Bobby Patel

Endodontic Diagnosis,
Pathology, and
Treatment Planning

Mastering
Clinical Practice

123
Endodontic Diagnosis, Pathology,
and Treatment Planning
Bobby Patel

Endodontic Diagnosis,
Pathology, and
Treatment Planning
Mastering Clinical Practice
Bobby Patel
Canberra, ACT
Australia

ISBN 978-3-319-15590-6 ISBN 978-3-319-15591-3 (eBook)

DOI 10.1007/978-3-319-15591-3

Library of Congress Control Number: 2015940815

Springer Cham Heidelberg New York Dordrecht London

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This book is dedicated to my endodontic mentor:
Ms Serpil Djemal
Preface

As both an undergraduate and postgraduate student, I was very much inter-

ested in evidence-based dentistry. Inherent questions would always be asked
as to ‘why is this practice best’ as opposed to the clinical adage of ‘it works
well in my hands so it must be good’. That is not to say that clinical experi-
ence and judgement are not important skills that we should all foster, but the
mastery of any subject must be accomplished at all levels. Endodontics, like
any discipline, has a multitude of research articles that are either evidence
based or practice related. The availability of evidence from the gold standard
double-blind randomized controlled trials (which yield the highest level of
evidence) is at best lacking. To attain excellence, one must gather the best
hierarchy of evidence available, with current clinical treatment strategies that
principally serve our patients.
The idea behind this clinical handbook was to provide both students and
dental practitioners a concise up-to-date book on both endodontic theories
and techniques. Emphasis is placed on presenting concepts based on current
literature that facilitate the process of applying knowledge to endodontic
clinical problems encountered within one’s daily practice. The core text is
supplemented with numerous figures, tables and photographs as well as
boxes highlighting relevant key text in a logical, systematic approach. Case
studies and clinical hints and tips are given at the end of some chapters in
order to further illustrate concepts described in the text. Although not intended
to provide a comprehensive review of the literature, this book is also intended
to stimulate the reader to read further regarding our current understanding
within endodontics. To aid the reader, a literature review has been provided
for each chapter, with a selective reference list of the classic and most current
references, where possible. In these various ways, the book serves as an edu-
cational repertoire for the clinician interested in the specialty of endodontics
and lifelong learning.
No student ever attains very eminent success by simply doing what is required of
him: it is the amount and excellence of what is over and above the required, that
determines the greatness of ultimate distinction. Charles Kendall Adams

Canberra, ACT, Australia Bobby Patel, BDS, MFDS, MClinDent,

MRD, MRACDS

vii
Acknowledgements

Firstly, I would like to thank my associate editor Antonia von Saint Paul and
project co-ordinator Wilma McHugh at Springer DE for bringing this project
to fruition. I would also like to express my deepest appreciation to Prakash
Jagannathan, Jayakumar Sendhilkumar and Nithyatharani Ramalingam who
were responsible for perfecting the language, design and layout of the book
and final copy-editing of the completed text. I also acknowledge Gursharan,
Girish, Rob, John and Tony Greenstein for allocating time out of their busy
schedules in order to contribute to their respective chapters and numerous
proof reads along the way.
I would like to acknowledge the staff (Lois, Kathleen, Julie, Jess, Jaimi,
Tiffany and Alana) and patients at Canberra Endodontics, who agreed to be
photographed for illustrative material; my wife Sarita, who has once again
supported me patiently while I compiled this book—she has been my inspira-
tion and motivation and has stood by me from the very beginning; and to my
three amazing children Raya, Sofia and Iyla for always making me smile and
for understanding on all those weekends when I was busy writing this book
instead of playing games. I hope that one day, you too follow your dreams
with hard work and conviction to make them a reality.

ix
Contents

1 Pain of Odontogenic and Non-odontogenic Origin. . . . . . . . . . 1

1.1 Overview of Orofacial Pain . . . . . . . . . . . . . . . . . . . . . . . . . 1
1.2 Odontogenic Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
1.3 Cervical Hypersensitivity . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
1.4 Traumatic Periodontitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
1.5 Myofacial Pain Syndrome. . . . . . . . . . . . . . . . . . . . . . . . . . . 9
1.6 Maxillary Sinusitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
1.7 Trigeminal Neuralgia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
1.8 Chronic Idiopathic Facial Pain . . . . . . . . . . . . . . . . . . . . . . . 15
1.9 Atypical Odontalgia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
1.10 Clinical Cases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16
1.10.1 Acute Exacerbation of Chronic Apical
Periodontitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16
1.10.2 Trigeminal Neuralgia . . . . . . . . . . . . . . . . . . . . . . . . 16
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18
2 Aetiology and Pathogenesis of Pulp Disease . . . . . . . . . . . . . . . 21
2.1 Overview of the Pulp–Dentine Complex . . . . . . . . . . . . . . . 21
2.2 Role of Bacteria in Peri-apical Disease . . . . . . . . . . . . . . . . 22
2.3 Route of Bacterial Entry into the Root Canal System . . . . . 22
2.4 The Spatial Distribution of Microflora Within
the Root Canal System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
2.5 Dentinal Tubule Invasion . . . . . . . . . . . . . . . . . . . . . . . . . . . 25
2.6 Fate of Bacteria Within the Root Canal System
and Their Interactions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
2.7 Provision of Nutrients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
2.8 Pathogenesis of Peri-apical Disease . . . . . . . . . . . . . . . . . . . 28
2.9 Biofilms and Endodontics . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
2.10 Microbiology of Intra-radicular Infections . . . . . . . . . . . . . . 29
2.11 Extra-radicular Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
2.12 Herpesvirus and Apical Periodontitis . . . . . . . . . . . . . . . . . . 30
2.13 Yeasts and Apical Periodontitis . . . . . . . . . . . . . . . . . . . . . . 31
2.14 Nonmicrobial Aetiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

xi
xii Contents

3 Classification of Pulpal and Peri-apical Disease . . . . . . . . . . . . 35

3.1 Diagnostic Terms for Pulpal and Peri-radicular
Health and Disease States . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
3.2 Clinically Normal Pulp . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36
3.3 Reversible Pulpitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
3.4 Irreversible Pulpitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38
3.5 Pulp Necrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38
3.6 Pulpless Tooth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
3.7 Degenerative Changes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
3.8 Normal Peri-radicular Tissues . . . . . . . . . . . . . . . . . . . . . . . 42
3.9 Acute Apical Periodontitis . . . . . . . . . . . . . . . . . . . . . . . . . . 42
3.10 Acute Apical Abscess . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
3.11 Chronic Apical Periodontitis. . . . . . . . . . . . . . . . . . . . . . . . . 43
3.12 Chronic Apical Periodontitis with Suppuration . . . . . . . . . . 44
3.13 Condensing Osteitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
4 Cystic and Non-cystic Lesions at the Peri-apex
of the Teeth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49
4.1 Overview of Peri-apical Pathologies in Endodontics . . . . . . 49
4.2 Differential Diagnosis of Radiolucent Lesions
of the Jaw . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53
4.3 Lesions of Endodontic Origin. . . . . . . . . . . . . . . . . . . . . . . . 53
4.4 Lesions of Non-endodontic Origin . . . . . . . . . . . . . . . . . . . . 56
4.5 Surgical Decompression . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58
4.6 Clinical Case . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
5 Ethics and Law. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65
5.1 Overview of Ethico-Legal Issues and Endodontics . . . . . . . 65
5.2 Negligence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
5.3 Dental Records . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
5.4 Informed Consent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
5.5 Referral for Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
5.6 Treatment Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72
6 Endodontic Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75
6.1 Overview of Infections of Endodontic
Origin and Management Thereof . . . . . . . . . . . . . . . . . . . . . 75
6.2 Facial and Neck Space Infections . . . . . . . . . . . . . . . . . . . . . 78
6.3 Management of Facial Cellulitis. . . . . . . . . . . . . . . . . . . . . . 84
6.4 Intra-oral Incision and Drainage . . . . . . . . . . . . . . . . . . . . . . 84
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
7 Infection Control in the Endodontic Office . . . . . . . . . . . . . . . . 87
7.1 Overview of Infection Control and Standard
Precautions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87
7.2 Hand Hygiene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90
7.3 Personal Protective Equipment . . . . . . . . . . . . . . . . . . . . . . . 91
7.4 Needlestick or Sharps Injury Prevention . . . . . . . . . . . . . . . 92
Contents xiii

7.5 Vaccination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
7.6 Cleaning, Disinfection and Sterilisation . . . . . . . . . . . . . . . . 94
7.7 Single-Use Endodontic Instruments
and Prion Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
8 Treatment Planning and the Decision-Making Process . . . . . . 103
8.1 Treatment Planning and the Decision-Making Process . . . . 103
8.2 Peri-Apical Pathology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106
8.3 Periodontal Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106
8.4 Restorative Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 108
8.5 Crown Lengthening. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
8.6 Alternative Prosthodontic Replacement Options . . . . . . . . . 110
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114
9 Endodontic Armamentarium . . . . . . . . . . . . . . . . . . . . . . . . . . . 117
9.1 Overview of Endodontic Instruments . . . . . . . . . . . . . . . . . . 117
9.2 Dental Magnification and Illumination. . . . . . . . . . . . . . . . . 121
9.3 Stainless Steel Instruments . . . . . . . . . . . . . . . . . . . . . . . . . . 123
9.4 Nickel–Titanium Alloy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
9.5 Engine-Driven Instruments . . . . . . . . . . . . . . . . . . . . . . . . . . 126
9.6 Sonic and Ultrasonic Instruments . . . . . . . . . . . . . . . . . . . . . 133
9.7 Microsurgical Instruments . . . . . . . . . . . . . . . . . . . . . . . . . . 134
9.8 Burs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
9.9 Instrument Packs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138
10 Antibiotics Use in Endodontics . . . . . . . . . . . . . . . . . . . . . . . . . . 141
10.1 The Role of Antibiotics in Endodontics . . . . . . . . . . . . . . . 141
10.2 Systemic Antibiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144
10.3 Local Adjunctive Antibiotics . . . . . . . . . . . . . . . . . . . . . . . 146
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147
11 Examination and Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
11.1 Overview of Endodontic Diagnosis . . . . . . . . . . . . . . . . . . 149
11.2 Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
11.3 Percussion and Palpation . . . . . . . . . . . . . . . . . . . . . . . . . . 153
11.4 Thermal Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155
11.5 Electric Pulp Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 158
12 Endodontic Radiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161
12.1 Overview of Radiology and Endodontics . . . . . . . . . . . . . . 162
12.2 Standard Equipment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 164
12.3 Plain Film Radiography . . . . . . . . . . . . . . . . . . . . . . . . . . . 166
12.4 Digital Radiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 170
12.5 Cone-Beam Computed Tomography . . . . . . . . . . . . . . . . . 172
12.6 The Tube Shift Technique. . . . . . . . . . . . . . . . . . . . . . . . . . 173
12.7 Differential Diagnosis of Radiolucent
and Radiopaque Lesions of the Jaw . . . . . . . . . . . . . . . . . . 175
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 176
xiv Contents

13 Anatomy and Root Canal Morphology . . . . . . . . . . . . . . . . . . . 179

13.1 Overview of Root Canal Anatomy . . . . . . . . . . . . . . . . . . . 179
13.2 Maxillary Central Incisor Teeth . . . . . . . . . . . . . . . . . . . . . 182
13.3 Maxillary Lateral Incisor Teeth. . . . . . . . . . . . . . . . . . . . . . 184
13.4 Maxillary Canine Teeth. . . . . . . . . . . . . . . . . . . . . . . . . . . . 184
13.5 Maxillary Premolar Teeth . . . . . . . . . . . . . . . . . . . . . . . . . . 186
13.6 Maxillary Molar Teeth . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188
13.7 Mandibular Incisor Teeth . . . . . . . . . . . . . . . . . . . . . . . . . . 191
13.8 Mandibular Canine Teeth . . . . . . . . . . . . . . . . . . . . . . . . . . 192
13.9 Mandibular Premolar Teeth . . . . . . . . . . . . . . . . . . . . . . . . 192
13.10 Mandibular Molar Teeth . . . . . . . . . . . . . . . . . . . . . . . . . . . 193
13.11 Incomplete Root Development . . . . . . . . . . . . . . . . . . . . . . 196
13.12 Dens Invaginatus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199
13.13 MB2 Canals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203
13.14 Middle Mesial Canals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 206
13.15 C-Shaped Canal Systems . . . . . . . . . . . . . . . . . . . . . . . . . . 207
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
14 Rubber Dam . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213
14.1 Overview of Rubber Dam Usage in Endodontics. . . . . . . . 213
14.2 Rubber Dam Armamentarium. . . . . . . . . . . . . . . . . . . . . . . 215
14.3 Clamp First Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 217
14.4 Bow First Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 218
14.5 Anterior Teeth Technique . . . . . . . . . . . . . . . . . . . . . . . . . . 218
14.6 Split/Slit Dam Technique . . . . . . . . . . . . . . . . . . . . . . . . . . 220
14.7 Latex Allergy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221
15 Analgesics, Anaesthetics, Anxiolytics
and Glucocorticosteroids Used in Endodontics. . . . . . . . . . . . . 223
15.1 Overview of Analgesics, Anaesthetics, Anxiolytics
and Glucocorticosteroids Used in Endodontics . . . . . . . . . 223
15.2 Analgesics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 226
15.3 Local Anaesthetic Solutions . . . . . . . . . . . . . . . . . . . . . . . . 227
15.4 Topical Anaesthesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230
15.5 Maxillary Infiltration and Blocks . . . . . . . . . . . . . . . . . . . . 230
15.6 Mandibular Infiltration and Blocks . . . . . . . . . . . . . . . . . . . 233
15.7 Supplemental Injections . . . . . . . . . . . . . . . . . . . . . . . . . . . 234
15.8 Delivery Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235
15.9 Anxiolytics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 236
15.10 Corticosteroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241
16 Endodontic–Periodontal Interrelationship . . . . . . . . . . . . . . . . 245
16.1 Overview of Endodontic–Periodontal Interrelationship . . . 246
16.2 Diagnosis of Endodontic–Periodontal Lesions. . . . . . . . . . 252
16.3 Management of True Combined
Endodontic–Periodontal Lesions . . . . . . . . . . . . . . . . . . . . 255
16.4 Craze Lines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
Contents xv

16.5 Fractured Cusp . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258

16.6 Cracked Tooth Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . 259
16.7 Vertical Root Fracture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261
16.8 Split Tooth. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261
16.9 Hemisection, Root Amputation and Root Resection . . . . . 262
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267
17 Orthodontic–Endodontic Interrelationship. . . . . . . . . . . . . . . . 271
17.1 Orthodontic Tooth Movement and Vital Teeth . . . . . . . . . . 271
17.2 Orthodontic Tooth Movement of Endodontically
Treated Teeth. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272
17.3 Factors Affecting Root Resorption During
Orthodontic Tooth Movement. . . . . . . . . . . . . . . . . . . . . . . 272
17.4 Management of Endodontic Procedures During
Orthodontic Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275
17.5 Orthodontics and Its Role in Trauma . . . . . . . . . . . . . . . . . 276
17.6 Effect of Orthognathic Surgery on Pulp Vitality. . . . . . . . . 277
17.7 Orthodontics to Aid Restorative Procedures. . . . . . . . . . . . 278
17.8 Clinical Cases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
17.8.1 Avulsion: Immediate Replantation Adult. . . . . . . . 278
17.8.2 Avulsion: Immediate Replantation Adult. . . . . . . . 279
17.8.3 Avulsion: Delayed Replantation Adolescent . . . . . 281
17.8.4 Avulsion: Delayed Replantation Adolescent . . . . . 283
17.8.5 Ankylosis: Late Adolescence . . . . . . . . . . . . . . . . . 283
17.8.6 Ankylosis: Preadolescence . . . . . . . . . . . . . . . . . . . 286
17.8.7 Lateral Luxation . . . . . . . . . . . . . . . . . . . . . . . . . . . 287
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 289
18 Systemic Diseases and Endodontics . . . . . . . . . . . . . . . . . . . . . . 293
18.1 Focal Infection Theory . . . . . . . . . . . . . . . . . . . . . . . . . . . . 293
18.2 Infective Endocarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 294
18.3 Prosthetic Joints . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 295
18.4 Irradiated Patients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297
18.5 Diabetes Mellitus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297
18.6 Osteoporosis and BRONJ . . . . . . . . . . . . . . . . . . . . . . . . . . 297
18.7 Bleeding Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 298
18.8 Cerebrovascular Accidents . . . . . . . . . . . . . . . . . . . . . . . . . 299
18.9 Respiratory Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 300
18.10 Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 300
18.11 Latex Allergy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301
18.12 Medical Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
Contributors

Sarita Atreya, BDS, MFDS RCS(ED) General Dental Practitioner,

Canberra, ACT, Australia
Ian Clarke, MBBS(Hons), FRCPA, MIAC, FASCP, IFCAP,
FAICD Capital Pathology, Canberra, ACT, Australia
Robert Fell, BDS, DClinDent, FRACDS, FRACDS Specialist
Periodontist, Canberra, ACT, Australia
Anthony Greenstein, BM, BS, MRCS, BDS, MFDS RCS (ED)
Oral & Maxillofacial Surgery, Pan Scotland Rotation, University
of Aberdeen School of Medicine and Dentistry, Aberdeen, UK
Gursharan K. Minhas, BDS, BSc, MSc, MFDS, MOrth, FDSOrth
The Royal Surrey County Hospital, Hampshire, UK
Hampshire Hospitals NHS Foundation Trust, Basingstoke, UK
John Mikhail Nakhla, B.Pharmacy Canberra, ACT, Australia
Girish Palnitkar, B Med Sc, MBBS, FANZCA Consultant Anesthetist
Canberra Hospital, Canberra, ACT, Australia
Bobby Patel, BDS, MFDS, MClinDent, MRD, MRACDS
Brindabella Specialist Centre, Canberra, ACT, Australia

xvii
 Pain of Odontogenic
and Non-odontogenic Origin 1

Summary
Patients can present with pain of odontogenic or non-odontogenic origin,
arising from the facial area, temporomandibular joints, ear, eyes, pharynx
and larynx. Often they may be complaining of pain from their teeth. The
dilemma the clinician faces is finding the correct origin of this pain whereby
an effective treatment will provide relief. Patients with neuropathic orofacial
pain may present to the clinician with a persistent, severe pain resulting in
multiple endodontic procedures being instigated or worse still extractions
recommended with no resolution of symptoms. The literature has demon-
strated that the incidence of pain following endodontic treatment is between
3 and 6 % in the absence of reliable clinical and/or radiographic evidence of
persisting disease. Management of orofacial pain is best by a multidisci-
plinary approach, and often the dentist is involved from the very beginning.
Where patient toothache symptoms are not reproducible or clinical signs do
not correlate, then a referral to an endodontist should be sought.

Clinical Relevance other potential causes of orofacial pain should be

The clinician must be able to differentiate and
accurately diagnose endodontic disease associ-
ated with both symptomatic and asymptomatic
teeth. A complete history recalled and recounted
by the patient combined with a careful clini-
cal and radiographic examination is the first
step in establishing a differential diagnosis.
The clinician must also have an understand-
ing of the pathways and mechanisms, possible
causes and different characters of orofacial pain
to be able to narrow this diagnosis to the prob-
able cause. Once odontogenic pain is excluded,
taken into consideration in order to arrive at the
likely diagnosis.
1.1 Overview of Orofacial Pain
The international association for the study of
pain defines pain as ‘an unpleasant sensory and
emotional experience associated with actual or
potential tissue damage, or described as such
damage’ [1]. Orofacial pain is defined as a term
referring to oral pain, dental pain and pain in the

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 1
DOI 10.1007/978-3-319-15591-3_1, © Springer International Publishing Switzerland 2015
2 1 Pain of Odontogenic and Non- odontogenic Origin

Table 1.1 Differential diagnosis for pain of dental origin Table 1.2 Differential diagnosis for pain of non-dental
origin
Origin Possible causes
Pulpal pain Dentine hypersensitivity Origin Possible causes
Dental caries Neurologic Trigeminal neuralgia
Defective restoration Glossopharyngeal neuralgia
Cracked tooth syndrome Post-herpetic neuralgia
Reversible pulpitis Bell’s palsy
Irreversible pulpitis Vascular Migraine
Pulp necrosis (partial) Cluster headaches
Periodontal pain Traumatic periodontitis Giant cell arteritis
Perio-endo lesion SUNCT
Endo-perio lesion Maxillary antrum Maxillary sinusitis
Combined endo-perio lesion Salivary glands Acute/chronic bacterial
Periodontal abscess sialadenitis
Gingival pain Gingivitis Sjogren’s syndrome
Acute necrotizing ulcerative Calculi causing duct stenosis
gingivitis or obstruction
Pericoronitis Soft tissue/oral Herpes zoster
mucosa Herpetic gingivostomatitis
Lichen planus
Mucous membrane pemphigoid Mucosal ulceration
Bone pain Acute alveolar osteitis (dry socket) Masticatory muscles/ Temporomandibular joint
jaws disorders
Ears/eyes/nose/lymph Otitis media
nodes Glaucoma
face above the neck, anterior to the ears and Psychogenic Chronic idiopathic facial pain
below the orbitomeatal line [2]. Although odon- Atypical odontalgia
togenic (dental) pain is the most commonly Burning mouth syndrome
reported form of orofacial pain when presenting
to the dentist, it should be recognised that this
symptom could be caused by painful disorders of The sensory innervation of teeth, terminating
non-odontogenic origin. Tables 1.1 and 1.2 and in the pulp–dentine complex, is made up of pre-
Fig. 1.1 provide a comprehensive list of possible dominantly A beta, A delta and C fibres. The A
diagnoses that need to be considered when deal- beta fibres are sensitive to mechanical (hydrody-
ing with a patient with orofacial pain. namic) stimulation of dentine. Myelinated A
Epidemiological studies show that the prevalence delta fibres, containing the neuropeptide calcito-
of orofacial pain in the population is between 14 nin gene-related peptide, are responsible for
and 19 % [3, 4]. A cross-sectional population strong, sharp, immediate well-localised pain.
study revealed that in the general population the Nonmyelinated, slow conducting C fibres,
prevalence of muscular-ligamentous/soft tissue responsive to inflammatory mediators, are
type of orofacial pain was 7 %, dentoalveolar responsible for dull, continuous and irradiating
7 % and neurological/vascular 6 % [5]. pain [8–10].
Pain management begins with developing an The hydrodynamic theory is the most acceptable
accurate differential diagnosis of dental pain based theory of pain transmission of pain stimuli through
on clinical signs and symptoms, special tests and the dentine [9]. According to this theory, pain pro-
radiographic findings. This is the critical first step in voked by stimuli is a consequence of fluid flow in
pain management and the clinical decision-making the dentinal tubules, stimulating mechanoreceptors
process allowing for an effective treatment that is (A beta fibres) leading to nerve impulses in the sub-
directed at treating the underlying disorder [6, 7]. odontoblastic plexus of Raschkow resulting in pain.
A detailed history of the patient is a prerequisite to The effect of thermal stimulus (hot or cold) is
establish a proper diagnosis (see Chap. 11). explained by the hydrodynamic theory in the
1.1 Overview of Orofacial Pain
a b
2 4
3 5
6
Fig. 1.1 (a) Diagrammatic representation and (b) lateral
skull x-ray demonstrating local and general causes of oro-
facial pain. (1) Eyes, (2) nose and sinuses, (3) oral, (4)
ears, (5) pharynx, (6) jaws and temporomandibular joints,
(7) psychogenic, (8) vascular, (9) neurological and (10)
referred pain from other sites. There are a multitude of
following way; application of hot stimuli on the
exposed dentine leads to expansion of fluid, whereas
cold application causes its contraction. This fluid
flow results in activation of mechanoreceptors of
the sensory nerves. Chemical stimuli applied (sweet
and salty foods) also lead to a faster flow of dentinal
fluid to the surface of teeth. This is due to the low
concentration of dentinal fluid and due to its lower
osmolarity causing fluid flow towards a higher con-
centration of liquids [11–13].
We can classify pulpal disease according to
several conditions: a healthy pulp; an inflamed
pulp, which has the capability of reversal (revers-
ible pulpitis); an inflamed pulp without the pos-
sibility of recovery (irreversible pulpitis); and
pulp necrosis [14, 15].
Dentine hypersensitivity is a direct conse-
quence of exposed dentine reacting to thermal
osmotic, chemical and tactile stimuli. The
diagnosis is made on symptoms eliciting a sharp
pain of short duration in the absence of any pulpal
pathology (based on clinical and radiographic
signs). Risk factors that contribute to developing
dentinal sensitivity include erosion, abrasion,
attrition, gingival recession, previous periodontal
3
7
9
2
10
non-odontogenic pains that can present at the site of a
tooth and can mimic a toothache. As a clinician, we
should also have an understanding of the complex mecha-
nism of odontogenic pain and the manner in which other
orofacial structures may simulate dental pain
treatment and anatomical defects. Management
strategies involve therapies aimed to reduce den-
tinal fluid flow (resin application to exposed den-
tinal tubules) or reduce dentinal neuron activity
(use of desensitising agents such as potassium
nitrate, strontium chloride, fluoride containing
medicaments and guanethidine) [16–21].
Reversible pulpitis indicates that the pulp is
vital with some areas of inflammation that has the
potential to heal provided the stimulus/irritant
has been removed. Symptoms can range from
none at all to intense sharp sensations often asso-
ciated with thermal stimulus [22].
In irreversible pulpitis, the pulp, although
vital, is severely inflamed and healing is an
unlikely event when steps are taken to try and
conservatively manage the pulp [23]. Symptoms
vary greatly with some patients complaining of
moderate to severe pain exacerbated with thermal
stimulus whilst others remain asymptomatic.
Indeed pulpitis may proceed to pulpal necrosis
without any symptoms at all [24]. Studies have
shown that there is a poor correlation between
clinical pain symptoms and the histopathological
status of the pulp [25].
4 1
Finally when the inflammation from the pulp
reaches the peri-radicular tissues, the patient is
usually able to locate the tooth responsible
(symptomatic periodontitis) and/or the clinician
is able to demonstrate by clinical and radio-
graphic examinations. Allodynia (a reduction in
pain threshold whereby a normal non-noxious
stimulus is perceived as pain) and hyperalgesia
(an increase in the magnitude of pain perception,
so that a previously painful stimulus is now per-
ceived as having a larger magnitude of perceived
pain) are symptoms of endodontic disease.
Inflammatory mediators are responsible for acti-
vation and sensitisation of nociceptors (a sensory
receptor that is capable of transducing and encod-
ing noxious stimuli) both peripherally and cen-
trally. This phenomenon can explain why some
patients experience pain postoperatively and is an
indicator that patients who experience preopera-
tive pain are more likely peri-operatively and
post treatment. Patients will often report mechan-
ical and thermal (heat or cold) hyperalgesia and
mechanical allodynia in relation to pulpal symp-
toms preoperatively. Examples include percus-
sion tenderness to a mirror handle that is not
painful when demonstrated on a control tooth but
obviously painful with a tooth that has pathology
of endodontic origin. Clinical pain is not simply
the consequence of a ‘switching on’ of the ‘pain
system’ in the periphery by a particular pathol-
ogy, but instead reflects the state of excitability of
central nociceptive circuits whose sensitivity can
be shifted by normal innocuous inputs [26–28].
In referred pain, the region of the body where
the pain is perceived is not the same as where the
pain originates. Clinically this type of pain is a
diagnostic challenge since effective treatment
needs to be directed at the cause, not the site. The
reasons behind referred pain are due to central
sensitisation and convergence of primary afferent
nerve fibres onto the same projection neurons
[29]. Afferent sensory nerve neurons have periph-
eral terminals that innervate different tissues, yet
their central terminals converge onto the same
second-order projection neuron located in the tri-
geminal nuclear complex. Examples in endodon-
tics include scenarios where the patient is
experiencing pulpitis on the right side and
Pain of Odontogenic and Non- odontogenic Origin
believes it is coming from the maxilla when it in
fact originates in the mandible. Another example
is when there is maxillary sinusitis and pain is
referred to the maxillary teeth on the affected
side. The condition of referred pain is a diagnos-
tic challenge whereby pain of non-odontogenic
origin can result in radiation of pain to distant
sites such as teeth. A typical example is a patient
suffering from myofacial pain who often com-
plains of a dull ache in their mandibular posterior
teeth. There are a multitude of non-odontogenic
pains that can present at the site of a tooth and
can mimic a toothache. Dental practitioners
should have an understanding of the complex
mechanism of odontogenic pain and the manner
in which other orofacial structures may simulate
dental pain. Failure to establish the aetiology of
the pain will result in incorrect diagnosis and
inappropriate treatment [30].
The International Association for the Study of
Pain (IASP) defines acute maxillary sinusitis as
‘constant burning pain with zygomatic and dental
tenderness from the inflammation of the maxil-
lary sinus’ [1]. In chronic cases, there may be no
pain or just occasional mild diffuse discomfort.
Aetiology is either bacterial or the more common
form due to allergies. The pain can be triggered
by bending forward, touching the area or pain on
biting associated with the upper teeth. Headache
is located over the antral area. Diagnosis can be
confirmed by maxillary sinus imaging revealing
fluid accumulation within the affected sinus.
Periapical periodontitis may result in maxillary
sinusitis of dental origin with resultant thicken-
ing and inflammation of the mucosal lining of the
sinus in areas adjacent to the involved teeth. In
cases of sinusitis of dental origin, conventional
endodontic treatment or re-treatment is the treat-
ment of choice [31]. Antibiotic therapy and the
use of nasal decongestants and analgesics are
indicated for the treatment of sinusitis or where
the sinus has been breached from nonsurgical or
surgical endodontics [32].
Temporomandibular disorder (TMD) is an
umbrella term associated with myofacial pain,
mandibular dysfunction, facial arthromyalgia and
masticatory myalgia. It encompasses pain related
to the masticatory muscles, the temporomandibular
1.1 Overview of Orofacial Pain
joint (TMJ) or both. Risk factors include female
gender, depression and multiple pain conditions
often suffering from chronic pain [33]. The rela-
tionship between TMD pain and clenching habit
or bruxism is controversial. One systematic
review showed no association between malocclu-
sion, functional occlusion and TMD in a
community-based population [34]. Management
strategies include conservative therapies such as
provision of information and reassurance, psy-
chological strategies, behavioural changes, pos-
ture training, thermal application and mechanical
exercises. Stabilisation splint therapy, which is
worn at night, prevents clenching and/or grinding
(parafunctional habits). Some appliances are
designed to realign the maxilla–mandible rela-
tionship. The devices are made of either soft plas-
tic or hard acrylic. Evidence for their efficacy has
not yet been proven. A number of medical thera-
pies involving a range of drugs from analgesics to
antidepressants are also available. Surgical proce-
dures including arthrocentesis and arthroscopy
have been advocated when there are functional
signs [35].
Trigeminal neuralgia (TN) is defined by the
International Association for the Study of Pain
(ISAP) as a ‘sudden and usually unilateral severe
brief stabbing recurrent pain in the distribution of
one or more branches of the fifth cranial nerve’
[1]. Trigeminal neuralgia presents with sharp,
shooting, unbearable pain in the distribution of
one or more branches of the trigeminal nerve, of
moderate to intense severity, lasting seconds. It is
precipitated by light touch, but may be spontane-
ous, and there are often associated trigger points.
These trigger points often present around the
teeth resulting in irreversible dental procedures
carried out unnecessarily [36]. Patients may have
periods of remission lasting days, weeks or lon-
ger. Symptomatic causes of trigeminal neuralgia
need to be excluded such as tumours, multiple
sclerosis and arteriovenous malformations [37].
Management includes medical with carbamaze-
pine or surgery (microvascular decompression,
ablative procedures and Gamma Knife) [37–39].
Atypical odontalgia clinically can present
with persistent pain, often commencing in con-
junction with some form of invasive dental
5
treatment such as root canal therapy, apicecto-
mies or history of multiple extractions. This typi-
cal presentation with no change in pain and no
obvious cause should alert the clinician to a neu-
ropathic cause. The pain is described as being
dull and throbbing in nature, often continuous,
which can be sharp at times. It can be light touch
provoked with features of allodynia at the pain
site. No clinical, laboratory or radiographic find-
ings demonstrate relevant abnormality [40, 41].
Chronic (persistent) idiopathic facial pain
(CIFP), previously atypical facial pain, is persis-
tent facial pain, which is poorly understood. The
diagnosis is often made when all other causes of
facial pain have been excluded. The pain is
described as aching, dull, nagging, sometimes
throbbing, sharp or stabbing. The pain is often
constant (mild to severe) with varying intensity
but not unbearable. The site of pain varies often
not following a neurological distribution. All
investigations are normal and patients are likely
to be suffering from other chronic pain condi-
tions elsewhere. A multidisciplinary approach
has been recommended using a combination of
drugs (antidepressants) and cognitive-behavioural
therapies [42, 43].
A recent systematic review found the preva-
lence of persistent pain after endodontic treat-
ment to be 5.3 %. Non-odontogenic pain is not
an uncommon outcome after root canal therapy
and may represent half of all cases of persistent
tooth pain. These findings have implications for
the diagnosis and treatment of painful teeth that
were previously root canal treated because ther-
apy directed at the tooth in question would not
be expected to resolve non-odontogenic pain
[44, 45].
Orofacial pain, its diagnosis and initial man-
agement fall between dentists and doctors and in
the secondary care sector among pain physicians,
headache neurologists and oral physicians.
Management of neuropathic pain is by accepted
pharmacotherapy with psychological support.
Facial pain patients should be managed in a mul-
tidisciplinary team [46].
Clinicians should always remember the old
saying ‘if you hear hoof beats, think of horses,
not zebras’. When a patient presents with a
6 1
disease, good diagnostic judgement should be
based on the most frequent cause of this pain, not
the obscure, seldom seen disease. A logical diag-
nosis can only be achieved through careful his-
tory taking and clinical assessment incorporating
diagnostic tests that will either confirm or dis-
prove your initial thoughts. As dentists we are
very good at diagnosing dental pain but should be
careful when contemplating irreversible treat-
ments in a patient based on symptomology with-
out clinical signs and radiographic findings which
would validate a correct course of action [47].
1.2 Odontogenic Pain
Odontogenic pain can originate from either
pulpal or periodontal tissue (see Fig. 1.2).
Although the mechanisms for pulpal and peri-
odontal pain are of inflammatory in origin, each
pain is perceived differently. Periodontal pain is
often well localised (due to proprioceptors pres-
ent in the periodontal ligament) and the patient
can usually point to the tooth, whereas pulpal
pain is poorly localised and may be referred to
another tooth (on the same side of the arch or the
opposite arch on the same side) or another region
of the jaw or face (sinuses, angle/ramus of man-
dible, ears, etc.). Pulpitis can be divided into two
categories: reversible and irreversible.
Reversible and irreversible pulpitis
Reversible pulpitis indicates that pulpal tis-
sues can repair once the noxious irritant has been
removed. It is often characterised by a short,
a b
Fig. 1.2 Diagrams showing the common causes of odon-
togenic pain. (a) Teeth, (b) bone, (c) periodontal and (d)
soft tissues. Common features of odontogenic pain include
Pain of Odontogenic and Non- odontogenic Origin
sharp pain upon provocation and does not occur
spontaneously. Irreversible pulpitis has a pro-
longed duration of pain when stimulated but may
also occur spontaneously. There is not usually
sensitivity to percussion until the inflammatory
process has reached the peri-apex of the tooth).
Necrotic pulp
A necrotic pulp can be completely asymptom-
atic or extremely painful. The tooth will not usually
respond to thermal stimulus such as cold or vitality
pulp testing (electric pulp testing). Occasionally
sensitivity testing may give a false positive result in
multi-rooted teeth where one canal is diseased
whilst the others remain vital. If the inflammation
has spread to the peri-apex of the tooth, then
extreme sensitivity to percussion can occur.
Periodontal pain may occur as a result of end-
odontic disease (primary endodontic), periodon-
tal disease (primary periodontal) or a combination
of both.
Acute apical periodontitis
Inflammation, as a direct consequence to irre-
versible pulpitis or a necrotic pulp, localises in
the apical periodontal ligament. The tooth
becomes sensitive to percussion and/or biting and
may be mobile.
Acute apical abscess
In this situation the inflammation, often a pro-
gression from a necrotic canal or sequelae to irre-
versible pulpitis, can result in spreading of
bacteria into the surrounding alveolar bone (oste-
itis) and beyond into the fascial planes of the soft
tissues (cellulitis). The host defence attempts to
counteract this foreign invasion by the release of
c d
the presence of aetiologic factors of an odontogenic origin
(e.g. caries, leakage of restorations, trauma, fracture, peri-
odontal disease, bone infection, soft tissue lesion)
1.3 Cervical Hypersensitivity 7

polymorphonuclear leukocytes resulting in
destruction of bacteria and formation of pus. Pain
associated with an abscess will be intense due to
a build-up of pus and confinement to bone result-
ing in pain as the pressure increases. The abscess
will try to find the pathway of least resistance as
the pressure continues to intensify as more and
more dead bacteria and host cells collect at the
zone of defence between bacteria and host.
Occasionally due to extensive bone loss, the cor-
tical plate is no longer intact allowing the abscess
to escape through a fistula or sinus. Sometimes
the abscess may drain through a narrow pocket
beside the tooth. Often we can provide effective
relief for the patient by incision and drainage
when the abscess is a fluctuant swelling beneath
the underlying mucosa. The cardinal signs of
acute inflammation such as pain, swelling, heat
and redness accompany an abscess as a result of
the inflammatory process.
Acute periodontal abscess
In this situation, the acute infection is a direct
result of an abscess within the soft tissue wall of
an existing periodontal pocket. The abscess will
often be well localised with moderate accompa-
nying pain and throbbing. The area may result in
a localised swelling as the abscess develops
resulting in fluid accumulation within the peri-
odontal ligament space causing the offending
tooth site to become more sensitive when chew-
ing/biting and with increased mobility. The over-
lying gingival tissues will appear swollen, and
the patient may have accompanying fever and
lymphadenopathy. Management of a periodontal
abscess is by providing effective drainage and
nonsurgical debridement of the pocket with
curettes and irrigation. Systemic antibiotics are
not usually indicated.
1.3 Cervical Hypersensitivity
In the absence of inflammation, dentine sensitiv-
ity is the mildest form of pulp irritation and is
completely reversible. The mechanism of dentine
sensitivity involves fluid flow in the dentinal
tubules that stretches or compresses the nerve
endings that pass alongside the tubular exten-
sions of the pulp odontoblasts (Fig. 1.3).
Aetiology
Dentinal sensitivity may develop when den-
tine is exposed as a result of dental caries or tooth
fracture (cracked tooth syndrome). A recently
placed restoration with marginal leakage or a
defective restoration, gingival recession, recent
periodontal treatment (nonsurgical and surgical)
and tooth surface loss (attrition, erosion and abra-
sion) can all result in dentine sensitivity.

a b

D DT O

OP

P P

EC

Fig. 1.3 Diagrams representing (a) typical tooth with exposed cementum (EC) and (b) odontoblast (O) and odonto-
blastic process (OP) within the dentinal tubule (DT). Note: intimate relationship between odontoblast and pulp (P)
8 1
The nerves in these exposed tubules respond
not only to heat and cold and sweet and sour but
also to scratching with an instrument or a finger-
nail and to tooth brushing. For this reason,
patients often avoid brushing the area. The subse-
quent plaque accumulation further aggravates the
situation.
Medical history may reveal a history of gastric
oesophageal reflux as a result of hiatus hernia or
eating disorders such as anorexia nervosa/
bulimia.
Signs and symptoms
There may be evidence of gingival recession,
caries, a fractured or leaking restoration or tooth
surface loss. The patient will often describe an
intense, sharp pain related to hot, cold or sweet
stimulus. The pain is never spontaneous, well
localised following application of the stimulus
and immediate relief following removal.
Diagnostic tests
The offending tooth is identified by applica-
tion of thermal stimulus (CO2 snow, ethyl chlo-
ride, cold air, hot gutta-percha or heat applicator).
Pulpal sensibility testing will be normal.
Management
Various treatment modalities exist for the
treatment of dentine sensitivity, and the aim is to
directly treat the cause or reduce fluid flow or
dentinal neuron activity. Prevention is aimed at
identifying and modifying potential risk factors
such as diet (excessive citrus fruit) or medical
history (excessive gastric acid production), which
contributes to exposed dentinal tubules. Brushing
habits need to be modified (modified Bass
technique) to reduce further gingival recession.
A fluoride mouth rinse can be used on a daily
basis (0.05 %).
Sealing dentinal tubules that terminate at the
cementum but become exposed to the oral envi-
ronment following periodontal surgery or due to
gingival recession may be accomplished by
applying potassium oxalate or strontium chlo-
ride, fluorides, or dentine-bonding agents.
Toothpastes that contain 5 % potassium nitrate do
not block the tubules but ‘numb’ the nerve end-
ings (Sensodyne). Although the fluid still flows in
the tubules, the nerves are ‘unexcitable’.
Pain of Odontogenic and Non- odontogenic Origin
An insulating cement base under amalgam
fillings will prevent the heat or cold irritating the
pulp. Eventually, irritation dentine (reparative
dentine) will build up to protect the pulp from
thermal shock.
Marginal microleakage around restorations may
also lead to hypersensitivity owing to bacterial
invasion and irritation. In the past cavity varnishes
were placed around newly placed amalgam resto-
rations to minimise microleakage and postopera-
tive sensitivity. Removal of the smear layer before
placing a restoration and coating the exposed den-
tine with a dentine-bonding agent serves to protect
the tubule opened during preparation and even acts
as insulation in place of a cement base.
1.4 Traumatic Periodontitis
This is inflammation of the periodontium and
injury to the underlying attachment apparatus
(occlusal trauma) due to excessive occlusal force.
Primary occlusal trauma is an injury resulting
from excessive occlusal forces applied to a tooth
or teeth with normal support. Examples include
high restorations, bruxism, recent fitting of a new
partial denture and excessive loading during orth-
odontic movement. Secondary occlusal trauma is
an injury resulting from normal occlusal forces
applied to a tooth or teeth with inadequate peri-
odontal support. Combined occlusal trauma is an
injury from an excessive occlusal force on a dis-
eased periodontium. In this case, there is gingival
inflammation and some pocket formation, and
the excessive occlusal forces are generally from
parafunctional movements.
Examination
Clinical signs and symptoms include progres-
sive mobility, pain on biting/chewing or percus-
sion, fremitus and occlusal premature contacts or
discrepancies. Teeth may be fractured or chipped.
Radiographic examination may reveal a wid-
ened periodontal ligament space. Bone loss (fur-
cal, infrabony vertical or circumferential) may be
evident. Characteristically bilateral infrabony
defects would be indicative of occlusal trauma as
opposed to periodontal disease.
1.5 Myofacial Pain Syndrome
Management
In a healthy dentition with no pre-existing
periodontal disease or reduced periodontal sup-
port (primary occlusal trauma), traumatic occlu-
sion can lead to hypermobility of some teeth. If
hypermobility, radiological widening of peri-
odontal ligament space or pronounced cervical
abfraction is found, the occlusion should be ana-
lysed and corrected.
In cases of a healthy dentition with no pre-
existing periodontal disease but reduced periodon-
tal support (secondary occlusal trauma), increased
mobility may also be reduced by occlusal adjust-
ment. Splinting of teeth may be indicated in those
cases where hypermobility is resulting in pain for
the patient.
In cases of combined occlusal trauma, treat-
ing the inflammation is of primary importance
and should be the first step in treatment plan-
ning. Premature contacts may play a role in
the progression of periodontitis. A simple cor-
rection of the occlusion, if necessary, should
be included in the initial phase of periodontal
treatment. This results in less attachment loss
during periodontal treatment and may contrib-
ute to better healing of the periodontal
tissues.
a b
Fig. 1.4 Diagrams showing (a) the temporalis muscles of mastication involved in elevation of mandible during mouth
closing and (b) referred pain pattern to the upper teeth and jaws and head
9
1.5 Myofacial Pain Syndrome
Temporomandibular disorders (TMD) encom-
pass pain affecting the masticatory muscles and/
or temporomandibular joints (TMJs). TMD has
been identified as a major cause of non-dental
orofacial pain. TMJ evaluation is based on joint
range of movements, pain on palpation and pres-
ence of joint sounds during mandibular and jaw
opening movements. Movement of the TMJ is
achieved by the muscles of mastication (Fig. 1.4).
Masseter, medial pterygoid and temporalis mus-
cles are associated with the elevation of the man-
dible (mouth closing). The digastric muscles are
involved in mandibular depression (mouth open-
ing). The inferior lateral pterygoid muscle is
involved in protrusion of the mandible, and the
superior lateral pterygoid muscle provides stabil-
ity for the condyle and disc during function.
Aetiology
Factors associated with TMD include trauma,
anatomical factors, pathophysiological factors
and psychosocial factors.
Physical trauma such as a direct blow to the
TMJ can result in injury and loss of function.
Parafunctional habits such as teeth clenching, tooth
grinding, lip biting and abnormal jaw posturing
10
a b
Fig. 1.5 Diagrams representing (a) superficial masseter muscles, (b) deep masseter muscle and (c) referred pain pat-
tern. Note: superficial (yellow) and deep (orange) muscles
a b
Fig. 1.6 Diagrams representing (a) lateral pterygoid, (b) medial pterygoid and (c) referred pain pattern. Note: lateral
pterygoid (orange) and medial pterygoid (yellow)
may exacerbate underlying TMD. Nocturnal brux-
ism may be exacerbated by stress, anxiety, sleep
disorders and medications. An indication of noctur-
nal bruxism is severity of dental attrition (Fig. 1.5).
The contribution of occlusion in the aetiology
of TMD is controversial, and the literature does
not support this view. Previously occlusal fea-
tures such as working and nonworking side inter-
ferences and discrepancies between retruded
contact position (RCP) and intercuspal position
(ICP) have been associated with TMD. As a
result, the management of TMD by direct occlu-
sal adjustment is no longer acceptable, and the
age-old concept of providing an ideal occlusion
to prevent TMD is based without scientific evi-
dence (Fig. 1.6).
Examination
The examination process includes a detailed
clinical history and a comprehensive physical
1 Pain of Odontogenic and Non- odontogenic Origin
c
c
examination. The patient may reveal some his-
tory of anxiety, depression or other chronic pain
conditions, which are associated with patients
suffering from TMD.
The patient may complain of unilateral or
bilateral dull pain within the TMJ and/or sur-
rounding muscles, occasionally on waking or
during eating or speaking. Referred pain causing
headaches, facial pain and neck pain may be a
common complaint.
TMJ tenderness is assessed by bimanual pal-
pation of the TMJs (by pressing on the lateral
aspect of the joint) and intra-auricular palpation
(by placing the little finger in the external auditory
meatus and gently pressing forwards) (Fig. 1.7).
TMJ sounds are checked during mouth open-
ing and mandibular excursions. Clicks are a result
of sudden movement of the disc relative to the
condyle (disc displacement with reduction).
1.5 Myofacial Pain Syndrome 11

a b

c d

Fig. 1.7 Clinical photographs demonstrating (a) intra-oral palpation of masseter muscle, (b) bimanual temporoman-
dibular joint palpation, (c) flat palpation of masseter and (d) flat palpation of the temporalis muscle

Clicks can be classified as early (early part of jaw
opening), late (indicating greater disc displace-
ment) and reciprocal (on opening and closing).
Crepitus (prolonged, continuous grating sound)
would indicate acute inflammation (recent
trauma) or degenerative disease.
Locking of the TMJ, due to malposition and
distortion of the disc, which is responsible for
condylar rotation, may be present. A closed lock
would be indicative of a disc displacement with-
out reduction.
Muscle palpation is carried out bimanually in a
relaxed position by pincer palpation (Fig. 1.7).
The three portions of the temporalis (anterior, pos-
terior and medial), superficial and deep masseter
as well as the insertion of the medial pterygoid
muscle are examined for any tenderness or pain.
The range of jaw movements is examined with
maximum pain-free jaw opening noted. Normal
maximal opening ranges from 45 to 55 mm
(Fig. 1.8). Any trismus (inability to open the
mouth) is noted. Centric relation (retruded con-
tact position (RCP) and intercuspal position
(ICP)) and lateral excursion movements and pro-
trusion are performed to assess mandibular devi-
ation or deflection.
Parafunctional habits are assessed by evidence
of scalloping of the lateral border of the tongue,
buccal mucosa ridging, tooth wear, occlusal wear
faceting, fractured restorations, dentine exposure
and dentine sensitivity.
Management
Patient education and self-care including any
parafunctional habits that have been identified and
methods of limiting and modification of these hab-
its by awareness and change are recommended.
The patient is instructed as to modifying behav-
iours such as avoiding gum chewing and yawning.
Heat therapy and warm compression packs are
indicated to provide relief of inflammation. Stress
12 1 Pain of Odontogenic and Non- odontogenic Origin

a b

c d

Fig. 1.8 Clinical photographs showing (a) measurement of interincisal distance, (b) RCP and ICP discrepancies (c) and (d)
lateral excursion movement

management may be indicated and patients may
need to seek counsel for therapy.
Pharmacological management includes use of
nonsteroidal anti-inflammatory analgesics, corti-
costeroids (intracapsular), anxiolytics (benzodi-
azepines), muscle relaxants and tricyclic
antidepressants (amitriptyline).
Physical therapy including posture-training exer-
cises to re-establish coordinated, rhythmic muscle
function, isotonic exercises to increase range of
motion and isometric exercises to increase muscle
strength are beneficial. Transcutaneous electrical
nerve stimulation (TENS) and electro-galvanic stim-
ulation (EGC) have shown some benefits.
Orthopaedic appliance therapy using inter-
occlusal splints, bite guards, night guards or brux-
ism appliances has been shown to provide some
benefit. Removable acrylic resin appliances that
cover the teeth have been used to alter the occlusal
relationship, redistribute occlusal forces, prevent
wear and reduce bruxism and parafunction.
Surgery such as arthrocentesis (intra-articular
irrigation of the TMJ with or without corticoste-
roid), arthroscopy and arthrotomy (open surgical
intervention of the TMJ) has been used with
some degree of success for cases that do not
respond to conservative and pharmacological
therapies.
1.6 Maxillary Sinusitis
Maxillary sinusitis causes a constant, boring pain
with zygomatic and dental tenderness from the
inflammation of the maxillary sinus usually as a
result of bacterial infection.
Aetiology
Predisposing factors include oral antral communi-
cation during tooth extraction, oral antral fistula, peri-
radicular infection, radicular cysts, foreign body within
the sinus (root canal materials/medicaments) and
patients suffering from recent colds or cystic fibrosis
1.6 Maxillary Sinusitis
a c
MS
b
R L
MS
Fig. 1.9 Diagram (a) showing lateral view of skull and
relationship of maxillary sinus (MS) with apices of poste-
rior molar teeth and image (b) showing a cross-sectional
CT image with complete opacification of the left maxillary
sinus with thickening of the bony margins. This finding
would be consistent with chronic sinusitis. (c) The roots of
patients with impaired drainage. Bacterial causes often
from respiratory tract infections include Haemophilus
influenzae, Streptococcus, Staphylococcus aureus,
alpha-haemolytic streptococcus and Pseudomonas
species.
The fungus Aspergillus fumigatus has been
associated with overfilled root canal medica-
ment/zinc oxide eugenol sealers in the sinus.
Examination
The patient may have a history of recent end-
odontic treatment, possible peri-apical infection
of an upper posterior tooth, history of recent
tooth extraction or cold.
A pain history of unilateral, dull, throbbing, con-
tinuous ache affecting the upper jaw and upper pos-
terior teeth and possible radiation to the eye is often
described. Pain may be worse in the evening, when
lying down or when bending. The affected side may
result in nasal discharge with possible mucopuru-
lent rhinorrhoea and fullness of the cheek. A number
13
Maxillary sinus
the maxillary molars are often in intimate contact with the
floor of the maxillary sinus and may be separated from the
sinus by only the sinus lining and a very thin layer of lam-
ina bone or in some cases no bone at all. Consequently
endodontic infections can cause sinus problems, and inde-
pendent sinus infections can cause referred pain to teeth
of posterior teeth may be tender to percussion, but
vitality testing will be normal (Fig. 1.9).
Radiographic examination of the sinuses
(occipitomental views 0 and 30°) may reveal
abnormal fluid accumulation or thickening of the
antral lining.
Management
If an endodontic cause is suspected such as peri-
apical pathology, then endodontic treatment or
extraction is indicated. If a non-dental cause is sus-
pected and first-line treatment does not appear to be
effective, then referral to ENT may be indicated.
Extrusion or inadvertent injection of sodium
hypochlorite into the sinus will result in acute
pain and swelling in the area requiring appropri-
ate medications such as steroids, analgesics and
antibiotics. The patient will need to be followed
up for risk of swelling, oedema, ecchymosis, tis-
sue necrosis, paraesthesia and scarring in the
area. Most cases should heal uneventfully.
14
a b
V1 Ocular division
V2 Maxillary
division
V3 Mandibular
division
Fig. 1.10 (a) Diagrammatic representation of trigeminal
nerve and its innervation of the face. (b) Note: V1
Ophthalmic branch supplying eye, eyebrow, forehead and
frontal portion of scalp. V2 Maxillary branch supplying
upper lip, maxillary teeth, gingivae, cheek, lower eyelid
and side of the nose. V3 Mandibular branch supplying
lower lip, mandibular teeth, gingivae and side of tongue.
Also covers a narrow area that extends from the lower jaw
in front of the ear to the side of the head. Trigeminal
Care must be taken during endodontic surgery
of maxillary premolar and molar teeth whose
roots may lie in close proximity to the sinus.
Inadvertent dislodgement of either resection
material, infected apical tissue or root tip into the
sinus would require appropriate referral for
retrieval using a Caldwell–Luc procedure.
Overfilled root canal medicaments/obturation
material can cause a persistent sinus infection
requiring either removal of the material or the
tooth. A specialist referral to ENT/Maxillofacial
surgery may be warranted.
Antibiotics such as amoxicillin, a nasal decon-
gestant (ephedrine nasal drops 0.5 %), inhalants
(Karvol inhalant capsule) and analgesics may be
prescribed to provide relief of symptoms.
1.7 Trigeminal Neuralgia
Trigeminal neuralgia is a sudden, very severe,
recurrent stabbing pain in the distribution of the
trigeminal nerve lasting from a few seconds to 2
minutes. Trigger points often evoke pain.
1 Pain of Odontogenic and Non- odontogenic Origin
Trigeminal
ganglion
V1
V2
Brainstem
V3
neuralgia (TN), also called tic douloureux, is a chronic
pain condition that affects the trigeminal or fifth cranial
nerve, one of the largest nerves in the head. The disorder
causes extreme, sporadic, sudden burning or shock-like
face pain that lasts anywhere from a few seconds to as
long as 2 min/episode. These attacks can occur in quick
succession. The intensity of pain can be physically and
mentally incapacitating
Aetiology
Eighty to ninety percent of cases are classified
as idiopathic and are caused by vascular com-
pression of the trigeminal ganglion close to its
exit from the brainstem by an aberrant loop of
artery or vein. Other causes (less than 10%)
include vascular compression due to a tumour or
cyst. One to five percent of patients with multiple
sclerosis develop trigeminal neuralgia (Fig. 1.10).
Examination
Patients will complain of unbearable, excruciat-
ing, short-lasting, electric-shock-type stabbing
pain affecting a particular site. Often a trigger zone
may be present along the distribution of the trigem-
inal nerve (most commonly second and third divi-
sions). Light touch of the trigger zone will induce
severe pain. Patients often avoid shaving or touch-
ing the area of the face where the trigger point lies
for fear of inducing an attack. Speech or swallow-
ing may be affected if the trigger zone involves the
mouth. The pain of trigeminal neuralgia never
crosses the midline. Pain of trigeminal neuralgia
will occur with periods of daily occurrence, then
periods of remission lasting days, weeks or months.
1.9 Atypical Odontalgia
Patients may present with spasmodic contrac-
tions of face muscles due to the pain of trigemi-
nal neuralgia (tic douloureux).
Management
The patient should be referred for specialist
care (oral medicine/oral maxillofacial surgeon/
neurologist) for appropriate management. Since
5–10% of cases carry the risk of tumours, the
patient will require further investigations such as
magnetic resonance imaging techniques to rule
out underlying pathology.
Several Cochrane systematic reviews have
shown the most effective medical treatment of
trigeminal neuralgia is with carbamazepine
(Tegretol®). The dosage is gradually titrated to a
therapeutic level that provides relief for the
patient (maximum maintenance dose 600–
1,200 mg/day divided dose regime). Phenytoin is
a second-line drug which is not as effective as
carbamazepine for the treatment of trigeminal
neuralgia.
Surgical management includes alcohol blocks,
neurectomy, radiofrequency gangliolysis, cryo-
surgery of the peripheral nerve as it exits from the
foramen and microvascular compression. The
risks associated with the surgical options must be
outweighed with the benefits and have associated
morbidity, mortality and reoccurrence.
1.8 Chronic Idiopathic
Facial Pain
Chronic (persistent) idiopathic facial pain (CIFP),
previously atypical facial pain, is persistent facial
pain described as continuous, daily pain affecting
one side of the face. The pain is described as ach-
ing, heavy, nagging, sometimes throbbing or
stabbing. The diagnosis cannot be made until all
other possibilities are excluded. Investigations
reveal no abnormalities or possible causes. A rel-
evant psychosocial history is important since
associated stress-related factors, anxiety, depres-
sion, sleep problems, employment status, family
life and marital status may all be contributing to
the pain.
Often these patients may have attended many
dentists, doctors and other specialists in a failed
attempt to cure the pain. Patients may also have
15
undergone serial extractions or multiple root
canal treatments to alleviate the pain.
Examination
The pain may be vague occurring all day every
day and poorly localised. The pain has often been
present for years with no provoking or relieving
factors. Clinical examination identifies no pathol-
ogy and will be inconsistent with history of com-
plaint. Vitality testing will be inconsistent and
variable. Sleep will be unaffected and patients
may describe the pain as crossing the midline.
The patient may have a detailed list of times,
dates and a written list of problems.
Management
A referral to an appropriate pain specialist or
psychiatrist once all local and systemic causes
such as dental, oral, facial, sinus, neuropathic and
intracranial have been eliminated.
1.9 Atypical Odontalgia
This is a form of atypical facial pain where the
patient attributes the pain experienced to the
teeth. By definition, this is toothache of
unknown cause. The condition has been referred
to as phantom tooth pain. Typically these
patients will be convinced that their pain is
coming from a tooth. Aetiology is unknown but
is often associated with prior trauma or inflam-
mation in the region. Multiple dental procedures
such as root canal treatments or extractions will
have been provided before a diagnosis has been
made in an attempt to provide relief for the
demanding patient who is at their wits end.
Often when the treatment fails, the patient will
insist on continuing treatment in other adjacent
teeth.
Examination
Atypical odontalgia will describe pain as dull,
aching and persistent and well localised to a par-
ticular tooth or area. The toothache will have
been present for months or years with no change
in characteristics. Clinical examination with
appropriate vitality tests and radiographic exami-
nations will reveal no obvious pathology. Thermal
stimulus such as heat and cold and percussion
tenderness does not consistently provocate the
tooth.
16
Management
Stop all treatment and refer to endodontic spe-
cialist to rule out any dental pathology. Once it
has been established that no obvious dental cause
is responsible, referral to a pain specialist would
be the next logical step.
There are no known effective treatments for
these patients, although drug therapy using tricy-
clic antidepressants has been used with some
success.
1.10 Clinical Cases
1.10.1 Acute Exacerbation of Chronic
Apical Periodontitis
A 39-year-old patient was referred for endodon-
tic management of tooth 47. Clinical examination
revealed a symptomatic tooth exhibiting pain on
biting and percussion. An intact temporary resto-
ration was noted. Radiographic examination
revealed a defective distal restoration overlying
the pulp chamber. Peri-radicular radiolucencies
were noted with the bulbous root anatomy of
tooth 47. The patient elected to have root canal
treatment, following which all his symptoms
resolved (Fig. 1.11).
1.10.2 Trigeminal Neuralgia
A 54-year-old male was referred to the practice
for non-specific constant dull ache associated
with the lower right posterior quadrant. The
patient insisted the pain was coming from tooth
47, which was subsequently extracted by his gen-
eral dental practitioner. Following extraction of
the tooth, the pain continued and the patient was
adamant that tooth 46 was the culprit. An end-
odontic referral was sought for further
management.
A detailed pain history revealed the patient
was experiencing episodic severe shooting pain
in the region of tooth 46 that felt like ‘electric
shocks’. The pain was spontaneous in nature and
exacerbated when touching the side of his face or
when chewing.
1 Pain of Odontogenic and Non- odontogenic Origin
Radiographic examination revealed tooth 46
had evidence of previous root canal treatment
which was deemed technically deficient. A provi-
sional diagnosis of trigeminal neuralgia was
made, but the patient was advised to consider
root canal re-treatment of tooth 46. Following
completion of endodontic re-treatment through
the existing cast restoration, the patient’s symp-
toms did not change. The patient was sent an
urgent referral to an oral maxillofacial surgeon
who agreed with the diagnosis, and the patient
was commenced on carbamazepine drug therapy.
After a 4-week period the patient reported a sig-
nificant improvement with his facial pain reduc-
ing dramatically. The patient was advised to
continue with his medication and warned of pos-
sible further episodes in the future requiring
additional medication and surgical intervention if
there was no response (Fig. 1.12).
Clinical Hints and Tips
Common features of odontogenic pain (pulpitis)
• Presence of aetiological factors for an
odontogenic origin (e.g. dental caries, leak-
age of restorations, trauma, fracture).
• Ability to reproduce chief complaint dur-
ing examination.
• Administration of local anaesthetic pro-
vides relief.
• Unilateral pain that does not cross the
midline.
• Pulpal pain qualities described as dull, ach-
ing and throbbing.
• Provocation of the tooth with thermal stim-
ulus (hot and/or cold) and percussion/pal-
pation reproduces the pain.
Common features of non-odontogenic pain
• No apparent aetiology for odontogenic
pain (e.g. no caries, leakage of restorations,
trauma, fracture)
• Bilateral pain sometimes affecting multiple
painful teeth
• Chronic pain that is not responsive to den-
tal treatment and has been present for
months without any change
• Pain qualities described as burning, electric
shooting, stabbing and constant vague dull
ache.
1.10 Clinical Cases 17

a b c

d e f

g h i

Fig. 1.11 Clinical radiographs of tooth 47 showing (a) ML which splits in the middle one third of the main distal
preoperative and (b) IAF. (c) Note: 90 degree curvature at canal, (g) mid-fill and (h, i) post-operative views with
apex of MB canal, (d) MAF preparation MB, ML and DB, mesio-angulation demonstrating complex anatomy
(e) additional mid-mesial confluent MB, (f) additional
18
a b
d e
Fig. 1.12 Clinical radiographs demonstrating (a, b) pre-
operative view showing recently extracted tooth 47 with no
change in pain. The patient insisted his pain was coming
from tooth 46. An endodontic referral was made and a deci-
sion to undertake root canal re-treatment. (c) MAF x-ray
following removal of old root filling and chemo-mechanical
• Pain that occurs with a headache
• Increased pain associated with palpation of
trigger point or muscles
• History of repeated dental therapies which
do not provide any relief or seeking opin-
ions from multiple clinicians
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 Aetiology and Pathogenesis
of Pulp Disease 2

Summary
Apical periodontitis is an inflammatory disorder of peri-radicular tissues
caused by aetiological agents of endodontic origin. The pulp–dentine
complex has only a limited ability to withstand microbiological, mechan-
ical, chemical or thermal insults by means of reactionary or reparative
dentine. Polymicrobial bacteria will eventually colonise the pulp result-
ing in a standoff between host defence mechanisms and bacterial coloni-
sation. Eventually bacteria will reach the apical tissues resulting in
clinical and radiographic signs and symptoms associated with apical peri-
odontitis. Effective treatment strategies should be aimed at reducing this
intra-canal biofilm to levels below a critical threshold conducive to
healing.

Clinical Relevance 2.1 Overview of the Pulp–

The primary aetiological factor for persist-
ing apical periodontitis is intra-canal bacte-
ria or bacterial biofilms. Treatment options
for the disease consist of chemo-mechanical
disruption of the biofilm removing or at least
reducing the intra-canal microbial load to
subcritical numbers achieved by root canal
instrumentation, use of sodium hypochlorite
irrigation, intra-canal antibacterial medication
and prevention of re-infection by obturation.
Any deviation from such protocols can only
lead to persistent microbes that may or may not
pose future hindrance for healing.
Dentine Complex
The dental pulp is a specialised connective tissue
entirely enclosed by dentine consisting of the pulp
periphery and pulp proper. The peripheral pulp can
be distinguished into three further zones including
the pseudo stratified layer of the highly differenti-
ated dentine producing odontoblast cells, a sub-
odontoblastic 40-μm cell-free zone and a cell-rich
zone. The terminal branches of the sensory and
autonomic nerve fibres are located in the sub-odon-
toblastic zone. The central pulp core consists of
mainly fibroblasts, collagen and elastin fibres, large
blood vessels and nerve bundles. The entire pulp is
embedded in a gel-like ground substance [1].

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 21
DOI 10.1007/978-3-319-15591-3_2, © Springer International Publishing Switzerland 2015
22
The odontoblasts are responsible for produc-
tion of mineralised dentine. Dentine is permeated
by millions of tubules each containing a cellular
process from an odontoblast. In a fully developed
tooth, the dentinal tubules have a diameter of 3 μm
at the outer periphery of dentine with a density
of approximately 15,000/mm2. As the dentinal
tubules converge towards the pulp, they are more
closely packed together with diameters reducing
to 1 μm with a density of 65,000/mm2 [1, 2].
The pulp–dentine complex has the ability to
respond to microbiological, mechanical, thermal
or chemical stimuli and insults, which are respon-
sible for inflammation within the pulp. Mild
insults may result in increased dentinogenesis as
a means of a protective mechanism whereby
increased peri-tubular dentine formation respon-
sible for the formation of sclerotic dentine can
occur. Tertiary dentine, either reactionary or
reparative in origin, can also be formed in
response to dentine injuries or toxic products that
reach the pulp–dentine complex. Reactionary
dentine, typically produced by pre-existing odon-
toblasts, may be a response to a freshly cut cavity
or a response to the restorative interface. Newly
differentiated odontoblastoid cells, on the other
hand, form reparative dentine, when the primary
odontoblast is irreversibly damaged. Growth fac-
tors such as transforming growth factor-β are
responsible for the initiation of odontoblast dif-
ferentiation and stimulation of dentine formation.
Release of growth factors typically occurs during
carious attacks to the tooth and injuries sustained
following cavity preparation and subsequent res-
toration of the tooth [2–4].
2.2 Role of Bacteria in Peri-
apical Disease
The presence of organisms in a necrotic dental
pulp was observed by Miller [5], but their role in
the development of apical periodontitis was not
confirmed until 70 years later. A definitive rela-
tionship between bacteria and peri-apical disease
is credited to Kakehashi and colleagues, demon-
strating that a normal oral microbiota was nec-
essary to produce pathologic changes resulting
2 Aetiology and Pathogenesis of Pulp Disease
from untreated experimental pulp exposures [6].
Numerous human and animal studies have con-
firmed the importance of bacterial infection in
the development of apical periodontitis [7–11].
The polymicrobial nature of the root canal flora
has been studied extensively, and obligate anaer-
obes, mainly Gram-negative bacteria (Prevotella
spp., Porphyromonas spp., Fusobacterium spp.,
Veillonella spp.) and some Gram-positive bacte-
ria (Actinomyces spp., Propionibacterium spp.,
Peptostreptococcus spp., Eubacterium spp.) have
been suggested as putative pathogens [9, 10, 12–
14]. Using a monkey model to evaluate the peri-
apical response to indigenous bacterial infections,
it was shown that, over time, facultative anaerobic
species and obligate anaerobes in combination
have been found to be capable of inducing inflam-
mation. It was found that bacteria inoculated in
combination in root canals had the capacity to
induce peri-apical changes and in such cases the
bacteria were re-isolated in equal proportions to
those recovered in the primary infection [15, 16].
Uncertainty about the bacterial origin of peri-
apical disease had allowed other aetiological the-
ories to become established. These included the
disproved hollow tube theory stating that necrotic
pulp tissue and stagnant tissue fluid were respon-
sible for irritation of the peri-apical tissues [16–
18]. Necrotic pulp tissue [19], bacterial products
[20] and viruses [21] have all been investigated,
but no definitive causal evidence was found.
2.3 Route of Bacterial Entry into
the Root Canal System
The root canal represents a special environment
in which selective pressures result in the estab-
lishment of a restricted group of the oral flora
[22, 23]. This selection process begins by a mode
of entry, which may ultimately affect the pattern
of infection within the root canal. The major
pathways of pulpal contamination are open com-
munication to the salivary plaque microorgan-
isms, exposed dentinal tubules [24–27], carious
exposure through crown or root [28], lateral
canals [29], microleakage [25–27, 30, 31], trau-
matic injury and anachoresis [32–34]. This latter
2.4 The Spatial Distribution of Microflora Within the Root Canal System
route, whereby bacteria reach the pulp and canal
system via severed blood vessels in the periodon-
tium, was proposed to explain findings in which
bacteria were isolated from teeth with necrotic
pulps and apparently ‘intact crowns’ [9, 10, 12].
Results of experiments carried out by Möller and
Delivanis and Fan [11, 35] conclusively exclude
this as a potential cause. Microleakage through
enamel cracks has been identified as the most
probable route of endodontic infection [24].
Pulpal infection is also possible through exposed
dentinal tubules at the cervical root surface
because of congenitally missing cementum at the
cement–enamel junction, which occurs in 10 %
of the population; exposed dentine in periodonti-
tis; or after loss of cemental covering due to
periodontal treatment [36].
a b
Fig. 2.1 Light microscopy longitudinal section of an
artificially created endodontic infection within a tooth
created using human saliva, serum and a constant depth
film fermentor after 28 days. Original magnifications: (a)
10×, (b) 50×, (c) and (d) 1,000×. Note: the presence of
23
2.4 The Spatial Distribution
of Microflora Within the Root
Canal System
A light microscopy (LM) study described the dis-
tribution of microorganisms within the root canal
as being polar in nature with a greater concentra-
tion of bacteria found in the bucco-lingual plane. It
was demonstrated that bacteria were able to pene-
trate up to half the thickness of dentine with more
bacteria present in the coronal segment as com-
pared to the apical [37]. With LM, by using specific
stains, i.e. Gram stain, it is possible to visualise and
characterise cells by their colouration (see Fig. 2.1).
However, by virtue of using such stains, several
bacteria may display similar staining characteris-
tics making identification difficult.
d
biofilm (yellow arrowhead) and dense aggregate of bac-
teria (black arrowhead) sticking to the dentinal wall (D)
along with a loose collection of bacteria suspended
within the lumen (L). (white circle) this area is magnified
in (c) and (d)
24
a b
Fig. 2.2 Light microscopy longitudinal section of an arti-
ficially created endodontic infection within a tooth created
using human saliva, serum and a constant depth film fer-
mentor after 28 days. Original magnifications: (a) 1,000×
A significantly greater percentage of coccoids
and rods have been seen in the coronal third than
in the apical third of root canals of teeth with
pulpal necrosis in a dark-field study. The percent-
age of filaments and spirochaetes, although not
significant, was shown to be slightly higher in the
apical than in the coronal root segment. The
quantification method used was based on the
observation of 200 bacteria, which were classi-
fied into morphological categories (coccoids,
2 Aetiology and Pathogenesis of Pulp Disease
and transmission electron microscopy view (b) 4,000×.
Note: structurally at the dentine (D) and biofilm (BF)
interface, a variety of morphologically distinct but taxo-
nomically unidentifiable bacteria can be seen
straight rods, filaments, spirochaetes and motile
rods) [38].
The morphological structure of the root canal
flora as seen by both LM and transmission elec-
tron microscopy (TEM) (see Figs. 2.2 and 2.3)
has been described as consisting of cocci, rods,
filamentous organisms and spirochaetes.
Structurally, the bulk of the root canal flora was
described as loose collections of a variety of
morphologically distinct planktonic bacteria
2.5 Dentinal Tubule Invasion
b c
Fig. 2.3 Transmission electron microscopy views of lon-
gitudinal section of an artificially created endodontic
infection within a tooth created using human saliva, serum
and a constant depth film fermentor after 28 days. Original
suspended in an apparently moist canal lumen.
Less frequently, the bacterial flora formed clus-
ters of ‘self-aggregating’ colonies of one distinct
type or ‘coaggregating’ communities of several
types sticking to the dentinal wall of the root
canal or existing free among vast numbers of
PMNs in the canal lumen [39]. Further work
demonstrated and confirmed the great anatomi-
cal complexity of the root canal and the ecologi-
cal organisation of the flora into protected sessile
biofilms [40].
Further SEM studies reported the existence of
cocci, which seemed to attach themselves to fila-
ments giving a ‘corncob’-like appearance in the
apical 2 mm of root canals associated with peri-
apical disease [41] (see Fig. 2.4). A study using
SEM examining the entire length of the canal
showed a continuous biofilm along the canal
wall [42].
25
d
magnifications: (a) and (b) 1,000× and (c) and (d) 4,000×.
Note: morphological appearance of cocci, rods and fila-
ments associated with a polymicrobial infection within a
tooth
2.5 Dentinal Tubule Invasion
Some research has been done on the penetration
of bacteria into the dentinal tubules. Bacteria
were seen to invade the dentinal tubules in early
studies, and the extent of bacterial invasion was
seen to be time dependent [37]. Later studies
investigated the depth of penetration of the den-
tinal tubules, and the reported depths vary from
150 to 2,000 μm, consisting of predominantly
Gram-positive rods and cocci [14, 42, 43].
Bacterial penetration of teeth with peri-apical
radiolucencies was examined using culturing and
histological techniques. Bacteria were found in
62 % of teeth in the layer closest to the cementum
layer. Microbiological examination of dentine
samples taken at different distances from the
canal lumen revealed 90 % of the dentine grind-
ings to show quantitative evidence for penetration
26
Fig. 2.4 Scanning
electron microscopy views
of longitudinal section of
an artificially created
endodontic infection
within a tooth created
using human saliva, serum
and a constant depth film
fermentor after 28 days.
Original magnification
1,000×. Note: morphologi-
cal appearance of coccoid
and filamentous organism
of bacteria towards the CEJ. Gram staining of his-
tological specimens, however, could only detect
bacteria from the pulpal–dentinal junction as far
as 375 μm. Perhaps this discrepancy was associ-
ated with contamination from adjacent layers of
dentine during processing or attributed to the lack
of sensitivity of LM to detect the low numbers of
bacteria from the small dentine sample [14]. Intact
cementum may be a limiting factor in bacterial
penetration from the pulpal surface, and its
absence enhances bacterial penetration [24, 44].
It has been speculated that bacterial adhesion
specificity plays a major role in determining the
invasion of the dentinal tubules. Recognition of
type І collagen may facilitate bacterial adhesion
to dentine [45]. Antigen І/ІІ family polypeptides
produced by some oral streptococci mediate pri-
mary binding of bacteria to intratubular collagen
type І. Once the cells had adhered to the collagen,
colonisation down the length of the tubule
occurred following an upregulation of antigen І/
ІІ polypeptides, stimulated by the release of pep-
tides during the demineralisation process. This
results in an increase in community growth
within and along the dentinal tubule. It has been
hypothesised that tissue fluid from the periodon-
tal ligament and alveolar bone bathing the root of
a tooth may provide sufficient nutrition to bacte-
ria within radicular dentinal tubules or the
obturated root canals [46], accounting for the
presence of streptococci and enterococci in failed
endodontically treated cases [47, 48].
2 Aetiology and Pathogenesis of Pulp Disease
2.6 Fate of Bacteria Within
the Root Canal System
and Their Interactions
The microbial composition of an infected root
canal is determined by [1] the route by which the
bacteria gain access to the root canal and [3] the
number and quality of ecological factors [49]. In
autogenously infected monkey teeth, the most
common bacterial strains were found to be facul-
tative anaerobic streptococci, obligate anaerobic
non-sporulating bacteria and coliform rods [11].
Further studies on monkeys found that when com-
binations of bacterial species were retrieved from
infected root canals and inoculated into unin-
fected root canals in equal amounts, the original
proportions became re-established, indicating that
selective mechanisms allow certain bacteria to
survive and multiply more than others [50].
In a succession of studies, the associations
between microbial species in dental root canal
infections of teeth with intact pulp chamber
walls were examined, and it was concluded that
commensal and antagonistic relationships
existed. Strong positive associations were found
between Fusobacterium nucleatum and
Peptostreptococcus micros, Porphyromonas
endodontalis, Selenomonas sputigena and
Wolinella recta. There was also a positive
association between Prevotella intermedia and
P. micros, P. anaerobius and the eubacteria.
Species of streptococci, Propionibacterium
2.7 Provision of Nutrients
propionicus, Capnocytophaga ochracea and
Veillonella parvula showed no or negative asso-
ciations with the other bacteria [22, 23].
Certain bacteria only become pathogenic in the
presence of other species. It has been suggested
that bacteriocins (proteins which have the capacity
to inhibit growth of a limited number of species)
are responsible for negative associations [51].
2.7 Provision of Nutrients
The root canal is a unique environment providing
a sanctuary to a biologically select anaerobic
milieu, which interacts with microbial factors and
the availability of nutrients. This restricted inter-
acting group of species are dependent on one
another for nutrition as the metabolism of one spe-
cies supplies essential nutrients for growth of other
members of the populations [22]. Nutrients may
be derived from the oral cavity (saliva), degenerat-
ing connective tissue, dentinal tubule contents or
a serum-like fluid from the peri-apical tissues
Fusobacterium
Eubacterium
Bacteroides Capnocytophaga
Eikenella corrodens
Peptostrepto-
coccus
NH4
CO2
Succinate
HEMIN
Porphyromonas endodontalis Campylobacter
porphyromonas gingivalis Wollinella
prevotella intermedius Bacteroides gracilis
Fig. 2.5 Possible nutritional relationships between bacteria in an infected root canal (Adapted from Sundqvist [22])
27
[52, 53]. Such predominating factors, within the
root canal environment, permit the growth of
anaerobic bacteria fermenting amino acids and
peptides apically [22, 23], whereas bacteria that
previously obtained energy by fermenting carbo-
hydrates may be restricted more coronally due to
dominance of such nutrients there. Growth of
mixed bacterial populations may depend on a food
chain in which metabolites of one species supply
essential nutrients for the growth of other mem-
bers of the population [23] (Fig. 2.5).
The relatively increased proportion of strict
obligate anaerobic organisms and the reduction
in facultative anaerobic organisms, over time, in
the apical portion are not only nutrient driven but
also partly due to the decrease in available oxy-
gen [15, 50]. It is likely that within a tooth with
necrotic pulp tissue, apical infection is main-
tained mainly by apical seepage of inflammatory/
serum exudate or possibly blood (such as trau-
matic instrumentation) [54].
It has been suggested that bacteria invad-
ing dentinal tubules may also gain nourishment
Streptococcus
Veillonella
Actinomyces
LACTATE
Formate Acetate
H2 Menadione
Eubacterium alactolyticum
28
from interstitial fluid originating from alveo-
lar bone and periodontal ligament and as such
would resemble serum. This fluid may sustain
cells within the tubules allowing for subsequent
growth [46].
2.8 Pathogenesis of Peri-apical
Disease
Peri-apical disease is the result of the interactions
between bacteria (and their by-products) and the
host defences. The non-specific and specific
branches of the host defences are recruited to
defend against the potential invasion of the body
by bacteria. The peri-apical lesion represents
resorption of bone away from the source of infec-
tion, whereby space is created for the migration
of the body’s defensive elements to counteract
the ongoing infection. In the early stages, follow-
ing acute inflammation, as a result of host/bacte-
rial interactions at the peri-apex of an infected
tooth, slight widening of the periodontal ligament
space may be evident radiographically. In the
absence of treatment intervention, bone destruc-
tion progresses from an acute to chronic state
resulting in marked radiographic radiolucency
that is clinically detectable. In animal models, the
area of bone destruction has been shown to
increase with time with a rapid phase between 7
and 15 days and stabilisation after 30 days. The
proportion of anaerobic bacteria, species present
and interaction with host dictates the amount of
bone destruction. Clinically there can be a wide
range in presentation from the absence of any
signs and symptoms (chronic apical periodonti-
tis), a discharging sinus (chronic suppurative api-
cal periodontitis) and the presence of pain and
swelling (acute exacerbation of chronic apical
periodontitis) [55–57].
2.9 Biofilms and Endodontics
A biofilm is defined as an aggregation of bacteria
associated with a solid surface, embedded in an
extracellular matrix of polysaccharide and other
metabolic products [58]. Plaque is a classic
2 Aetiology and Pathogenesis of Pulp Disease
example, which becomes spatially differentiated
after attachment and growth of pioneer species,
allowing secondary colonisers, not able to colo-
nise the surface alone, to adhere.
As the biofilm develops, gradients in factors
such as oxygen levels, redox potentials and pH
develop and permit the co-existence of species
that would be incompatible with each other in a
homogenous environment. Microbial communi-
ties usually develop on environmentally exposed
surfaces as a biofilm. Bacteria, which first colo-
nise a habitat, have been termed ‘pioneer spe-
cies’. The metabolism of these organisms can
modify the habitat and local environment to such
an extent as to make conditions more suitable for
the growth of ‘secondary colonisers’ with more
demanding requirements [59].
The early colonisers of tooth enamel include
streptococci (especially Streptococcus sanguis
and Streptococcus oralis) (Nyvar 1987) and
Neisseria spp. that consume oxygen and liberate
carbon dioxide and hydrogen, creating micro-
environments suitable for facultative anaerobes
and eventually obligate anaerobes [60].
The process of changes in bacterial species and
their proportions in a habitat during colonisation
is termed ‘succession’. Eventually, the composi-
tion of the microbial community at a site becomes
stable over time, known as the ‘climax commu-
nity’. The composition of this climax community
can, however, change further depending on key
environmental factors such as nutritional status or
local environmental conditions at a site, which
ultimately control the composition or activity of
microbial communities during development [59].
Free-floating bacteria existing in an aqueous
environment, so-called planktonic microorgan-
isms, are a prerequisite for biofilm formation.
Planktonic organisms in saliva serve as the pri-
mary source for the organisation of a specific bio-
film. The establishment of a micro-community
on a surface seems to follow essentially the same
series of developmental stages, including deposi-
tion of a conditioning film, adhesion and coloni-
sation of planktonic organisms in a polymeric
matrix, co-adhesion of other organisms and
detachment of biofilm microorganisms into the
surroundings [61] (Fig. 2.6).
2.10 Microbiology of Intra-radicular Infections
Fig. 2.6 Development of
biofilm on surface
(Adapted from Svensater
and Bergenholtz [61])
Adhesion
Protein
absorption
Adsorption of
proteins to form a
Conditioning film
As far as endodontic infections are concerned,
the ‘biofilm concept’ has thus far gained limited
attention. Bacterial ‘condensations’, representing
biofilms, have been discussed either within the
framework of appearances on root tips with non-
vital pulps [62–64] or on the walls of infected
root canals [39–41].
Biofilm structures may provide protection and
may allow better resistance to adverse external
influences for the organisms incorporated as com-
pared with the planktonic state [65]. From this
aspect, the formation of biofilms carries particular
clinical significance not only from a host defence
mechanism point of view, but also therapeutic
efforts including chemical, mechanical and anti-
microbial treatment measures. Investigative tools
for studying biofilms and the dynamics of ecology
in infected root canals should be developed further
to enhance our current knowledge, understanding
and management of apical periodontitis [66].
2.10 Microbiology of Intra-
radicular Infections
Collectively more than 400 different microbial
taxa have been identified when using anaerobic
culturing and culture-independent molecular
techniques. These taxa are usually found in com-
binations with fewer species number when com-
paring secondary/persistent disease (103–107)
and primary infections (103–108). In addition to
bacteria, fungi, archaea and herpesviruses have
also been found in intra-radicular infections and
lesions of apical periodontitis. Microorganisms
29
Detachment
Co-adhesion Detachment
Surface
Growth and metabolism
Adhesion and co-adhesion of
by adherent microorganisms
Planktonic microorganisms
ingress the root canal system from the oral cavity
resulting in a unique microbial infection that is
dictated by ecological and environmental factors
that allow for the differences seen in the untreated
root canal and root-filled canal with persistent
infection (see Table 2.1). It has been recognised
that uncultivable species may be present in root
canals, contributing to the disease process, and so
as technology improves, so too does our under-
standing of the endodontic pathogens that define
the underlying disease process.
Primary infections
Primary intra-radicular infections are character-
ised by a mixed partnership of 10–30 species per canal
[67]. The most prevalent and abundant taxa/groups
in primary infections include black-pigmented
Gram-negative anaerobic species (Prevotella
and Porphyromonas species), Fusobacterium
nucleatum, streptococci, spirochaetes (Treponema
species), Dialister species, Pseudoramibacter alac-
tolyticus, Propionibacterium species, Parvimonas
micra, Tannerella forsythia, Filifactor alocis,
Eubacterium species and Olsenella species [10, 11,
15, 50, 68–74].
Persistent/secondary infections
The major cause of post-treatment apical
periodontitis is persistent or secondary intra-
radicular infections. Most studies have revealed
an overall higher incidence of Gram-positive
bacteria. Enterococcus faecalis has been the
most frequently detected species in root canal-
treated teeth [75–77]. Several as-yet unculti-
vated bacteria have also been identified in root
canal-treated teeth [78]. This suggests that the
microbiota associated with posttreatment
30 2 Aetiology and Pathogenesis of Pulp Disease

Table 2.1 Distinctive features of the microbiota associated with different types of endodontic infections

Persistent/ secondary
Chronic apical periodntitis Acute apical abscess
infections
Mixed
Community Mixed Mixed
single
No. taxa 10–20 10–20 1–30

Gram negative anaerobes Gram positive facultative

Most prevalent groups
Most frequent taxa
Gram positive anaerobes
Actinomyces
Campylobacter spp
dialister spp
Eikenella corrodes
Fusobacterium nucleatum
Lactobacillus
Porphyromonas spp
Prevotella spp
Propionibacterium
Parvimonas micra
Peptostreptococcus spp
Treponema spp
Gram negative anaerobes
anaerobes
Dialister spp Actinomyces spp
Eikenella corrodes Candida abicans (yeast)
Fusobacterium Enterococcus faeclis
Lactobacillus Enteric rods
Peptostreptococcus Fusobacterium nucleatum
Porphyromonas spp Lactobacilli
Prevotella spp Propionibacterium spp
Streptococcus Peptostreptococcus spp
Streptococcus spp

persistent disease is a mixed bacterial popula- Propionibacterium propionicum [82], in a

tion that is more complex than previous cultural
studies suggest [79, 80]. Gram-positive
facultative anaerobes commonly associated
with samples from root-treated teeth affected
by apical periodontitis include Enterococcus
faecalis, streptococci, lactobacilli, Actinomyces,
Peptostreptococcus spp. and yeasts.
2.11 Extra-radicular Infections
It has been suggested that the main bacterial
species implicated in independent extra-radicu-
lar infections are Actinomyces species [81] and
pathologic entity named apical actinomycosis
[83]. The ability of these bacteria to form
cohesive colonies within the lesion has been
regarded as an important mechanism to evade
phagocytosis [84].
2.12 Herpesvirus and Apical
Periodontitis
Several viruses have been detected in periodontal
pockets using polymerase chain reaction (PCR)
technology suggesting herpesvirus as a cofactor
in destructive marginal periodontitis [85]. Over
2.14 Nonmicrobial Aetiology
the past decade studies have been published rais-
ing the possibility of herpesvirus participation in
the pathogenesis of apical periodontitis in the
same way as it has been proposed for marginal
periodontitis [86, 87]. Among the members of
the herpesvirus family, human cytomegalovirus
(HCMV) and Epstein–Barr virus (EBV) are the
most frequently detected in samples of peri-
apical lesions. Although the association of her-
pesviruses with some forms of apical periodontitis
has been suggested, a causative role remains to
be proven. It has been proposed that unfavour-
able changes in environmental exposure or alter-
ations in gene expression of the immune system
might periodically suppress the peri-apical host
defence. This then might lead to reactivation of
resident herpesviruses and increases in proin-
flammatory mediators, followed by overgrowth
of pathogenic bacteria [88].
2.13 Yeasts and Apical
Periodontitis
Yeasts have been commonly isolated from root
canal infections usually (both primary and post-
treatment) in low numbers and all belonging to
the genus Candida with C. albicans being the
predominant species [48, 89–91]. Other isolates
detected include C. glabrata, C. guilliermondii,
a b
Fig. 2.7 Clinical photographs showing pulse granuloma.
It can often be found in peri-apical areas of growly
decayed teeth or retained roots and teeth with a history of
endodontic therapy, where the root canal system has been
left open at some stage. The essential histopathological
features consist of a connective tissue stroma containing
31
C. inconspicua and Geotrichum candidum.
A variety of virulence factors enable C. albicans
to adhere to and penetrate into dentine, and its
ability to tolerate harsh ecological conditions
including high alkalinity (calcium hydroxide
therapy) may account for its low prevalence in
persistent cases of apical periodontitis [92].
2.14 Nonmicrobial Aetiology
Nonmicrobial aetiological factors, located within
inflamed peri-apical tissues beyond the root canal
system, can maintain peri-apical disease in root-
filled teeth. These factors include foreign body reac-
tion to exogenous materials [93] or endogenous
cholesterol crystals and a cystic condition of the
lesion [94]. The overall prevalence of foreign body
reaction at the peri-apex is currently unknown.
There is clinical and histological evidence that
the presence of tissue-irritating foreign materials
at the peri-apex, such as extruded root-filling
materials, endodontic paper points, particles of
foods (Fig. 2.7) and accumulation of endogenous
cholesterol crystals, adversely affect posttreat-
ment healing of the peri-apical tissues [95].
Conventional orthograde re-treatment may not be
sufficient, particularly if the foreign body reac-
tion is due to extruded gutta-percha beyond the
confines of the canal.
variable numbers of inflammatory cells and foreign body
giant cells associated with hyaline rings and ovoid fibril-
lary or amorphous hyaline masses. Treatment is by local
curettage and excision. Note: light microscopy (a) ×100
and (b) ×200 (Courtesy of Dr. Ian Clarke, Capital
Pathology, Canberra ACT)
32
Despite there being great advancements in the
field of endodontic microbiology and technology
over the past four decades, evidence of improved
outcome is still lacking. Many issues related to
the basic and applied science of endodontic
microbiology still remain unanswered, and it is
hoped that continued research, knowledge and
insights may provide the key equated to clinical
success rather than failure.
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 Classification of Pulpal
and Peri-apical Disease 3

Summary
Current diagnostic terminology used to describe pulpal and peri-radicular
states is presented with an attempt to provide minimum confusion for the
practitioner. In order to carry out proper endodontic treatment, a complete
diagnosis must include both a pulpal and peri-apical diagnosis for each
tooth evaluated.

Clinical Relevance
Modern endodontics is not only interested in
treatment modalities of pulpal extirpation pro-
cedures aimed at treating diseased pulps. More
so, in recent times, the advent of ‘regeneration’
procedures holds the belief that conservative
procedures aimed at preserving pulpal vitality
or healing of diseased pulps may be possible.
Without the correct diagnosis, the correct treat-
ment cannot be prescribed. Clinical terminology
in regard to diagnosis is based on assumptions
by correlating signs and symptoms and radio-
graphic findings often confusing with presumed
histopathological status. The clinician is pre-
sented with simple diagnostic terminology based
on clinical findings underpinning the progres-
sive nature of pulpal disease, which ensures the
most appropriate treatment strategy is selected.
Traditional histopathological based diagnos-
tic terminology should be disregarded for this
purpose.
3.1 Diagnostic Terms for Pulpal
and Peri-radicular Health
and Disease States
Many different classification systems have been
proposed to describe the various states of pulpal
health and disease based on either histopatho-
logical findings or clinical findings. The majority
of classifications advocated are a combination of
the two [1–9]. Even when the ‘gold standard’ of
histological findings was correlated with pulpal
clinical signs and symptoms, no direct correla-
tion could be made, further proving this fallacy
[10–12]. The clinician should be aware that we
are only able to indicate the probable pulpal
status of any tooth based on both clinical and
radiographic findings [13–15]. Often our treat-
ment decisions based on presumed diagnosis are
only proven once treatment has been initiated.
It is therefore of paramount importance that we

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 35
DOI 10.1007/978-3-319-15591-3_3, © Springer International Publishing Switzerland 2015
36 3 Classification of Pulpal and Peri-apical Disease

Table 3.1 Comprehensive clinical diagnostic system Table 3.2 Comprehensive radiographic diagnostic
system
Clinically normal pulp Vital, asymptomatic healthy
pulp Normal peri-radicular Teeth with normal peri-
Reversible pulpitis Presence of mild inflammation tissues radicular tissues that will not
Acute where the pulp is capable of be abnormally sensitive to
Chronic healing percussion or palpation testing
Irreversible pulpitis Presence of more degenerative Acute apical Inflammation usually of the
Acute processes within the pulp periodontitis apical periodontium producing
Chronic whereby the pulp is not Symptomatic apical clinical symptoms including
capable of healing periodontitis painful response to biting and
Pulp necrosis The end result of irreversible percussion (mechanical
Necrobiosis (partial pulpitis. Subsequent bacterial allodynia)
necrosis) invasion will lead to an Acute apical abscess An inflammatory reaction to
Complete pulp infected pulpal necrosis Acute alveolar pulpal infection and necrosis
necrosis abscess characterised by rapid onset,
Sterile Dentoalveolar spontaneous pain, tenderness
Infected abscess of the tooth to pressure, pus
Pulpless tooth Previously initiated treatment Phoenix abscess formation and swelling of the
(pulpotomy, pulpectomy) associated tissues
Degenerative changes Pulp atrophy or fibrosis is a Chronic apical Inflammation and destruction
Atrophy degenerative change that is periodontitis of apical periodontium that is
Pulp canal not clinically discernable Asymptomatic of pulpal origin, appears as a
calcification PCC sometimes referred to as apical peri-radicular radiolucent area
Partial pulp canal obliteration or periodontitis and does not produce clinical
Complete calcific metamorphosis symptoms
Hyperplasia Pulp polyp Acute exacerbation of Inflammation and destruction
Internal resorption Pathological state of the pulp chronic apical of apical periodontium that is
Surface where multinucleate giant periodontitis of pulpal origin, appears as a
Inflammatory cells begin to remove the peri-radicular radiolucent area
Replacement dentinal walls of the pulp that produces clinical
space symptoms
Previous root canal Previously treated teeth Chronic apical An inflammatory reaction to
treatment periodontitis with pulpal infection and necrosis
No signs of infection suppuration characterised by gradual onset,
Infected little or no discomfort and the
Technical standard intermittent discharge of pus
Adequate through an associated sinus
Inadequate Condensing osteitis A diffuse radiopaque lesion
Other problems believed to represent a bony
Perforation, missed reaction to low-grade
canals, fractured inflammatory stimulus, usually
instrument seen at the apex of a tooth in
Adapted from Abbott [21] which there is long-standing
pulp pathosis
Adapted from American Association of Endodontist
correctly diagnose the pulpal status along the (2003) and Terms from the American Board of Endodontics
continuum of health and disease with as much (2007)
confidence as possible. A starting point on this
road to success is identifying and understanding
correct terminology when attempting to address
the endodontic health of any given tooth and 3.2 Clinically Normal Pulp
eliminating terminology related to histopathol-
ogy that cannot be attained in the clinical situa- This is equivalent in meaning to a vital, asymp-
tion [16–24] (see Tables 3.1 and 3.2). tomatic or healthy pulp (Fig. 3.1).
3.3 Reversible Pulpitis
a b
Fig. 3.1 Clinical photographs and radiographic exami-
nation used when determining the probable pulp status
of a tooth. Following history taking and chief complaint,
a thorough examination is performed including (a) per-
cussion, (b) palpation, (c) thermal sensitivity testing and
(d) pulp electrical vitality testing. Radiographic exami-
nation should include a long cone parallel image of the
Chief Electric
Radiographic
complaint History findings pulp test
Normal pulp None Normal Responsive
Teeth with a normal pulp and peri-radicular
tissues demonstrate no signs or symptoms to
suggest any disease is present. Depending on the
age of the tooth, there may or may not be evi-
dence of pulp calcification and pulpal fibrosis.
The pulp will generally respond to cold or elec-
tric stimuli, and the response will not linger for
more than a few seconds. Percussion, palpation
and bite tests elicit no pain and the radiographic
appearance is normal. A suitable control tooth
must be selected for comparison, and pulpal test-
ing should include both thermal and electrical
testing to determine the most probable pulpal
diagnosis.
37
c d
tooth in question showing the entire tooth and anatomy
beyond the root apices. (e) Shows tooth 16 which was
determined to be normal after careful examination.
Degenerative changes can be seen in the coronal pulp
chamber but they do not indicate whether the tooth is
healthy or unhealthy
Thermal Percussion
Palpation Differential
testing Treatment diagnosis
Mobility
No treatment
Normal Nil indicated
3.3 Reversible Pulpitis
This refers to a pulp that has mild inflammation due
to pulpal irritation that is capable of healing and
returning to a clinically normal pulp if appropriate
treatment therapy is performed. Reversible pulpitis
is a result of caries, trauma, defective or new restora-
tions, mechanical pulp exposures, tooth brush abra-
sion, cracked tooth syndrome or recent subgingival
scaling and curettage. The pain is characterised as
mild to severe elicited by stimuli (e.g. thermal, bit-
ing, sweet or sour stimuli) (Fig. 3.2 and 3.3).
The pain will resolve after a few seconds once
the stimulus has been removed and there is no
38 3 Classification of Pulpal and Peri-apical Disease

a b

Fig. 3.2 Clinical radiographs demonstrating reversible the pulp chamber with no obvious peri-apical changes.
pulpitis. A 15-year-old patient presented with gross car- (b) Final post-operative radiograph demonstrating deep
ies in tooth 36 (a). The patient was asymptomatic other restoration using MTA as an indirect pulp capping
than occasional sharp pain with the tooth on eating. agent, glass ionomer cement and composite resin
Radiographic findings confirmed deep caries overlying restoration
Chief Electric Thermal Percussion
Radiographic Palpation Differential
complaint History findings pulp test testing Treatment diagnosis
Mobility
Sharp and
fleeting Caries, cracks,
Reversible Hot/Cold Normal Responsive Normal/ Nil Removal restorative
related to Exaggerated cause
pulpitis sensitivity thermal prodedures or
challenge trauma

history of spontaneous pain. There will be no
response to percussion or palpation, and the
radiographic appearance is generally normal.
Reversible pulpitis must be distinguished from
dentine sensitivity whose aetiology is due to
exposed root dentine.
3.4 Irreversible Pulpitis
A pulpal condition is usually caused by deep
dental caries or restorations, previous pulp cap-
ping procedure, crack or any other pulpal irri-
tant. Spontaneous pain may occur or be
precipitated by thermal or other stimuli. The
pain may last for several minutes to several hours
described as a sharp or dull exaggerated painful
response that lingers after the stimulus has been
removed. The nature of the pain depends on the
type of nerve fibre responding to the inflamma-
tion within the pulp (either A delta fibres that
mediate sharp pain or C fibres responsible for
dull throbbing pain). This disease entity implies
that the pulpal state will not heal and if left
untreated will result in pulpal necrosis followed
by apical periodontitis.
The tooth may or may not be sensitive to per-
cussion and the radiographic appearance may be
unremarkable other than the aetiology (deep
restoration) (Fig. 3.4).
Occasionally the patient may present with
asymptomatic irreversible pulpitis whose onset is
precipitated by previous carious exposure, caries
excavation or trauma.
3.5 Pulp Necrosis
Pulp necrosis is the end result of irreversible pul-
pitis that usually occurs over a variable period of
time. On rare occasions such as trauma, the onset
of necrosis may be sudden and immediate.
3.5 Pulp Necrosis
a b
e f
i j
Fig. 3.3 Clinical photographs demonstrating indirect
pulp capping procedure using MTA. Note (a–h) caries
removal leaving in situ stained dentine overlying pulp, (i)
Symptoms will vary according to the stage of
necrosis (partial or complete) with some patients
giving a history of previous pain to those who
experienced none. Percussion sensitivity may be
evident if necrosis has resulted in an infected root
canal system with bacteria reaching the apical
portions of the tooth and beyond. Occasionally
the tooth may become discoloured as a direct
result of altered translucency of the tooth or hae-
molysis of red blood cells during pulp decomposi-
tion. Pulp tests will demonstrate no response to
both electric pulp testing and thermal stimulus in
cases where complete necrosis has taken place. In
multi-rooted teeth where partial necrosis may
have occurred, pulpal sensibility testing may
prove positive, making diagnosis difficult in the
early stages (Fig. 3.5).
The distinction between partial necrosis
and complete necrosis is important in the
39
c d
g h
k l
MTA placement, (j) GIC base, (k) acid etching and (l)
placement of composite resin restoration
management of trauma and immature teeth
with open apices particularly when deciding
whether to perform an apexogenesis or apexifi-
cation procedure.
Sterile necrosis is a histological term that
can only be presumed based on continued unre-
sponsiveness to pulp testing and the presence of
no peri-apical lesion at the apex of the tooth.
This is usually the case in unrestored teeth that
have sustained trauma where no reliable clini-
cal and radiographic signs or symptoms can
confirm the presence of apical periodontitis.
Usually a waiting period of 3 months is advised
with periodic pulp testing. In such cases, the
decision to wait longer with the benefit of
pulpal revascularisation must be weighed
against the possibility of developing apical
periodontitis, which statistically reduces the
overall success rate.
40 3 Classification of Pulpal and Peri-apical Disease

a b c

Fig. 3.4 Clinical radiographs demonstrating a case obvious cracks or fractures were seen. The patient’s dis-
treated with irreversible pulpitis. A 48-year-old patient comfort did not improve and following application of
complained of sensitivity to both hot and cold liquids with CO2 snow pain lingered for several minutes. Response to
the discomfort becoming spontaneous. (a) Preoperative percussion and palpation was normal and radiographic
radiographic demonstrating a large MO amalgam restora- findings indicated no osseous changes. (c) Nonsurgical
tion. The patient was aware of pain on release with the endodontic treatment was indicated and following com-
MB cusp. (b) A composite restoration was placed and no pletion her pain resolved
Chief Electric Thermal Percussion
Radiographic Palpation Differential
complaint History findings pulp test testing Treatment diagnosis
Mobility
Intense, Caries,
prolonged defective Caries, cracks,
Irreversible Hot/Cold Exaggerated
spontaneous restorations, Exaggerated Nil Endodontic therapy restorative
pulpitis sensitivity pain related to PDL Lingering procedures or
heat stimulus space may be trauma
widened

a b c d e

Fig. 3.5 Clinical radiographs and photographs demon- electric pulp testing and thermal stimulus. A decision
strating pulpal necrosis. A 12-year-old patient sustained was made to commence nonsurgical root canal therapy.
an uncomplicated crown fracture (enamel–dentine) in (b) Intra-operative view following access cavity con-
tooth 11. The patient was asymptomatic. Pulpal testing firmed a necrotic pulp chamber. (c) Master apical file
revealed negative responses 5 months after the initial radiograph and (d) and (e) post-operative radiographs
injury. Radiographic findings (a) revealed no osseous demonstrating obturation following warm vertical com-
changes. Tooth 21 (control) responded normally to both paction using gutta-percha and AH plus cement
Chief Electric Thermal Percussion
Radiographic Palpation Differential
complaint History findings pulp test testing Treatment diagnosis
Mobility

Endodontic
Pulp No symptoms Variable Normal PDL or No No Nil treatment when
Variable hot/cold widened PDL response clinical and/or Trauma
necrosis response
sensitivity radiographic signs
develop
3.7 Degenerative Changes
a b
Fig. 3.6 Clinical radiographs demonstrating pulpless
teeth. (a) A 54-year-old patient presented with tenderness
and pain associated with tooth 46. The crown was con-
structed 10 years earlier. The patient had severe localised
pain which improved following pulp extirpation with her
general dental practitioner. Microscopic examination of
the access revealed an unlocated MB canal which would
account for her continuing discomfort with the tooth
Chief
Radiographic
complaint History findings
Previous
Nil pulpotomy,
Pulpless pulpectomy Normal PDL or
Percussion/ widened PDL
tooth Palpation or
tenderness root canal
treatment
3.6 Pulpless Tooth
Occasionally a tooth may present with previously
started but not completed endodontic therapy
including pulpotomy or pulpectomy procedures
that provide predictable pain reducing strategies in
endodontic emergency patients. Treating the
unscheduled emergency patient by the ‘prescription
pad’ (i.e. antibiotics) should be an adjunct for cases
where systemic involvement is evident (i.e. acute
apical abscess) and where local measures such as
incision and drainage have been carried out.
These teeth may or may not present with signs
and symptoms of pulpal and peri-radicular disease
depending on the type of procedure carried out.
Radiographic evidence of prior endodontic access
should be noted with possible radiopaque inter-
appointment medicament within the canals.
Completion of endodontic treatment is indicated to
ensure the tooth remains asymptomatic (Fig. 3.6).
41
despite pulp canal extirpation. Ultrasonic troughing was
necessary to locate the calcified canal orifice. (b) Prior
endodontic access with pulp extirpation carried out with
minimal instrumentation by the patient’s general dental
practitioner provided immediate and complete relief.
Patient presented with a pulpless tooth and no symptoms.
Upon access four canal were noted with sedative dress-
ings confirming provisional diagnosis
Electric Thermal Percussion
Palpation Differential
pulp test testing Treatment diagnosis
Mobility
Traumatic
occlusion
No No Nil Endodontic
response Non odontogenic
response treatment
pain
Myofacial pain
3.7 Degenerative Changes
Partial or complete obliteration of the root canal
space is a common finding following a history of
traumatic luxation injuries and root-fractured
teeth. Pulpal sensibility testing may be normal,
weaker or negative in teeth depending on the
amount of obliteration within the pulp canal space.
Clinically a yellowish shade may be seen in teeth
with coronal pulp canal obliteration (Fig. 3.7).
These teeth have a good prognosis with evi-
dence of peri-apical radiolucency developing in
13–16 % of cases after periods of up to 20 years.
Discolouration alone is not an indication for end-
odontic intervention, and only complex restor-
ative treatment may provide an effective solution
with the possibility of the demise of the pulp. The
prognosis of treating such cases may be guarded
with the risk of iatrogenic perforation high during
the search for the elusive calcified canal space.
42
a b
Fig. 3.7 Clinical radiograph and photograph demonstrat-
ing degenerative changes. (a) A 30-year-old patient was
referred regarding assessment of pulp vitality of tooth 11.
The patient recalled trauma at the age of nine whilst ice
skating and also mentioned orthodontic fixed appliance
therapy during her teenage years. The tooth has been
gradually getting more discoloured over time. (b) Clinical
Chief
Radiographic
complaint History findings
Degenerative
changes Tooth has Previous Normal PDL or
e.g. Pulp canal gradually history of
widened PDL
obliteration/ got darker trauma
Calcific (yellow)
metamorphosis
3.8 Normal Peri-radicular
Tissues
Normal peri-radicular tissues will not be sensi-
tive to percussion or palpation testing.
Radiographically the peri-radicular tissues are
normal with an intact lamina dura and a uniform
periodontal ligament space (Fig. 3.8).
The clinician must bear in mind the significance
of assessing the presence or absence of peri-apical
radiolucencies that can be extrapolated from stud-
ies where artificial peri-apical lesions were created
in posterior region of dry jaws. These lesions were
not easily visualised on radiographs when confined
to the cancellous bone due to masking by the more
mineralised and therefore denser overlying cortical
bone. Peri-apical radiolucent lesions are usually
only diagnosed when there has been perforation or
erosion of the overlying cortical plate.
3 Classification of Pulpal and Peri-apical Disease
examination revealed obvious discolouration of the crown
(Yellow). The tooth was nonresponsive to thermal and
electrical pulp testing. Radiographic findings confirmed a
diagnosis of pulp canal calcification. No endodontic inter-
vention was required. The patient decided to accept the
discolouration rather than risk pulp necrosis following
restorative intervention
Electric Thermal Percussion
Palpation Differential
pulp test testing Treatment diagnosis
Mobility
No
No Nil No
response response treatment
3.9 Acute Apical Periodontitis
Acute apical periodontitis occurs when pulpal
disease extends into the surrounding peri-
radicular tissues causing inflammation. The
patient will generally complain of discomfort
when biting, chewing, and eating or when the
teeth come into contact. Sensitivity to percussion
is a telltale diagnostic sign synonymous with
acute apical periodontitis. Palpation testing may
or may not elicit a sensitive response (Fig. 3.9).
Radiographic findings may vary from no obvi-
ous observable change to widening of the peri-
odontal ligament space at the apex of the tooth.
Occlusal reduction may aid in the reduction
of post-instrumentation pain in patients whose
teeth exhibit preoperative pain, pulp vitality, per-
cussion sensitivity and/or the absence of a peri-
radicular radiolucency. The biologic rationale
3.11 Chronic Apical Periodontitis 43

Fig. 3.8 Clinical radiograph showing normal peri-radicu- examination revealed no abnormalities associated with
lar tissues. Tooth 47 had mesial–occlusal caries, and the the peri-apex of tooth 47. Treatment would be excavation
patient has been complaining of sensitivity to sweets and of caries followed by placement of a permanent restora-
cold liquids. There was no discomfort to biting and pres- tion. If the pulp is exposed, treatment would be nonsurgi-
sure. The tooth was hypersensitive to thermal stimulus cal endodontic treatment followed by a permanent cast
(CO2 snow) with no lingering pain. Radiographic cuspal coverage restoration
Chief Electric Thermal Percussion
Radiographic Palpation Differential
complaint History findings pulp test testing Treatment diagnosis
Mobility

Normal Normal Nil No

None Normal Response response
periradicular Variable treatment
tissues

for the relief of pain provided by occlusal trauma
is due to the reduction of mechanical allodynia
(i.e. sensitivity to percussion) of sensitised
nociceptors.
including lymphadenopathy and the presence of
pyrexia. Prompt management will be required to
prevent potentially life-threatening spread of
infection and urgent referral if local measures do
not provide adequate relief.

3.10 Acute Apical Abscess

Patients will present with a very painful tooth and
pulp testing will indicate a necrotic pulp. Swelling
is often present and it may be either localised to
the mucogingival area, or it may involve fascial
planes and spaces (Fig. 3.10).
The tooth is very sensitive to percussion and
palpation and may exhibit varying degrees of
mobility. Radiographic examination may reveal
no anatomic changes in some cases and obvious
peri-apical pathology in others. The patient may
or may not exhibit systemic manifestations
3.11 Chronic Apical Periodontitis
When bacteria and bacterial products from a
necrotic pulp ingress into the peri-apical tissues,
the patient’s immune system may become
engaged in a chronic conflict. The resultant
inflammatory process causes peri-radicular
bone resorption that is demonstrated as a
peri-radicular radiolucency on the radiograph
(Fig. 3.11).
Clinically the patient is asymptomatic with
no tenderness to percussion or palpation in the
44 3 Classification of Pulpal and Peri-apical Disease

a b

Fig. 3.9 Clinical radiographs showing endodontic case obvious peri-radicular pathology was noted. (b) Nonsurgical
diagnosed as acute apical periodontitis. (a) Following endodontic treatment was initiated through the crown using
placement of a full gold crown restoration on tooth 36, the sodium hypochlorite irrigation. All symptoms resolved fol-
patient complained of sensitivity to hot and cold liquids. lowing the cleaning and shaping procedure. An intra-canal
Upon application of thermal stimulus (CO2 snow), the dressing of calcium hydroxide was placed for a 2-week
patient experienced lingering pain that lasted up to a minute period prior to obturation using a warm vertical compaction
after removal of the stimulus. There was obvious tender- technique using AH plus cement and gutta-percha
ness to biting and pain to percussion. Radiographically no
Chief Electric Thermal Percussion
Radiographic Palpation Differential
complaint History findings pulp test testing Treatment diagnosis
Mobility

Moderate to
Acute apical Discomfort when ?Recent Normal or Response/ servere pain
Variable with or Endodontic Occlusal trauma
periodontitis biting or chewing restoration windened PDL No treatment
response without
mobility

region. Pulp testing confirms a necrotic pulp. exacerbation of an otherwise asymptomatic

Effective nonsurgical root canal treatment will
often tip the balance in favour of the host
immune response by reducing the bacterial load
within the tooth and peri-apical tissues, allow-
ing healing to take place. In cases where no
treatment is provided, the temporary balance
between bacteria and host will be eventually
altered with patients often experiencing pain as
a result of this shift and further bacterial migra-
tion, cortical bone erosion and lesion expansion.
Clinically the symptomatic patient presenting
with a radiolucent lesion can be classified
as acute exacerbation of chronic apical peri-
odontitis. Phoenix abscess is a term applied to
tooth during instrumentation. The process of
instrumentation (and possibly overinstrumenta-
tion) may inadvertently inoculate the peri-apical
tissues with bacteria creating an inflammatory
reaction and flare up.
3.12 Chronic Apical Periodontitis
with Suppuration
Clinically the patient is asymptomatic with little
or no discomfort. There will be a history of inter-
mittent discharge of pus through an associated
sinus tract allowing drainage. The tooth will be
3.13 Condensing Osteitis 45

a b

Fig. 3.10 (a) Clinical photographs showing endodon- old patient was referred due to difficulties with root
tic cases diagnosed as acute apical abscess. (a) Swelling canal treatment with tooth 36. The patient presented
localised to mucogingival area adjacent to tooth 16. with an obvious buccal space infection which did not
Prior endodontic access was attempted by the general respond to local measures of incision and drainage and
dental practitioner, but the canals were difficult to oral antibiotics. The patient was referred to the local
locate through the crown. The patient was experiencing maxillofacial department where the tooth was subse-
localised pain in the overlying gum and the tooth was quently extracted
very sensitive to pressure. (b) A fit and healthy 40-year-
Chief Electric Thermal Percussion
Radiographic Palpation Differential
complaint History findings pulp test testing Treatment diagnosis
Mobility
Incision and
drainage
Acute apical Pain with or Recent Normal or No No Exquisitely Root canal
abscess without swelling deep windened PDL response response painful and treatment Necrotic or
restoration tenderness +– Antibiotics if pulpless tooth
in overlying systemic
mucosa involvement

nonresponsive to electric pulp testing and ther-
mal stimulus. Percussion and palpation testing
will be nonresponsive. A sinus will be present
which may or may not be draining exudate
(Fig. 3.12).
Radiographic examination will reveal osseous
destruction with radiolucency. To confirm the
source of the draining sinus, when present, a
gutta-percha cone is carefully placed through the
sinus or opening until it stops and a radiograph is
taken. Occasionally root-treated teeth or pulpless
teeth where bacterial infection persists can
present with a draining sinus of pulpal origin.
Endodontic treatment or re-treatment is indicated
and the sinus will resolve following adequate
chemo-mechanical debridement to reduce micro-
bial load.
3.13 Condensing Osteitis
Localised area of bone sclerosis associated with
the apices of teeth presenting with pulpitis. The
involved tooth will often have a history of low-
grade, chronic inflammation such as a necrotic
pulp, extensive restorative history or a cracked
tooth. The patient may be asymptomatic or
demonstrate a wide range of pulpal symptoms.
46 3 Classification of Pulpal and Peri-apical Disease

a b

Fig. 3.11 Clinical radiographs demonstrating an end- revealed no tenderness or pain associated with tooth 47.
odontic case diagnosed as chronic apical periodontitis. (a) Preoperative examination confirmed extensive peri-radic-
A fit and healthy 42-year-old gentleman was referred for ular radiolucencies associated with the root apices of
an endodontic opinion regarding tooth 47. The patient tooth 47. (b) Final post-operative radiograph. Note no
gave a history of thermal sensitivity and pain on release obvious cracks or fractures were detected internally and
for several months on the right side. He recalled some probing profile for the tooth was within normal limits. An
localised pain exacerbated when biting and chewing but orthodontic band was provisionally placed until definitive
this resolved on its own accord. Clinical examination crown restoration with his general dental practitioner
Electric Thermal Percussion
Chief Radiographic Palpation Differential
complaint History findings pulp test testing Treatment diagnosis
Mobility

Asymptomatic
Chronic apical None Radiographic Necrotic or
periodontitis Periapical No No Nil Endodontic
evidence during radiolucency response response treatment pulpless?
routine Transient apical
examination resorption (trauma)

a b c

Fig. 3.12 Clinical radiographs and photograph demon- respond to thermal (CO2 snow) and electric pulp testing.
strating chronic apical periodontitis with suppuration. Both percussion and palpation elicited normal responses.
(a) Tooth 16 demonstrates a calcified root canal system (b) and (c) A draining sinus was noted in the overlying
with a relatively large peri-radicular radiolucent lesion alveolar mucosa which was traced with a gutta-percha
associated with the fused peri-apex. Periodontal probing cone to confirm involvement of tooth 16. Nonsurgical root
profile was within normal limits. The tooth did not canal treatment was recommended
Electric Thermal Percussion
Chief Radiographic Palpation Differential
complaint History findings pulp test testing Treatment diagnosis
Mobility

Chronic Bad taste

apical or gum boil/
periodontitis Asymptomatic Periapical No No Nil Endodontic Perio-Endo lesion
swelling radiolucency response response treatment Vertical root
with noted
suppuration fracture
besides
tooth
References 47

a b

Fig. 3.13 Clinical radiographs demonstrating an end- tenderness to percussion and pain on biting. Pulpal
odontic case diagnosed as condensing osteitis. responses were negative to both thermal stimulus (CO2
(a) Mandibular left first molar had been hypersensitive to snow) and electric pulp testing. Nonsurgical endodontic
cold over the last few months following placement of an treatment is indicated followed by cast cuspal coverage
extensive amalgam restoration with near pulp exposure of restoration. Over time the condensing osteitis should
the mesial canals. At consultation, the patient reported regress
Electric Thermal Percussion
Chief Radiographic Palpation Differential
complaint History findings pulp test testing Treatment diagnosis
Mobility

Focal
sclerosing Asymptomatic Extensive
osteomyelitis or variable restorative Increased Response Sensitive or
radiopacity Variable Endodontic
(condensing pulpal or history or no non treatment
osteitis) symptoms of crack response responsive

Electric pulp testing and thermal stimulus may
or may not be responsive. Percussion and
palpation tenderness may be present or absent
(Fig. 3.13).
Radiographic examination will reveal an
increased radio-opacity associated with the
peri-apex of the offending tooth. Nonsurgical
endodontic treatment is the treatment of choice if
the patient wishes to retain the tooth.
References
1. Ingle J, Bakland L. Ingle’s endodontics. 6th ed.
Hamilton: BC Decker; 2009.
2. Torabinejad M, Walton R. Endodontic principles
and practice. 4th ed. St. Louise: Saunders/Elsevier;
2009.
3. Cohen S, Hargreaves K. Pathways of the pulp. 9th ed.
St. Louis: Mosby; 2006.
4. Gutmann JL, Dumsha TC, Lovdahl P, et al. Problem
solving in endodontics. 4th ed. St Louis: Mosby;
2004.
5. Wiene F. Endodontic therapy. 6th ed. St. Louise:
Mosby; 2004.
6. Bergenholtz G, Horsted-Bendslev P, Reit C. Textbook
of endodontology. London: Blackwell Munksgaard;
2003.
7. Whitworth JM. Rational root canal treatment in prac-
tice – quintessentials series. 2nd ed. London:
Quintessence publishing Co Ltd; 2002.
8. Orstavik D, Pitt Ford TR. Essential endodontology.
London: Blackwell; 1998.
9. World Health Organization. Application of the inter-
national classification of diseases to dentistry and sto-
matology. 3rd ed. Geneva: World Health Organization
(WHO); 1995. p. 66–7.
10. Seltzer S, Bender IB, Zionitz M. The dynamics of
pulp inflammation: correlations between diagnostic
data and actual histologic findings in the pulp (part I).
Oral Surg Oral Med Oral Pathol. 1963;16:846–71.
11. Seltzer S, Bender IB, Zionitz M. The dynamics of
pulp inflammation: correlations between diagnostic
48
data and actual histologic findings in the pulp (part II).
Oral Surg Oral Med Oral Pathol. 1963;16:969–77.
12. Dummer PM, Hicks R, Huws D. Clinical signs and
symptoms in pulp disease. Int Endod J. 1980;13:
27–35.
13. Jafarzadeh H, Abbott PV. Review of pulp sensibility
tests. Part I: general information and thermal tests. Int
Endod J. 2010;43:738–62.
14. Jafarzadeh H, Abbott PV. Review of pulp sensibility
tests. Part II: electric pulp tests and test cavities. Int
Endod J. 2010;43:945–58.
15. Newton CW, Hoen MM, Goodis HE, Johnson BR,
McClanahan SB. Identify and determine metrics,
hierarchy and predictive value of all the parameters
and/or methods used during endodontic diagnosis.
J Endod. 2009;35:1635.
16. Morse DR, Seltzer S, Sinai I, Biron G. Endodontic
classification. J Am Dent Assoc. 1977;94:685–9.
17. Glickman GN, Mickel AK, Levin LG, Fouad AF,
Johnson WT. Glossary of endodontic terms. 7th ed.
Chicago: American Association of Endodontists;
2003.
3 Classification of Pulpal and Peri-apical Disease
18. American Board of Endodontics. Pulpal & periapical
diagnostic terminology. Chicago: American Association
of Endodontics; 2007.
19. Abbott PV, Yu C. A clinical classification of the status
of the pulp and the root canal system. Aust Dent J.
2007;52(Suppl):S17–31.
20. Abbott PV. Classification, diagnosis and clinical man-
ifestations of apical periodontitis. Endod Top. 2004;8:
36–54.
21. Abbott PV. Endodontics and dental traumatology: an
overview of modern endodontics – teaching manual.
Perth: The University of Western Australia; 1999. p. 11–5.
22. Gutmann JL, Baumgartner JC, Gluskin AH, Hartwell
GR, Walton RE. Identify and define all diagnostic
terms for peri-apical/peri-radicular health and disease
states. J Endod. 2009;35:1658.
23. Levin LG, Law AS, Holland GR, Abott PV, Roda RS.
Identify and define all diagnostic terms for pulp health
and disease states. J Endod. 2009;35(12):1645–57.
24. Green TL, Walton RE, Clark JM, Maixner D.
Histological examination of condensing osteitis in
cadaver specimens. J Endod. 2013;39:977–9.
 Cystic and Non-cystic Lesions
at the Peri-apex of the Teeth 4

Summary
The most common peri-radicular lesions of the jaws are inflammatory
lesions caused by infection of the dental pulp. Peri-apical granuloma,
chronic peri-apical abscess, peri-apical pocket cysts, radicular cysts, extra-
radicular infections, foreign body reactions and fibrous scar tissue typi-
cally present as unilocular peri-apical radiolucencies of varying size and
degrees of circumscription. The need to differentiate can only be based on
a careful history taking, clinical signs and symptoms and equivocal pulpal
sensibility testing followed by commencement of nonsurgical root canal
treatment to tip the balance in favour of healing.

Clinical Relevance 4.1 Overview of Peri-apical

Clinically peri-apical lesions cannot be differen-
tially diagnosed as either cystic or non-cystic
lesions based on conventional radiographs. An
accurate diagnosis can only be made following
histopathological serial sectioning of the lesion
in its entirety. Unlike true radicular cysts, peri-
apical pocket cysts (Bay cysts) may heal after
nonsurgical root canal therapy. The clinician
must also be aware of other radiopaque jaw
lesions that mimic lesions of endodontic origin
that may not respond to conventional treatments
requiring careful follow-up and in some cases
surgical exploration and biopsy to confirm the
true nature of the problem.
Pathologies in Endodontics
A cyst, derived from the Greek Krystis mean-
ing sac or bladder, is defined as a closed path-
ological cavity, lined by an epithelium that
contains a liquid or semisolid material [1].
Radicular cysts are inflammatory jaw cysts
that commonly occur at the peri-apex of a
necrotic, infected pulp as a direct sequel to
apical granuloma, although a granuloma need
not always develop into a cyst. Occasionally
they may also be found on the lateral aspects
of the root in relation to a lateral accessory
canal [2].

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 49
DOI 10.1007/978-3-319-15591-3_4, © Springer International Publishing Switzerland 2015
50 4 Cystic and Non-cystic Lesions at the Peri-apex of the Teeth

a b c

Fig. 4.1 Clinical radiographs showing resolution of peri- graph following completion showing significant reduction
apical endodontic lesion following nonsurgical root canal in lesion size and (c) 12-month follow-up demonstrating
therapy. Note (a) preoperative view of tooth 22 showing intact periodontal ligament space associated with the
distinct peri-radicular lesion, (b) 6-month review radio- peri-apex

Persistent peri-radicular radiolucencies of Table 4.1 Surgical sieve for radiolucent and mixed
endodontic origin are commonly due to intra- lesions of the jaw
radicular infection [3], extra-radicular infection Well-circumscribed radiolucent lesions
[4–6], foreign body reactions [7], true cysts [8, 9] Developmental
and fibrous scar tissue [10]. Orthograde root Nasopalatine duct cyst
canal treatment or re-treatment with the intention Dentigerous cyst
to remove/eliminate microorganisms below a Odontogenic keratocyst
Inflammatory
critical threshold conducive to healing is the first
Peri-apical granuloma
line of treatment in all cases. Lesions associated
Peri-apical pocket cyst
with extra-radicular infections, true cysts and for-
Radicular cyst
eign body reactions can only be managed by peri- Neoplastic
radicular surgery. Peri-apical lesions that heal by Multiple myeloma
fibrous scar tissue require no treatment (Fig. 4.1). Ameloblastoma
Many lesions that occur in the jaw including Traumatic
lesions of endodontic origin (inflammatory cysts, Traumatic bone cyst
granulomas, abscesses or fibrous scars) have similar Metabolic
radiological appearances often making it difficult to Giant cell lesions of hyperparathyroidism
differentiate among them (Table 4.1 and Fig. 4.2). Idiopathic
Although rare, other clinically confusing peri-apical Aneurysmal bone cyst
lesions have been documented including lesions of Central giant cell granuloma
4.1 Overview of Peri-apical Pathologies in Endodontics 51

Table 4.1 (continued) malignancy. It is therefore imperative to have an

Ill-defined radiolucent lesions understanding of the pathogenesis of common end-
Inflammatory odontic lesions and their management to ensure that
Acute osteomyelitis misdiagnosis is avoided. Careful history taking and
Neoplastic clinical findings should be evaluated taking into con-
Osteogenic sarcoma sideration radiographic findings to help in narrowing
Chondrosarcoma down the differential diagnosis. Follow-up is impor-
Metastatic lesions tant not only to ensure that any therapeutic treatment
Lesions with mixed and/or variable radiological
approach has been successful but also to confirm the
appearances
Developmental
correct diagnosis has been made [11, 12].
Fibrous dysplasia Two distinct categories of radicular cysts have
Inflammatory been reported in the literature making a distinc-
Condensing osteitis tion between those cavities containing completely
Neoplastic enclosed epithelium (true radicular cyst) and
Osteochondroma (benign) those containing epithelium-lined cavities that are
Ossifying (cement-ossifying) fibroma open to the root canals (bay cyst or peri-apical
Osteosarcoma (malignant) pocket cyst) (Fig. 4.2). The former is an indepen-
Normal anatomical structures dent entity resulting in a lesion that is self-sustain-
Mental foramen ing and no longer dependent on the presence or
Maxillary sinus absence of root canal infection. As a result surgi-
Nutrient canals cal excision would have to be performed following

a b c

Fig. 4.2 Diagrams showing (a) non-vital tooth with a
peri-radicular lesion that cannot be distinguished radio-
graphically from a peri-apical granuloma, abscess or cyst.
Note (b) a peri-apical pocket cyst that by definition has an
epithelium-lined cavity that communicates with the root
canal system and (c) a radicular cyst where the epithelium-
lined cavity is completely enclosed from the root canal
system. The former will often resolve following nonsurgi-
cal root canal therapy, whereas the latter may require sur-
gical enucleation
52 4 Cystic and Non-cystic Lesions at the Peri-apex of the Teeth
conventional root canal treatment to ensure heal-
ing. In the latter nonsurgical root canal treatment
carried out effectively would eliminate the infec-
tion within the root canal space, ensuring peri-
apical pocket cysts would heal [8, 9].
Currently the gold standard for diagnosis of a
peri-apical lesion is based on clinical and histologi-
cal findings using serial sectioning of the lesion in
its entirety [11]. In the past, assumptions were
made based on radiological findings to differentiate
between a true radicular cyst and peri-apical granu-
loma, which were scientifically unsound.
Often lesion size was measured and larger
radiographic diameters were more likely thought
of as cystic as opposed to granulomatous in
nature, which was not always the case [13–15].
Radiological appearances of cysts are often
described as round or ovoid radiolucencies sur-
rounded by a narrow radiopaque demarcating
margin, which extends from the lamina dura of
the involved tooth. In infected or rapidly growing
cysts this margin may not be present and these
features are therefore not correlative with the
definitive diagnosis of a true radicular cyst [16].
Several surgical approaches exist for the man-
agement of cystic lesions of the jaws including
enucleation, marsupialisation and decompres-
sion. Enucleation comprises of complete removal
of the cyst lining which is a definitive treatment
modality not usually requiring further interven-
tion. The risk of morbidity is higher as
nearby structures and teeth may be damaged.
Marsupialisation is the conversion of a cyst into a
pouch. The cystic roof is removed in its entirety,
and the cut edges of the remaining cyst are
sutured to the adjacent soft tissue lining the oral
cavity, maxillary sinus or nasal cavity into a con-
tinuous pouch. Surgical decompression is a mini-
mally invasive technique whereby a large cystic
lesion is converted into a small one with the aim
of any future surgical intervention having reduced
morbidity when considering enucleation.
Decompression involves the insertion of a
decompression stent/drainage tube into the peri-
apical lesion, regular irrigation, periodic length
adjustment and maintenance of the drain for
varying lengths of time. It is contraindicated in
cases of large dental granulomas or any solid cel-
lular lesion for the reason that there is an absence
of a fluid-filled cavity to decompress [17–21].
There have been numerous reports of non-
odontogenic benign and malignant lesions present-
ing in the peri-apical area mimicking lesions of
endodontic origin. The frequency and distribution of
radiolucent jaw lesions in a retrospective study
revealed that most non-healing lesions submitted for
biopsy were classified as either apical granulomas
(40.4 %) or apical cysts (33.1 %), and they were often
from the maxillary anterior jaw. Over 20 % of the
reported non-healing radiolucent lesions submitted
had a more severe pathologic implication, such as
odontogenic keratocysts (8.8 %), central giant cell
lesions (1.3 %), ameloblastomas (1.2 %) and even
the small but important number of metastatic lesions
(0.26 %). Most of these lesions were located in the
posterior mandible. Granulomas or cysts (73 %)
were often from the anterior maxillary jaw. Thus
non-healing radiolucent jaw lesions other than granu-
lomas or cysts were reported over 20 % of the time
and may have more severe pathological implications,
suggesting the value of differential diagnoses [22].
Common cysts that mimic lesions of endodon-
tic origin include odontogenic keratocysts [23],
residual cysts [24], lateral periodontal cysts [25]
and nasopalatine duct cysts [26].
Benign aggressive lesions that cause locally
destructive lesions mimicking peri-apical pathosis
include central giant cell granulomas [27, 28], central
ossifying fibroma [29], calcifying epithelial odonto-
genic tumour (Pindborg tumour) [30, 31], osteoblas-
toma [32] and central odontogenic fibroma [33].
Benign cemento-osseous dysplasia including
peri-apical cemental dysplasia can develop
around the apices of the teeth, representing a
well-recognised diagnostic challenge that is dif-
ficult to distinguish from peri-apical granulomas
in the early stages [34, 35].
Granulomatous inflammation distinguished
from granulation tissue associated with peri-
apical granulomas is a distinct entity that has
been reported in the literature elicited by foreign
material. It has been proposed that foreign body-
induced granulomatous inflammation at the peri-
apex of the teeth may result in endodontic
treatment that fails to heal [7, 36, 37].
A variety of misdiagnosed malignant neoplas-
tic lesions have been reported in the endodontic
literature, masquerading at the peri-apex of the
teeth similar to lesions of endodontic origin. As a
result of clinical and radiographic similarities,
4.3 Lesions of Endodontic Origin
these lesions may be mistaken with inflammatory
or infectious diseases of the jaws, creating a
dilemma for the clinician. Histopathological
evaluation is of paramount importance when the
lesion fails to respond to routine treatments [12,
31, 38–45].
4.2 Differential Diagnosis
of Radiolucent Lesions
of the Jaw
The most common peri-radicular lesions of the
jaws are peri-apical granuloma, peri-apical cyst
(radicular and peri-apical pocket cyst) and the
chronic dental abscess, which are inflammatory
in origin due to the demise of the dental pulp. All
three lesions typically present as unilocular, peri-
radicular radiolucencies of varying sizes.
Unequivocal results of clinical signs and symp-
toms including pulp vitality testing and radio-
graphic diagnosis often lead to commencement
of root canal treatment which tips the balance for
healing to occur. The need for follow-up is a pre-
requisite not only to determine the outcome of
treatment but also to ensure that a correct diagno-
sis was reached. In the cases of lesions that fail to
respond, a surgical approach may be necessary to
confirm histopathologically the underlying rea-
son for failure and also rule out the possibility of
other lesions that mimic endodontic pathology.
a b
Fig. 4.3 Clinical photomicrographs showing distinct his-
topathological features of a peri-apical granuloma.
Typical features include chronically inflamed granulation
tissue at the apex of a non-vital tooth surrounded by
53
4.3 Lesions of Endodontic Origin
Peri-apical granuloma
A chronic inflammatory reaction that consists
of granulomatous tissue predominantly infiltrated
with lymphocytes, plasma cells and macro-
phages. The lesion is maintained by persistent
necrotic pulpal contents resulting in a well-
circumscribed radiolucent lesion around the peri-
apex of a tooth. Occasionally the lesion may
present laterally in response to a lateral canal or
perforation. Nonsurgical endodontic therapy will
eradicate the lesion (Fig. 4.3).
Peri-apical condensing osteitis
Reactive hyperplasia at the peri-apex of a
tooth in response to a low-grade pulpal infection
can lead to condensing osteitis. Typically seen in
young adults and teenagers, affecting mandibular
molars and premolars most commonly. The bone
is compact and dense with minimal chronic
inflammation appearing more radiopaque at the
peri-apex of the tooth. Endodontic treatment is
required to resolve the problem.
Acute apical abscess
An abscess is defined as a ‘localised collection
of pus’ that can occur around the peri-apex of an
endodontically infected tooth. An abscess is a
focus of acute inflammation characterised by a
distinct collection of polymorphonuclear leuko-
cytes within a pre-existing chronic inflammatory
lesion (e.g. granuloma). An acute peri-apical
fibrous connective tissue and lymphatic (plasma cells,
neutrophils, mast cells, etc.). Note light microscopy (a)
×100, (b) ×200 (Courtesy of Drlan Clarke Capital
Pathology Canberra ACT)
54 4 Cystic and Non-cystic Lesions at the Peri-apex of the Teeth

a b c d e

f g h i

Fig. 4.4 Clinical radiographs and photograph demon-
strating case diagnosed as chronic apical abscess. Note (a)
and (b) parallel peri-apical and mesial 20° shift showing
extensive peri-radicular radiolucent lesion extending from
the peri-apex of teeth 32, 31 and 41. Following pulp sen-
sibility testing, a diagnosis of chronic apical periodontitis
31 was made. Teeth 32 and 41 were deemed vital.(c) MAF
preparation was completed using hand files, (d) patency
filing was used and pus exudate was noted, (e) intra-canal
medication was placed for 3 months, and (f) review
appointment showed dressing resorbed and peri-apical
lesion reduced considerably in size. (g–i) Nonsurgical
endodontic treatment completed. Patient has been placed
on further review

abscess is a very painful condition that is charac-
terised by intense throbbing; extreme pain to
touch, biting and percussion; palpation tender-
ness; and increased mobility of the tooth. An
intra-oral or extra-oral swelling may be evident.
Radiographically there may not be any signs.
Chronic apical abscess (phoenix abscess)
Chronic apical periodontitis with suppuration
These terms denote a peri-apical abscess that
arises from an acute exacerbation of a chronic
inflammatory peri-apical lesion (Fig. 4.4).
The lesion appears as a well-demarcated
radiolucency at the peri-apex of a tooth.
Histopathologically a variable mixture of fibrovas-
cular connective tissue, scar and chronic inflam-
matory cells is present with foci of neutrophils,
oedema and liquefaction necrosis. Often drainage
may be evident through a sinus intra-orally with or
without symptoms. Nonsurgical endodontic treat-
ment will eradicate the lesion.
Peri-apical pocket cyst
An inflammatory lesion that contains a
sac-like epithelium-lined cavity that is open
to and continuous with the root canal. Pocket
cysts are more likely to heal after nonsurgical
endodontic therapy of the tooth since the treat-
ment removes the source of irritation. A well-
defined radiolucency will be associated either
apically or laterally and indistinguishable
from peri-apical granuloma or radicular cyst.
Nonsurgical treatment will often eradicate the
lesion (Fig. 4.5).
Radicular cyst
An inflammatory lesion with a distinct patho-
logical cavity completely enclosed in an epithe-
lial lining so that no communication to the root
4.3 Lesions of Endodontic Origin
a b
Fig. 4.5 Clinical radiographs demonstrating manage-
ment of a large peri-apical lesion associated with the peri-
apices of teeth 31 and 41. Differential diagnosis includes
peri-apical granuloma, peri-apical pocket cyst and radicu-
lar cyst. (a) Initial preoperative radiograph. Note diffuse
peri-apical radiolucency. (b) Master apical file radiograph
canal exists. It occurs as a result of inflammation-
induced proliferation of rests of Malassez within
the peri-apical granuloma. The pathogenesis of
radicular cysts has been described as compris-
ing of three distinct phases: the phase of initia-
tion, the phase of cyst formation and the phase
of cyst enlargement. In the first phase as a result
of inflammation, proliferation of rests of
Malassez occurs within the peri-apical granu-
loma. The exact mechanism for inducing epithe-
lial proliferation is unknown, but inflammatory
mediators and bacterial toxins from within the
necrotic pulp are thought to play a central role.
During the second phase, a cyst cavity develops
lined by proliferating epithelium. Again, the
exact mechanism of cyst cavity formation is a
matter of debate. Three main hypotheses for the
development of cavity formation include the
possibility of epithelium proliferation to cover
the connective tissue surface of an abscess cav-
ity, cavity formation as a result of connective
tissue breakdown surrounded by sheets of epi-
thelium and epithelial degeneration in which
micro-cysts are formed at the centre of large
epithelial masses by epithelial cell degeneration
and autolysis.
Clinically small radicular cysts are often
asymptomatic and only discovered during rou-
tine radiographic examination. Over time, if the
55
c d
(no additional lingual canal noted). (c) Post-operative
view of obturated tooth 41 and (d) 6-month follow-up
showing complete resolution of the peri-radicular lesion
and confirming that tooth 31 was not involved (as demon-
strated by pulpal testing preoperatively)
cyst is undetected, it may slowly expand enlarg-
ing the jaw. The initial swellings are usually bony
hard, but as the cyst increases in size, the overly-
ing cortical bone may become very thin until
finally with progressive bone resorption the
swelling exhibits ‘egg shell crackling’. Eventually
complete loss of the overlying bone results in the
mucosa appearing bluish and the cyst becomes
fluctuant (Fig. 4.6).
Histopathologically an inflamed fibrovascular
connective tissue wall is evident with non-
keratinising, often hyperplastic stratified squa-
mous epithelium lining. Radiographically, a
well-defined radiolucency may be seen with
possible radioopaque borders occurring apically
and laterally that is indistinguishable from a peri-
apical granuloma or peri-apical pocket cyst.
The radicular cyst often contains large
amounts of cholesterol crystals (Fig. 4.7), which
cannot be removed by the host defence system,
thus helping to sustain this pathological condi-
tion. Endodontic surgery will be required with
curettage.
Residual cyst
A residual cyst arises from epithelial remnants
stimulated to proliferate by an inflammatory pro-
cess originating from pulpal necrosis of a non-
vital tooth that is no longer present. Usually a
non-vital tooth remains in situ long enough to
56 4 Cystic and Non-cystic Lesions at the Peri-apex of the Teeth
a b
c d
Fig. 4.6 Clinical case showing large radicular cyst occu-
pying left maxillary sinus as result of a non-vital central
incisor which had suffered trauma as a child. The patient
presented with a draining sinus in relation to tooth 21 but
no obvious facial swelling. (a) Initial intra-oral radiograph
develop chronic peri-apical pathosis (i.e. a radic-
ular cyst). Eventually the tooth is extracted with
little regard to the peri-apical pathosis, which
remains within the jaw as a residual cyst. Over
the years, the cyst may regress, remain static or
grow. Ongoing clinical symptomology or chance
radiographic findings may alert the clinician to
the presence of a radicular cyst requiring excision
and histopathological examination to confirm
diagnosis.
Peri-apical fibrous scar tissue
A well-circumscribed persistent lesion that
may be present after completion of either nonsur-
gical or surgical endodontic therapy. Healing fol-
lowing resolution of inflammation occurs by
fibrous scar tissue filling the defect rather than
bone. Minimal or no inflammatory cell infiltrate
will be present histopathologically. This type of
e f
demonstrated a large peri-radicular lesion whose margins
could not be visualised completely. A cone beam CT scan
was arranged. Note the extent of expansion in the left
maxillary sinus seen on (b) rotational tomogram and (c–f)
sagittal slices
lesion may be interpreted as ‘failure’ during fol-
low-up procedures and must be distinguished
from a true failure from persistent inflammation.
Scar tissue commonly occurs in through-and-
through lesions where bony infill is preceded by
fibrous tissue.
4.4 Lesions of Non-endodontic
Origin
Many anatomic structures and osteolytic lesions
can be mistaken for peri-radicular pathosis and
have been reported in the literature including
various developmental cysts, fibro-osseous
lesions, infections, granulomatous inflammatory
conditions and a wide range of benign or malig-
nant neoplasms. Additionally other radiographic
4.4 Lesions of Non-endodontic Origin
a b
c d
Fig. 4.7 Clinical photomicrographs using hematoxylin
and eosin staining demonstrating histopathological fea-
tures of a radicular cyst. These include (a–c) a cavity lined
by non-keratinised hyperplastic squamous epithelium and
anatomical superimpositions that have been mis-
taken for peri-radicular pathosis include the
maxillary sinus, nutrient canals, nasal fossa and
lateral or submandibular fossa. Many systemic
conditions can mimic or affect the radiographic
appearance of the alveolar process. A discussion
of these conditions is beyond the scope of this
chapter, but the reader is encouraged to read fur-
ther in any oral pathology textbook.
Cysts
Odontogenic keratocyst
A developmental cyst arising from the rests of
dental lamina, arising at any age and most com-
monly located in the posterior mandibular body
and ramus. Multiple lesions are often seen with
basal cell nevus syndrome (Gorlin–Goltz syn-
drome). Radiographically, it presents as a well-
57
ChCl
(d) cholesterol clefts (ChCl). Note light microscopy (a)
×100 and (b–d) ×200 (Courtesy of Dr Ian Clarke Capital
Pathology Canberra ACT)
circumscribed unilocular or multilocular lucent
lesion with well-corticated borders. An important
feature of these cysts is to grow in an anteropos-
terior direction with minimal cortical expansion.
These cysts will continue to persist and enlarge
following root canal therapy.
Nasopalatine duct cyst
A developmental cyst arising from the epithe-
lial remnants of the nasopalatine duct in the inci-
sive canal. Usually occurs in the midline of the
maxilla with occasional palatal swelling if large
enough. There is high risk of misinterpretation
when a coincident maxillary incisor tooth pres-
ents with questionable vitality.
Lateral periodontal cyst
A developmental cyst arising from the rests of
dental lamina. Usually occurs in middle-aged
58 4 Cystic and Non-cystic Lesions at the Peri-apex of the Teeth
adults in the mandibular and maxillary premolar
and canine regions. Typically occurs between the
roots of vital teeth.
Ameloblastoma
The majority of ameloblastomas are benign
with less than 1 % showing malignant behaviour.
Typically occur in adults between the 3rd and 7th
decade of life as asymptomatic lesions that can
cause facial swellings. The most common site for
occurrence is the ascending ramus and proximal
body of the mandible. Ameloblastomas are sub-
divided into either uni-cystic or multi-cystic.
Marked bucco-lingual cortical plate expansion
may be evident on radiographs, giving rise to a
‘soap bubble’ appearance. Tooth resorption and
displacement may be evident.
Central giant cell granuloma
These lesions can occur at any age but have a
propensity to occur in patients younger than
30 years of age and more commonly in females.
The lesion often presents in the anterior mandible
with a tendency to cross the midline. They may
cause a variable degree of bony expansion with
divergence of roots and root resorption. Brown
tumour of hyperparathyroidism can mimic
CGCGs radiographically as well as pathologi-
cally, requiring biochemical testing and radio-
logical findings in other bones to help
differentiate.
Benign fibro-osseous lesions
Peri-apical cemento-osseous dysplasia
A specific type of fibro-osseous lesion known
as ‘peri-apical cemental dysplasia’ develops
around the apices of teeth with a predilection for
mandibular incisors representing a diagnostic
challenge. In the early stages, it appears as a
well-defined radiolucent lesion, which gradually
becomes radiopaque with a thin lucent rim.
Careful clinical assessment including sensibility
testing and radiographic interpretation should
establish a reliable diagnosis. Endodontic treat-
ment is not indicated in these cases.
Malignant lesions
A wide range of primary or metastatic malig-
nant lesions have been reported in the literature
as lesions surrounding the peri-apex of a tooth
diagnosed as something more sinister following
failure of endodontic treatment to resolve symp-
toms or confirmation by way of histopathologi-
cal diagnosis. The astute clinician must be
aware of atypical features not commonly
reported with infections of endodontic origin
such as minimal caries, root resorption, irregu-
lar radiolucency, localised tooth mobility, anaes-
thesia and failure of the peri-apical lesion to
resolve after root canal treatment. Tooth vitality
is an important finding in the majority of these
cases although on rare occasion this has proved
to be inconclusive.
4.5 Surgical Decompression
Treatment options for the management of large
peri-radicular radiolucent lesions include nonsur-
gical root canal treatment, apical surgery or
extraction. If the lesion is in close proximity to
adjacent vital teeth and surrounding structures
(such as the maxillary sinus, floor of the nose,
mandibular canal or mental foramen), due con-
sideration must be given since the risks of dam-
age following a surgical approach are high. A
more conservative approach is to carry out a
decompression procedure. Surgical decompres-
sion allows continuous drainage often resulting
in a significant reduction in lesion size, which
may then respond more favourably when either a
nonsurgical or surgical approach is carried out.
The steps involved when carrying out such a pro-
cedure include:
1. Adequate anaesthesia is administered. A
block or infiltration is more than sufficient for
adequate anaesthesia of the area.
2. Decompression tube is fabricated from a stan-
dard intravenous setup. This type of tubing is
suitable due to having sufficient diameter to
prevent clogging and sufficient strength
to prevent collapsing and is readily available.
A section of tube is pre-cut and the terminal
end bevelled to a 45° angle.
3. A small vertical incision is made directed into
the centre of the lesion. The incision is placed
through the periosteum to bone usually pene-
trating the lesion.
4.6 Clinical Case
4. The bevelled end of the tube is inserted to the
depth of the lesion until resistance is met pos-
teriorly. The tube is adjusted so that the oppo-
site end is flush to the gingivae. This section of
tube is then pressed against a heated spatula to
create a button, which prevents tube slippage
posteriorly. On occasion, a suture may be
required either above or below the tube on the
vertical incision line to ensure close adaptation
of the tissue. The tubing can also be secured in
place by a non-resorbable suture as a
precaution.
5. The patient is instructed on the correct irriga-
tion technique. A 10-mL disposable Luer-Lok
syringe with an irrigating needle is given to
the patient along with a supply of sterile water.
The patient is instructed to irrigate a minimum
of three times daily using the entire contents
of the 10-mL syringe.
6. The patient is reviewed on a weekly basis
until there is no further evidence of fluid or
exudate contents being flushed from the
lesion. This course of treatment can take from
2 days to 4 weeks.
7. The involved tooth associated with the lesion
should be endodontically instrumented and
dressed with a suitable intra-canal medica-
ment (such as calcium hydroxide). This treat-
ment should be carried out prior to surgical
decompression or immediately after.
8. Once the tube is removed permanently, the
soft tissue defect should heal within a few
days or up to a week.
4.6 Clinical Case
A 56-year-old gentleman was referred regarding
a long-standing lesion associated with tooth 21.
The general dental practitioner had seen the
patient for numerous dressings, but despite his
best efforts, the canal could not be dried.
Clinical examination confirmed a distinct
peri-radicular radiolucency associated with the
peri-apex of tooth 21 extending to the adjacent
lateral incisor. Tooth 22 responded positively to
both electric pulp testing and thermal stimulus
59
(CO2 snow). At the first appointment, an exu-
date of pus was confirmed within the canal.
Chemo-mechanical canal preparation was com-
pleted using stainless steel hand files and
sodium hypochlorite solution with master api-
cal preparation completed to size #70. An intra-
canal calcium hydroxide medicament was
placed (Fig. 4.8).
The patient was forewarned about the possi-
bility of surgical intervention and that a surgical
decompression approach may help avoid this.
Following surgical decompression (Fig. 4.9), the
patient was seen a further 3 months later for com-
pletion of endodontic treatment (Fig. 4.10). No
further exudate was present within the canal and
the buccal draining sinus had resolved. The
patient has been placed on careful follow-up and
understands that any further issues with the tooth
will need to be addressed from a surgical
approach.
Clinical Hints and Tips
• A peri-apical granuloma or peri-apical
pocket cyst may heal after conventional root
canal therapy, whereas a true radicular cyst
will require surgical intervention. Treatment
of suspected cysts, therefore, require careful
follow-up over a period of time.
• If surgical intervention is necessary, the
decision as to whether to raise a flap and
completely enucleate or to try ‘decompres-
sion’ first is a consideration for some cases.
• Decompression may allow the lesion to be
predictably much smaller should enucle-
ation be necessary, and there may be less
damage to associated teeth and vital struc-
tures as a result.
• There is no standard protocol regarding
length of time needed for the drain. As a
practical matter, many patients may not be
willing to undergo prolonged treatments.
• Surgical decompression is a conservative
approach which requires patient co-opera-
tion, and appropriate informed consent
must be attained with the patient fully
understanding that further surgical inter-
vention may be necessary.
60 4 Cystic and Non-cystic Lesions at the Peri-apex of the Teeth
a b
d e
Fig. 4.8 Clinical case that was initially treated with a sur-
gical decompression approach. The patient had received a
traumatic blow to his upper jaw 2 years previously. He had
been seeing his general dental practitioner for root canal
treatment of tooth 21, but treatment could not be com-
pleted due to continuous exudate within the canal. An
endodontic referral was made and a decision made to
embark upon a nonsurgical approach. A recommendation
was made to also carry out surgical decompression to
c
f
ensure a dry canal prior to obturation. Radiographs dem-
onstrating (a, b) initial preoperative views showing large
radiolucent lesion encroaching on the floor of the nose
and involving the peri-apex of the vital adjacent tooth. (c)
MAF working length, (d) calcium hydroxide dressing
placement, (e) note decompression tubing barely visible
(red arrow) and (f) intra-oral view of tooth 21 dressed
with calcium hydroxide. In this case, the tubing was not
tolerated by the patient and removed after 2 days
4.6 Clinical Case 61

a b

c d

e f

Fig. 4.9 Clinical pictures demonstrating surgical decom- line), (c) insertion of tube to posterior margin, (d) tubing
pression of tooth 21. Note (a) preoperative view showing cutback flush to gingivae and sutures placed to secure, (e)
draining sinus in overlying alveolar mucosa (green decompression drain in place and (f) irrigation of lesion
arrow), (b) vertical incision made overlying sinus (dotted using Leu-Lock syringe 10mL flush of sterile saline
62 4 Cystic and Non-cystic Lesions at the Peri-apex of the Teeth
a b
Fig. 4.10 Clinical radiographs showing (a) preoperative
view and (b) post-operative view of tooth 21. A warm ver-
tical compaction technique using AH plus cement and
gutta-percha was used. The patient has been placed on
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21. Sammut S, Morrison A, Lopes V, Malden
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23. Wright BA, Wysocki GP, Larder TC. Odontogenic
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 Ethics and Law
5

Summary
Endodontic procedures are both challenging and technically demanding
resulting in treatments that may have fallen short of acceptable guidelines.
Occasionally the dentist may be open to litigation on the basis of clinical
negligence. Failure to communicate with patients about the procedure and
not obtaining consent for treatment is a key area of complaint, as is inad-
equate record keeping. When treatment is undertaken within the frame-
work of accepted guidelines, it would be very difficult for a patient to open
a claim for clinical negligence should a failure occur.

Clinical Relevance Receiving a complaint from a patient can be

Endodontics is an area of dentistry which gives
rise to an increasing amount of complaints and
litigation. Valid consent is an absolute require-
ment for legal and ethically correct treatment.
Appropriate consent, through good communica-
tion, plays an important role in overall risk man-
agement that can reduce the chances of
complaints. Warning patients about the risks
associated with endodontics is an important part
of obtaining a valid consent. Where treatment
will be complex, a referral to a specialist should
be offered.
5.1 Overview of Ethico-Legal
Issues and Endodontics
Today, we live in a world of ever-increasing con-
sumerism and high expectations where patients are
sometimes dissatisfied resulting in a complaint.
very confronting and stressful. Patients gener-
ally complain because they may be dissatisfied
with their experience, they may seek information
that is not forthcoming or they may be unhappy
with the result of care provided [1]. The dimen-
sions of patient satisfaction include the art of care
(caring attitude), technical quality of care, acces-
sibility and convenience, finances (ability to pay
for services), physical environment, availability,
continuity of care, efficacy and outcome of care
[2]. A complaint can be defined as ‘an expression
of dissatisfaction with the practice’s procedures,
charges, personnel or quality of service’ [3].
Good communication, both verbal and non-
verbal, is a key to reducing patient complaints [4].
The clinician must be astute in determining patient
expectations, addressing previous misconceptions
and being able to ensure that the divide between
the patients’ expectations and what can actually be
achieved has been modified, reduced or eliminated.

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 65
DOI 10.1007/978-3-319-15591-3_5, © Springer International Publishing Switzerland 2015
66
Table 5.1 Key clinical risk management checklist
Always attempt to develop rapport and communication
with the patient
Before performing any endodontic procedure, obtain
informed consent
Document clearly, fully and legibly where applicable
Know when to refer the patient for a second opinion
Have all necessary equipment before beginning
endodontic procedures
Good radiographic technique should be applicable with
preoperative, peri-operative and post-operative films
demonstrating technique
Rubber dam use is mandatory both from an aseptic
point of view and medicolegally
Any iatrogenic errors during the procedure should be
discussed with the patient and documented and
appropriate referral option given where necessary
Be knowledgeable in the recognition and management
of common endodontic complications including
hypochlorite accidents and post-treatment flare-ups
Consider appropriate referral to endodontic specialist
where applicable
This process fathomed from careful history taking,
clinical examination and overall assessment will
aim to address any unmet patient expectations
thereby reducing the cause of many complaints
[5]. Early recognition of patient unhappiness will
help to resolve concerns quickly and prevent
patient complaints from escalating [6].
With dental practitioners performing more
endodontic procedures in their office, the expo-
sure to possible malpractice litigation increases
significantly. It is not enough to possess good
skills and techniques; dentists must actively and
diligently adhere to risk-reduction strategies to
help minimise or eliminate future lawsuits [3, 7].
Clinical risk management is the process by which
a framework of protocols is in place in order to
prevent complaints or at least help minimise their
impact (see Table 5.1).
Valid consent is a continuous evolving process
rather than a single event, leading to patient
understanding and permission for the clinician to
deliver treatment, fundamental to clinical, as well
as ethical and legal, risk [8].
Clinical and ethical risk management
requires not only the correct treatment being
5 Ethics and Law
provided, and appropriate consent obtained, but
also good records of that treatment. Good
record keeping is fundamental in managing risk
and preventing and resolving complaints and
legal claims [9, 10].
Ethics is a branch of the discipline of philoso-
phy that studies morality associated with human
behaviour. Professional ethics in dentistry from
the time of Hippocrates to the present day is
based on the ‘duty of care’ and providing justice
and fairness to the patient including beneficence,
respect for autonomy, veracity, quality care, con-
tinued learning and fidelity [11, 12]. The princi-
ple of beneficence is based on the fact that the
patient is seeking care from a clinician to gain
benefits in his/her oral health. The clinician pro-
vides the highest quality of care subject to cur-
rent scientific understanding, the clinical
circumstance and the patients’ desires. Respect
for autonomy, derived from the Greek meaning
of self-rule or governance, means that it is mor-
ally correct to acknowledge and affirm the rights
of the patients and their self-determination,
important in the process of gaining both a moral
and legal valid consent. Truthfulness or veracity
is a moral duty to all patients whereby valid con-
sent is achieved without manipulation, deception
or coercion. A prima facie duty of dentists is to
ensure that the upmost quality of care is pro-
vided to the patient ensuring maximum benefit.
Any treatment therapy provided must be appro-
priate for the specific problem addressed based
on both sound scientific knowledge and estab-
lished technical standards. One cannot provide
quality care or care consistent with the profes-
sion’s knowledge base, if one is not familiar with
that knowledge base. Hence continued learning
(CPD) is a further professional moral duty for
the dentist [13, 14]. Fidelity or faithfulness is the
promise of the dentist to patients to be there for
them; to place their interests as primary; to do
for them the best that can be done with regard to
oral health, and to not abandon them in a time of
their need [15].
A dentist assumes a duty of care under com-
mon law when a patient is accepted for treatment.
5.1 Overview of Ethico-Legal Issues and Endodontics
Complaints as a direct result of any treatment
provided by the dentist can result in disciplinary
matters with the governing body that regulates
the profession or civil and/or criminal proceed-
ings. The former may result in suspension or era-
sure with revoking of their dental licence and
ability to practice. The latter may be brought
before either a judge or jury, resulting in either
compensation or direct criminal proceedings.
Civil and criminal matters brought before a judge
may arise as a resultant of either intent such as
assault (battery), negligence or strict liability
(problems arising from the use of dental
products).
To bring an action of negligence under law,
the judge needs to be satisfied that a duty of care
existed between the defendant (the clinician) and
the plaintiff (the patient), that the duty of care
was breached and that there is a causal link
between the breach of duty and injury sustained
by the patient.
Duty of care (doctor–patient relationship)
requires that the clinician provides a quality of
care in accordance with their appropriate skill
and knowledge. Valid informed consent helps
protect the clinician from complaints, civil
claims, criminal charges and disciplinary matters
with the relevant governing body.
In the English law (UK) the Bolam principle
for negligence was derived from the direction
given by McNair J to the jury in the case of Bolam
v. Friern Hospital Management Committee.
Mr Bolam, a manic–depressive, was given elec-
troconvulsive therapy. Risks of the procedure
including seizures that could result in fractures of
the patient’s bones were not discussed. Measures
such as restraints and the use of muscle relaxant
drugs to reduce these dangers were not given or
discussed either. Being ignorant of these issues,
he did not ask for them and following therapy sus-
tained severe fractures to his pelvis [16]. The
Bolam principle was formulated as a rule that a
doctor is not negligent if he acts in accordance
with a practice accepted at the time as proper by a
responsible body of medical opinion even though
other doctors adopt a different practice. In short,
67
the law imposes the duty of care, but the standard
of care is a matter of medical judgement.
The Sidaway case was another landmark case
concerning the duty of the surgeon in terms of
informing the patient of the potential risks before
undergoing an operation. The claimant suffered
from pain in her neck, right shoulder, and arms. Her
neurosurgeon took her consent for cervical cord
decompression, but did not include in his explana-
tion the fact that in less than 1 % of the cases, the
said decompression caused paraplegia. She devel-
oped paraplegia after the spinal operation. In this
case the judge ruled that the clinician was not negli-
gent if he had informed the patient of the same risks
as a responsible body of medical opinion, analo-
gous to the Bolam test of negligence [17].
Inherent problems in the paternalistic
approach to the Bolam test as applied to consent
to treatment and the disclosure of risk have been
exposed through a series of cases that have moved
the law step-wise to a position more in alignment
with that of North American jurisdictions and
Australia. At the age of two Patrick Bolitho was
diagnosed with a patent ductus arteriosus, a con-
dition that prolongs the foetal circulation after
birth to the detriment of the normal oxygenation
of the blood. An operation to correct the anomaly
had been undertaken in 1983 from which he
made a good recovery. A year later he was admit-
ted to St Bartholomew’s Hospital with croup.
During the course of his admission, a sequence of
events culminated in a respiratory collapse and
cardiac arrest, from which Patrick emerged with
severe brain damage and subsequently died. The
hospital admitted breach of duty for the failure of
the paediatric senior registrar, Dr Horn, to attend
when she was called on account of being detained
in the outpatient clinic. Experts for the claimant
asserted that endotracheal intubation would have
been the correct course of action under the cir-
cumstances, but Dr Horn maintained that even
had she attended she would not have attempted
intubation and cited Bolam to demonstrate that a
responsible body of opinion would have endorsed
her decision. Therefore, the failure to attend was
not causally linked with the respiratory arrest
68
since, hypothetically, had she attended the out-
come would have been the same. It was however
concluded that in rare cases, where a reasonable
body of professional opinion is not capable of
withstanding logical analysis, the judge is enti-
tled to hold that the opinion is not reasonable or
responsible [18].
The High Court of Australia rejected the
Bolam test of medical negligence with respect to
giving information and obtaining consent in
Rogers v Whitaker. Mrs Whitaker developed an
extremely rare condition in her left eye after
undergoing surgery on her right eye. She had been
blind in the right eye for many years as a result of
a penetrating injury. Her treating surgeon advised
her that surgery could improve the appearance of
the eye and probably improve her sight. What the
surgeon did not tell her was that there was a
1:14,000 risk of developing ‘sympathetic ophthal-
mia’. Unfortunately she developed this condition
and was rendered totally blind. She sued
Dr Rogers on the basis that he had been negligent
in failing to provide her with the relevant advice
about the surgical risk, and further, that if she had
been given that information, she would not have
consented to the surgery. Dr Rogers argued that
the matter should be resolved by reference to the
Bolam test because there was evidence that a
body of reputable medical practitioners would not
have warned the plaintiff of the danger of sympa-
thetic ophthalmia. He could not, therefore by law,
be found to have been negligent. The trial judge
ruled that Mrs Whitaker had not been properly
warned about the risks and that had she been
warned she would not have undergone the surgery
to the right eye. She was awarded over $800,000
damages as a result [19, 20]. Ideally, all risks
(however low) should be discussed before
embarking upon endodontic treatment.
In the USA, a different principle has been long
accepted and upheld the patient’s right not to be
given medical tests or treatment without fully
informed consent on his or her part for such tests
or treatment. The case involved a 19-year-old boy
who underwent surgery for severe back pain and
experienced complications that resulted in paral-
ysis. The physicians failed to warn the patient of
any risk of paralysis from the procedure, and the
5 Ethics and Law
patient sued for malpractice and failure to fully
disclose the risks necessary to allow the patient to
make an informed consent. If harm resulted, the
patient could sue and recover damages. The
patient must be told of all material risks, compli-
cations and side effects without which the pro-
cess of consent is invalid [21–23].
Strictly speaking the patient should give con-
sent (both implied and expressed). In the man-
agement of minors (under 16) and incompetent
adults, the clinician must seek agreement with
either the parent or carer, although one can still
go ahead with treatment if this is denied, and it is
deemed in the best interests of the patient (e.g.
life-threatening). With respect to minors, a child
under the age of 16 must be considered sufficient
maturity to be able to give valid consent. This is
termed Gillick competence following a judge-
ment in 1985 [24]. Legislation also defines paren-
tal responsibility but with the proviso that the
child’s own understanding of, and consent to,
treatment must be taken into account [25].
Current mental health legislation permits only
the patient’s psychiatric condition to be treated
compulsorily. If a clinician acts in the ‘best inter-
ests’ of the patient, despite the lack of consent by
the patient themselves, then the treatment would
be deemed lawful. This decision must be made
with immediate family, carers and doctors
involved. Furthermore, any issues related to
adults with diminished or absent capacity to con-
sent are legislated by the Mental Capacity Act,
which provides a legal framework to protect the
autonomy of patients when considering issues
with consent [26–28].
A clinician must not disclose information about
a patient unless legally obliged to do so.
Consultation with a defence organisation is recom-
mended before any information is divulged [29].
The impact of failed or unsatisfactory endodon-
tic treatment is arguably greater than for many other
dental procedures. The higher-value endodontic
claims frequently necessitate remedial work or
result in the loss of the tooth and replacement with
costly bridgework or dental implants adding sub-
stantially to any settlement value [30, 31].
If any endodontic treatment has been carried
out in accordance with current teaching and
5.3 Dental Records
recognised procedures, the treatment has been
explained to the patient, valid consent has been
given including all benefits and risks, careful
records have been kept and good communication
maintained at all times, the chances of litigation
should be greatly reduced. Where problems have
arisen, the patient should be informed and appro-
priate referral sought to try and rectify the
situation.
5.2 Negligence
Whilst a decade or more ago it was unusual for
the profession to be sued, recently the ‘culture of
litigation’ has become much more prevalent
worldwide. There has been an increase in the
number of claims management firms and an
increase in advertisement of typical ‘no win no
fee’ slogans resulting in a compensation culture
fuelled by rising worthless claims. According to
indemnity organisations, endodontic treatment is
a common source of claims related to clinical
negligence that not only results in the dentists
untarnished record becoming the source of scru-
tiny but also leading to compensation claims and
possible recriminations as a result of professional
misconduct allegations. A letter received from a
solicitor regarding claims of negligence can be an
obvious unnerving experience for any practitio-
ner that on occasion may have a lasting effect.
For a patient to succeed in any claim of negli-
gence, three essential features must be present
and proved in a court of law. These include the
fact that a duty of care was owed by the dentist to
the patient, that there was a breach of that duty of
care in failing to reach the standard of care
expected and that the patient suffered as a direct
result of this breach resulting in harm or loss.
Dental negligence is the failure of a dentist to
treat and care for a patient with a reasonable
degree of skill and care. If the dentist was care-
less, lacked proper skills or disregarded estab-
lished standards of practice when treating a
patient, then it may be possible for medical/dental
malpractice solicitors to claim compensation for
any personal injury. The test to be applied in den-
tal negligence cases is one of ‘reasonable care’,
69
and the standard is not determined solely or even
primarily by reference to the practice followed or
supported by a responsible body of opinion in the
dental profession. The High Court in Australia
has ruled that the test is not what other dentists
say they would or would not have done in the
same or similar circumstances.
Where a failed endodontic case results in the
loss of a tooth, the settlement cost is often higher
than the original cost of the endodontics because
of the cost of the alternative replacement options
including dental implants that may often be rec-
ommended as the ‘treatment of choice’ to replace
the lost tooth.
5.3 Dental Records
Contemporaneous dental records are designed to
record treatment carried out on a patient and to
act as a historical record. When a patient com-
plains, makes a claim of negligence or something
goes wrong, then the records themselves act as
evidence proving or disproving the standard of
care provided. Written dental records should con-
tain details of the patient’s identification data,
medical history including known allergies, dental
history, clinical examination, diagnosis, radio-
graphic findings, treatment plan, reference to
consent and progress notes (see Table 5.2).
Table 5.2 Good record keeping
Completed and signed patient medical and dental
history form including any known allergies
Radiographs (labelled and dated) and radiographic
findings/diagnosis
Patient identification details including telephone
number, date of birth and age
Date and time of each entry
Clinical examination findings
Treatment plan discussed including alternative
treatment options
Diagnosis and treatment notes with full details of any
episodes, discussions and incidents including options
discussed
All quotes given to the patient and payments made
Consents obtained and warnings and information given
Drugs and dosages used including any prescriptions
given to the patient
70
The governing bodies of different countries
have set out professional standards and guidance
on what is to be expected by dentists. Good record
keeping and the contemporaneous nature of such
records is highlighted, and with failure to comply,
fraudulent record keeping or alterations may
result in serious professional misconduct allega-
tions. Often patient complaints that are investi-
gated by the professional misconduct committee
may cite poor record keeping as a contributing
factor further adding weight to any claims made.
Dental records may be recorded on paper, but
with the digital revolution, more and more prac-
tices are converting to computer-based records.
The establishment of integrated digital records
provides an efficient administrative solution with
ease of data extraction both internally and exter-
nally. Computer records by nature of their soft-
ware programme ensure that contemporaneous
notes are recorded, and the possibility of embel-
lishing, altering, deleting or interfering with the
integrity of such records is not possible. Data
protection and security is important for both
types of records and confidentiality is important.
Computer systems offer used password-protected
access ensuring confidentiality provided the user
keeps these secure.
If treatment has been clearly unsuccessful for
whatever reason, then the issue of blame or liabil-
ity is rarely in doubt. On the other hand, if there
is a dispute as to what occurred before, during or
after treatment, then the contents of the dental
records are crucial to proving the facts. It goes to
say that excellent dental records will therefore
provide a good defence as opposed to poorly doc-
umented or in rare instances no records at all.
With respect to the latter, it is also important to
remember that a complaint or claim cannot be
defended against and will certainly increase the
probability of the claim succeeding even where
there is no ground such as those of malicious
intent.
Documentation should never contain any per-
sonal views or opinions with regard to the patient,
speculation, derogatory statements or inappropri-
ate references that can be read by anyone that the
patient authorises in the future. Dental records
should provide the objective facts rather than
5 Ethics and Law
subjective opinions, and the time spent in creat-
ing comprehensive treatment records may just be
the solution when dealing with any false claims
and allegations made by a patient.
5.4 Informed Consent
The process of obtaining informed consent from a
patient prior to embarking upon any invasive end-
odontic procedure is a well-established necessity
both from an ethical/professional and also legal
standpoint. A well-informed patient is more likely
to have a reasonable expectation to both the out-
come and also any possible complications that
may occur during the course of any treatment pro-
posed. The clinician must address patient precon-
ceived expectations as often complaints may arise
when this expectation has not been met. Informed
consent is a continuous process based on the fol-
lowing three principles where the patient must:
• Be informed – the patient is given all relevant
information as to the nature and purpose of the
procedure along with risks and benefits
• Be competent (having legal capacity) – the
patient is able to understand what is proposed
by way of treatment
• Be free to decide – the patient should give
consent voluntarily and not be subjected to
any coercion or undue influence
Informed consent has evolved from repeated
interpretations of courts and legislations within
different countries of the patient’s right to partici-
pate in the decision-making process regarding
the type of treatment he/she is about to undergo.
The provision of adequate information in relation
to the inherent risks associated with the proposed
treatment must be highlighted to the patient. The
amount of information given has shifted from the
previously held view (and still held in certain
countries) of warning the patient of all substantial
risks deemed appropriate by responsible and rel-
evant professional bodies. In Australia and the
USA this shift has moved towards what the ‘rea-
sonable patient needs to know’ resulting in fore-
warning of all risks that might influence the
patient’s choice in determining a proposed course
of treatment.
5.6 Treatment Complications
In general terms, the endodontist needs to dis-
close the following information in appropriate lay
terms that are understandable to the patient with-
out the use of jargon in order to satisfy both the
morale and legal doctrine of informed consent:
• Diagnosis of the existing problem
• Nature of the proposed treatment or procedure
• Inherent risks associated with the proposed
treatment or procedure
• Prognosis
• Feasible alternative treatment options includ-
ing doing nothing or extraction with/without
prosthodontic replacement (denture, bridge
and osseointegrated implants)
• Inherent prognosis and risks associated with
alternative treatment options
• Cost estimates involved
The patient should be provided with an oppor-
tunity to question the clinician about any of the
above.
5.5 Referral for Treatment
The purpose of a referral letter is to assist the
recipient in making administrative decisions
regarding acceptance of the referral, prioritisation
and contacting the patient for a suitable appoint-
ment. Referrals to an endodontic specialist may
be made for a myriad of reasons including prob-
lems associated with diagnosis, treatment or re-
treatment procedures, which may be beyond the
scope of the referring dentist. The decision to
refer to endodontic specialist services should be
based on the individual clinician’s ability as deter-
mined by his/her training and experience. On
occasion the patient may be deemed difficult or
the tooth may be complex requiring specialist
attention. Careful case pretreatment assessment
and the decision to refer early are important in
avoiding unnecessary complaints later. Patients
that are referred following difficulties encoun-
tered during treatment procedures or where iatro-
genic mishaps have occurred will often be
aggrieved when a referral is sought later, particu-
larly when the cost of ongoing treatment increases.
It is the duty of the referring dentist to have
provided the endodontist with relevant informa-
71
tion with regard to the case including history of
presenting complaint, investigations and inter-
ventions carried out as well as relevant medical,
dental and social history that may bear relevance.
The dentist should assume some responsibility in
terms of consent regarding any intended treat-
ment sought by way of the referral. Treatment
mishaps or complications should have been care-
fully discussed with the patient prior to referral.
Likewise, it is the endodontists duty to com-
municate with the referring dentist with a detailed
initial consultation report highlighting the rele-
vant clinical findings, diagnosis, radiographic
assessment, treatment options discussed, progno-
sis, treatment plan and risks where appropriate. It
is also useful to reconfirm with both the dentist
and patient any proposed restorative or periodon-
tal treatment that may be required and clearly
stated in the documentation that is sent. A copy
of the referral letter may be appropriate for some
patients who require written confirmation of pro-
posed treatment discussed.
At the end of treatment, the patient is often sent
back to the referring dentist to carry out any post-
endodontic restoration necessary for the longevity
of the tooth. A detailed letter outlining the final
treatment radiograph, final temporisation and rec-
ommendations for definitive restorations should
be sent including any provisos for future review
appointments. Occasionally a patient may return
for a review in 6 months; the temporary restora-
tion may have deteriorated and signs and symp-
toms of disease persisted. The difficulty in such a
situation is the remedial costs of re-treatment or
worse still a fractured tooth beyond repair. Both
referring dentist and endodontist must be clear in
their ability to have informed the patient of treat-
ments proposed including the final definitive res-
toration of the tooth. Clear lines of communication
are essential in preventing poor outcomes result-
ing in patient dissatisfaction.
5.6 Treatment Complications
Endodontic mishaps (see Fig. 5.1) can occur, but
this in itself does not render the case negligent.
Separation of an endodontic instrument within
72
a b
Fig. 5.1 Clinical photographs and radiographs showing
potential mishaps occurring with endodontic treatment and
file/instrument separation. Note (a) general dental practitio-
ner attempted removal of separated file rather than endodon-
tic referral. The file was further displaced beyond the
the root canal system and an inadvertent iatro-
genic perforation when trying to locate canals are
both risks that can occur. Prior to treatment com-
mencement, the patient would be warned of the
possible risks. If an iatrogenic error or complica-
tion does occur, then the patient is subsequently
informed in the first instance. Arrangements
should then be made to remedy the situation
including a prompt referral where appropriate. It
is suffice to say that good documentation is nec-
essary whenever such an event occurs.
References
1. Lim HC, Tan CB, Goh LG, Ling SL. Why do patients
complain? A primary health care study. Singapore
Med J. 1998;39(9):390–5.
2. Ware JE, Davies-Avery A, Stewart AL. The measure-
ment and meaning of patient satisfaction: a review of
the literature. Santa Monica: Rand Corp; 1977.
3. Rattan R, Tiernan J. Risk management in general den-
tal practice. London: Quintessence Publishing; 2004.
4. DiMatteo MR, Hays RD, Prince LM. Relationship of
physicians’ nonverbal communication skill to patient
satisfaction, appointment noncompliance, and physi-
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5. D’Cruz L. Risk management in clinical practice. Part
1. Introduction. Br Dent J. 2010;209(2):19–23.
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plaints happen and how to prevent them. Dent Update.
2014;41:168–73.
5 Ethics and Law
c
confines of the canal requiring surgical referral. (b) Fractured
rosehead bur and (c) separated Ni-Ti rotary file. Mishaps can
occur provided the patient is informed and appropriate mea-
sures such as referral are arrange then further problems from
a legal standpoint can usually be avoided
7. Dym H, Ogle OE. Risk management techniques for
the general dentist. Handbook of dental practice. Dent
Clin North Am. 2008;52:3.
8. Collier A. The management of risk part 2: good con-
sent and communication. Dent Update. 2014;41:
236–41.
9. Collier A. The management of risk part 3: recording
your way out of trouble. Dent Update. 2014;41:
338–40.
10. D’Cruz L. Off the record. Dent Update. 2006;33:
390–400.
11. Edelstein L. The Hippocratic oath: text, translation
and interpretation, Bulletin of history of medicine.
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12. Beauchamp TL, Childress JF. Principles of biomedical
ethics. 4th ed. New York/Oxford: Oxford University
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13. Council GD. Continuing Professional Development
(CPD) for dental care professionals. London: General
Dental Council; 2008.
14. Dental Board of Australia. Communique March 2014.
http://www.ada.org.au/dentalboardofaustralia.aspx
15. Nash DA. Ethics in dentistry: review and critique
of Principles of Ethics and Code of Professional
Conduct. J Am Dent Assoc. 1984;109(4):
597–603.
16. Bolam v Friern Hospital Management Committee
(1957) I WLR 582
17. Sidaway v Board of Governers of Bethlem Royal and
the Maudsley Hospital (1985) 2 WLR 480
18. Bolitho v City and Hackney Health Authority (1997)
39 BMLR 1: (1998) I Lloyds Rep Med 26
19. Rogers v Whitaker (1992) 67 AWR 47
20. Kirby M. Patients’ rights – why the Australian courts
have rejected “Bolam”. J Med Ethics. 1995;21:5–8.
References
21. Schloenforff v Society of New York Hospital 211 NY
124; 105 NE 92, 93 (1914) (NYCA)
22. Canterbury v Spence 464 F 2d (1972) (USCA)
23. King JS, Moulton B. Rethinking informed consent:
the case for shared medical decision-making. Am J
Law Med. 2006;32:429–501.
24. Gillick v West Norfolk and Wisbech AHA (1985) 3
All ER 402–437
25. Children’s’ Act 1998 and 2004
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26. Mental Health Act 1983 (Amended 1995 and 2007)
27. F v West Berkshire Health Authority (1990) HL
28. Mental Capacity Act 2005
29. The Medical Defence Union Ltd. Confidentiality.
London; MDU 1997
30. Nehammer C, Chong BS, Rattan R. Endodontics. Clin
Risk. 2004;10:45–8.
31. Webber J. Risk management in clinical practice. Part
4. Endodontics. Br Dent J. 2010;209(4):161–70.
 Endodontic Emergencies
6

Summary
Severe odontogenic infections in endodontics can be a serious potentially
life-threatening illness that can, on many occasions, respond favourably to
appropriate management. Delayed or inappropriate treatment may result
in sepsis or airway embarrassment requiring a surgical airway (tracheos-
tomy), inotropic support and close monitoring, on an intensive care unit.
The anatomical basis of the spread of these infections and techniques rel-
evant to their management will be discussed.

Clinical Relevance ultimately colonise the entire root canal system

Endodontic infections arising locally from an
infected tooth can potentially spread along the
route of least resistance along fascial planes exten-
sively and are rapidly potentially becoming fatal.
Prompt pharmacological and surgical interven-
tions including incision and drainage procedures
are discussed in an attempt to control the spread of
infection. The general dentist should be aware of
the potential sites of spread based on anatomy and
the relevant rationale for management including
referral to hospital when indicated.
6.1 Overview of Infections
of Endodontic Origin
and Management Thereof
The pathogenesis of endodontic disease has been
attributed to inflammation of the dental pulp (pul-
pitis) from bacteria and their metabolites, which
affecting the peri-radicular tissues (apical peri-
odontitis) [1–3].
Controlling an endodontic infection is dependent
on the host defence system, occasional systemic
antibiotics (when indicated), chemo-mechanical
instrumentation, locally used inter-appointment
intra-medicaments, root canal filling and coronal
restoration of the tooth [4]. In untreated teeth or
inappropriately and ineffectively managed previ-
ously root-filled teeth, a unique combination of oral
obligate anaerobic and facultative anaerobic bacteria
may continue to induce inflammation around the
root apex [5–7]. Host inflammatory mediators,
produced by macrophages and lymphocytes, will
recruit and activate osteoclasts resulting in
peri-radicular bone loss that can be histologically
classified as apical granuloma, abscess or cyst.
Interaction between host immune defence and viru-
lent organisms will result in undisturbed periods fol-
lowed by exacerbation and acute pain when the

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 75
DOI 10.1007/978-3-319-15591-3_6, © Springer International Publishing Switzerland 2015
76 6 Endodontic Emergencies

Table 6.1 Anatomical spaces involved in the spread of maxillofacial infections

Space Anatomical boundary Contents
Buccal Between buccinator and masseter muscle Buccal fat pad, parotid duct and facial
artery
Submasseteric Between masseter and ascending ramus Ramus and parotid fascia posteriorly
Pterygomandibular Between medial pterygoid and ascending ramus Mandibular nerve and vessels
Submandibular In split of deep cervical fascia Submandibular gland
S: mylohyoid Facial vessels
L: mandible, platysma Lymph nodes
M: hyoglossus
I: digastric
Sublingual Above mylohyoid Submandibular gland
S: mucosa Sublingual gland
AL: mandible Wharton duct
M: genioglossus Lingual nerve and vessels
P: hyoid bone Hypoglossal nerve
Submental S: mylohyoid Anterior jugular veins
I: hyoid musculature Lymph nodes
L: anterior belly of digastric
Lateral pharyngeal M: lateral wall pharynx Carotid arteries
S: base of skull Jugular veins
L: medial pterygoid and parotid gland Vagus, hypoglossal, glossopharyngeal
and accessory nerves
P: carotid sheath/styloid apparatus Sympathetic chain
Lymph nodes
Retropharyngeal S: skull base Loose connective tissue
A: post wall of pharynx
P: prevertebral muscles
L: carotid sheath
Infraorbital S: levator labii superioris alaeque nasi, Connective tissue
zygomaticus major
A:orbicularis oris Fat
P: buccinator Infraorbital nerve and vessels
Infratemporal A: maxillary tuberosity Pterygoid plates
S: infratemporal crest of sphenoid Maxillary artery
L: coronoid and temporalis Mandibular nerve
M: lateral and medial pterygoids Chorda tympani
Pterygoid muscles
Note: S superior, L lateral, M medial, I inferior, AL anterolateral, P posterior

balance is tipped in favour of the bacteria [8]. On
occasion pus may accumulate as a result of the api-
cal focus proceeding to abscess formation culminat-
ing in localised swelling, pain and redness (the
cardinal inflammatory signs). The risk of spreading
infection is along the path of least resistance dictated
by bone and periosteum, muscle and fascia by way
of haematogenous dissemination, lymphogenous
dissemination or direct extension into fascial spaces.
If perforation of the cortical bone exists, drainage
into the oral cavity, usually through a fistula, pro-
vokes a marked reduction in symptoms. In some
instances the infection may spread to neighbouring
regions such as the maxillary sinus; sublingual, sub-
mandibular and infraorbital regions; or orbit and
brain and even to the parapharyngeal space resulting
in a descending necrotising mediastinitis (Table 6.1
and Fig. 6.1) [9–12].
Direct extension of infection along the fas-
cial planes is the most common route for spread of
6.1 Overview of Infections of Endodontic Origin and Management Thereof 77

a b

c d

Fig. 6.1 Clinical photographs demonstrating (a) draining tion, (c) a long-standing parulis and (d) a fluctuant abscess
sinus in relation to tooth 46, (b) a gutta-percha placed into overlying tooth 22 with pus exudate
the sinus to confirm radiographically the source of infec-

odontogenic infections if drainage of the accumulat-
ing pus and exudate does not occur. Fascial planes
enfold and buttress visceral (vessels, nerves and
glands), muscular and bony structures forming planes
of least resistance that can form anatomical spaces.
These potential anatomical spaces are created when
blood, gas, inflammatory exudate, exogenous flu-
ids or surgical exploration dissects the fascial plane.
Dissemination of infection is dictated by the morphol-
ogy of tooth root involved, the extent of the lesion, the
anatomy of the alveolus and the location of surround-
ing muscular and fascial attachments [9–12].
Haematogenous spread of odontogenic infec-
tions can lead to serious and life-threatening com-
plications such as septic cavernous thrombosis,
orbital cellulitis and cerebral abscess [13–15].
The principal management of severe odon-
togenic infections is to establish drainage of
the pus with concomitant appropriate antibi-
otic therapy and pain management. Where
conservative management has failed to resolve
the problem, it would be in the best interests
of the patient to consider immediate referral to
a specialist oral maxillofacial surgeon with
possible admission and inpatient intravenous
antibiotics, surgical intervention and possible
extraction of the involved tooth. Ultimately
serious airway obstruction can result in poten-
tial death of patients with severe uncontrolled
spreading infections as in the case of life-
threatening conditions such as Ludwig’s
angina [16–22].
78
6.2 Facial and Neck Space
Infections
Most odontogenic infections are a sequel to pulp
necrosis resulting in an inflammatory process at
the peri-apex of the tooth. If left untreated, the
inflammatory process can result in either facial
cellulitis (defined as an acute and oedematous
spread of an inflammatory process through the
facial planes of the soft tissues) or an abscess
(collection of pus).
Established pus may form a fistulous pathway
eroding through the cancellous alveolar bone,
perforating the cortical plate and periosteum and
spreading into the surrounding soft tissues
a b
c d
Fig. 6.2 Clinical photographs and radiographs demon-
strating (a) draining cutaneous fistula in relation to tooth
15 (green arrow), (b) preoperative film demonstrating
6 Endodontic Emergencies
eventually discharging into the mouth with suppu-
ration. The spread of odontogenic infections is dic-
tated primarily by the thickness of overlying bone
and location of the infected tooth in relation to mus-
cle attachments as well as host defences taking the
least path of resistance. Infections of endodontic
origin often present as intra-oral pustules or
rarely extra-oral, small, elevated, circumscribed,
suppuration-containing lesions of either the skin or
oral mucosa. Placing a gutta-percha cone into the
overlying fistula tract and taking an intra-oral radio-
graph will often establish the source of the estab-
lished pathway confirming the diagnosis (Fig. 6.2).
Cellulitis of the face and neck will result in
pain, tenderness and redness and diffuse oedema
peri-apical lesion in relation to 15, (c) gutta-percha placed
in sinus tract and (d) gutta-percha sinus tracing radiograph
confirming tooth 15 is responsible for draining sinus
6.2 Facial and Neck Space Infections 79

of the soft tissue spaces causing a large firm
swelling with accompanying pyrexia, regional
lymph node enlargement and possible spasm of
adjacent muscles and trismus. Infections will
spread either locally along fascial spaces or by
lymphatics to regional lymph nodes and rarely by
the bloodstream (haematogenous) leading to
thrombophlebitis, bacteraemia or septicaemia.
The fascial spaces most commonly affected
include the sublingual, submandibular, pterygo-
mandibular and buccal spaces. Others such as the
temporal, masseteric, parotid, lateral pharyngeal
and retropharyngeal spaces are less frequently
involved (Figs. 6.3 and 6.4).
Maxillary sinusitis may occasionally result as
a direct extension of the odontogenic infection
into the overlying sinus. Dysphagia and oedema
of the larynx may follow a lateral pharyngeal
space infection. Infections of both the subman-
dibular and sublingual spaces (Ludwig’s angina)
may lead to trismus, swelling and an elevated
tongue leading to potential airway obstruction
and respiratory distress. Other rare complications
include orbital cellulitis, cavernous sinus throm-
bosis, meningitis and blindness which may occur
if the infection spreads either through local tissue
planes or through the valveless facial and angular
veins.

Fig. 6.3 Diagrammatic

Sinusitis
representation of possible Sinus tract
pathways of infection or cellulitis
arising from maxillary and Palatal abscess
mandibular molars. The Muscle
most common and least
dangerous path is for the
infection to tract through Sinus tract
the gingivae or mucosa (parulis) Tongue
(sinus tract)
Muscle
Ludwigs angina

Sinus tract Muscle

or cellulitis

Medial pterygoid
Parotid salivary gland
muscle
Parotid space

Masseter muscle Parapharyngeal space

Superior
constrictor muscle
Submasseteric space
Peritonsillar space

Buccal space Pterygomandibular

space

Buccinator muscle
Mylohyoid muscle

Fig. 6.4 Diagram highlighting the potential tissue spaces around the posterior mandible
80 6 Endodontic Emergencies

Orbit

Infratemporal
Canine space
space

Maxillary teeth

Parotid space Buccal space

Mandibular teeth

Masseter
Submandibular Pterygoid
and sublingual Temporal
spaces spaces

Lateral
pharyngeal
space
Carotid Retro
sheath pharyngeal
space

Cranium Mediastinum

Fig. 6.5 Diagram showing potential fascial space infections and route of spread from maxillary and mandibular teeth

Multiple fascial planes constitute important
anatomical limitations for the spread of infection
and serve to direct the spread of infection once
their natural resistance is overcome. Anatomical
understanding is essential when investigating the
pathways of spread of infection not only when
planning treatment strategies, but also to guard
against potential complications that may occur
(Figs. 6.3, 6.4 and 6.5).
Submental space
The submental space is located between the
mylohyoid muscles superiorly and the investing
layer of deep cervical fascia below covered by
platysma, superficial fascia and skin. It is
bounded laterally by the anterior bellies of the
digastric muscle and contains the submental
lymph nodes.
Teeth commonly involved are the apices of the
mandibular anterior teeth whereby the infection
perforates lingually below the attachment of the
mentalis muscle resulting in a firm swelling
beneath the chin.
Sublingual space
The sublingual space is between the lingual
oral mucosa beneath the tongue above the origin
of the mylohyoid muscle.
Infections associated with the mandibular
molars and premolars can result in a swelling
beneath the tongue when viewed through the
mouth. The swelling may deflect the tongue
medially and superiorly. Speech and swallowing
may be affected (‘hot-potato’ voice) with the air-
way becoming compromised. It may spread to
involve the submandibular space or across the
6.2 Facial and Neck Space Infections
a b
c d
Fig. 6.6 Clinical photographs showing Ludwig’s angina.
A 34-year-old patient presented to the outpatient clinic
with a history of left-sided facial pain, fever and left neck
swelling. Left tender submandibular brawny indurated
midline to involve the contralateral sublingual
space.
Submandibular space
The submandibular space is a compartment
containing the submandibular salivary gland and
lymph nodes beneath the investing layer of deep
cervical fascia and platysma and the inferior bor-
der of the mandible. The mylohyoid muscle
superiorly and anteriorly communicates with the
submental space and anteromedially with the
sublingual space.
Infections of the second or third molars within
the submandibular triangle can lead to obvious
swelling over the lower border of the mandible.
Ludwig’s angina
When all three primary spaces (submandib-
ular, submental and sublingual) become
infected bilaterally, it is termed Ludwig’s
81
swelling with elevation of the tongue, trismus and diffi-
culty with breathing were noted. (a–d) Early surgical
decompression, extra-oral drain placements, tracheos-
tomy and tooth extraction were carried out
angina. It is characterised by a rapidly progres-
sive cellulitis of the floor of the mouth with
swelling, pain, malaise, fever, neck swelling,
dysphagia and an elevated tongue (Fig. 6.6).
Mandibular molar teeth are commonly
involved, and the clinician must act promptly
due to the risk of rapid progression and possi-
bility of airway compromise. Urgent referral is
warranted for possible tracheostomy to prevent
or correct airway obstruction, intravenous anti-
biotic therapy and appropriate surgical drain-
age and tooth extraction.
Canine fossa
The canine fossa occupies the anterior maxilla
with borders extending from the infraorbital mar-
gin to the alveolar process vertically and from the
zygomaticomaxillary suture to the anterior nasal
aperture horizontally.
82
Commonly if the root of the maxillary canine
tooth lies superior to the insertion of the levator
anguli oris muscle, patients will present with a
swelling lateral to the nose. Loss of the labio-
nasal fold may be evident on the affected side.
Buccal space
The buccal space is located between the buc-
cinator muscle and the skin of the cheek. The
buccinator is a wide thin horseshoe-shaped mus-
cle which runs along the alveolar process from
the upper first molar posteriorly round onto the
mandibular third molar with attachment to the
pterygomandibular raphe. The fibres decussate
into the upper and lower lip anteriorly.
Infection in maxillary or mandibular molar
teeth may be directed into the mouth (gum boil)
or into the face (cheek swelling) depending upon
whether the source of infection lies within or out-
side the perimeter of the buccinator attachments.
Palatine space
A palatal abscess can often be observed in the
premolar–molar region or as a result of the lateral
incisor, which often has a disto-palatal curvature
at the apex. A compressible mass or swelling may
be evident lateral to the midline or in the anterior
maxilla. Occasionally the swelling may perforate
the underlying bone to reveal a draining fistula.
Submasseteric space
The submasseteric space exists beneath the
masseter muscle on the lateral aspect of the man-
dible with the ascending ramus of the mandible
on the medial aspect.
This space is often involved when infection
spreads posteriorly from the buccal space or due
to soft tissue infection associated with third
molars. Significant trismus and acute tenderness
on palpation of the masseter muscle extra-orally
may be evident. Fluid accumulation in the sub-
masseteric space may lead to a pronounced
swelling at the angle of the mandible.
Pterygomandibular space
The pterygomandibular space is an area
between the medial surface of the mandible and
the medial pterygoid muscle. The two heads of
the medial pterygoid muscle arise from the
medial surface of the lateral pterygoid plate and
the lateral surface of the tubercle of the palatine
bone and tuberosity of the maxilla. Within the
6 Endodontic Emergencies
pterygomandibular space runs the lingual nerve,
the mandibular nerve and the inferior alveolar
artery. The space communicates posteriorly with
the lateral pharyngeal space.
Posterior spread of infection from the sub-
mandibular or buccal spaces may result in limita-
tion of mouth opening. The abscess usually
points at the anterior border of the ascending
ramus.
Infratemporal fossa
The temporal space is confined laterally by the
temporalis fascia and medially by the skull. Soft
tissue infections from maxillary third molars may
result in a noticeable swelling over the temporal
region with possible trismus.
Parapharyngeal space
The medial wall is comprised of the superior
constrictor muscle with styloglossus and stylo-
pharyngeus. The lateral wall is fascia covering
the medial pterygoid, the angle of the mandible
and the submandibular salivary gland. Posteriorly
the space abuts on the parotid gland. The poste-
rior border is the prevertebral fascia and upper
part of the carotid sheath.
Systemic symptoms are frequently noted with
a lateral pharyngeal infection with pain on swal-
lowing and trismus common complaints. The
tonsil and lateral pharyngeal wall are pushed
towards the opposite side of the mouth, and the
uvula can be deflected medially. Urgent hospital
referral is warranted before respiratory distress
ensues.
Retropharyngeal space
The retropharyngeal space lies in a posterior–
medial direction to the parapharyngeal space
occupying the space posterior to the pharynx and
oesophagus. The superior pharyngeal muscle and
its investing fascia bound the retropharyngeal
space anteriorly. Prevertebral fascia binds the ret-
ropharyngeal space posteriorly.
Patients may present with neck pain, neck
swelling, fever, dysphagia and dyspnoea or noisy
breathing suggestive of a compromised upper air-
way. Urgent referral and admission to hospital is
warranted.
Cavernous sinus thrombosis (CVS)
The two cavernous sinuses are situated on
either side of the sella turcica and are
6.2 Facial and Neck Space Infections
a b
Fig. 6.7 Clinical photographs demonstrating (a) preop-
erative and (b) post-operative views of odontogenic
orbital cellulitis associated with a necrotic maxillary cen-
tral incisor. The patient experienced right maxillary
toothache prior to orbital swelling. At examination the
patient presented with diplopia, restricted right eye motil-
ity and pain that worsened during eye movement. The
interconnected by the intercavernous sinus.
Within the lateral walls of the sinuses run the cra-
nial nerves III, IV, VI and V. Septic thrombi most
often occur as a result of mid-face infections via
facial veins (superior or inferior ophthalmic vein
anteriorly and emissary veins posteriorly) or
direct extension.
Patients may present with headache, retro-
orbital pain, periorbital oedema, fever and pro-
ptosis. A multidisciplinary approach may be
needed to manage such cases with mortality rates
less than 30 % if the diagnosis is not made or
where treatment is not instituted.
83
right eye itself demonstrated ptosis, proptosis and slight
exotropia. The patient underwent urgent right orbitotomy
for incision and drainage of the right orbital abscess.
Following discharge, there was complete resolution of
the proptosis and diplopia and return of 20/20 vision in
the right eye
Orbital cellulitis
Orbital cellulitis although not commonly
associated with odontogenic infections may arise
as a result of infections from maxillary incisor
teeth that spread via the angular and facial veins,
which connect with the superior and inferior oph-
thalmic veins. In the posterior direction the ptery-
goid plexus connects the orbit with the oral
cavity. Patients may present with a painful and
erythematous swelling of the eyelid. Loss of
visual acuity, proptosis, pain, limited ocular
motility and optic nerve damage may proceed if
left untreated (Fig. 6.7).
84 6 Endodontic Emergencies

6.3 Management of Facial Table 6.2 Common antibiotic regimes employed for man-
agement of endodontic facial infections in adult patients
Cellulitis
Dose and
Antibiotic route Comments
The prerequisite for successful management of
Amoxycillin Oral 500 or Analogue of penicillin
any facial swelling includes proper prompt diag-
250 mg that is rapidly
nosis and treatment with emphasis on controlling 8 hourly absorbed with a
the airway, effective antibiotic therapy and timely 5–7 days longer half-life
surgical intervention. IV 1 g
Patients with facial swellings often present 8 hourly
with a multitude of signs and symptoms that must Amoxycillin with Oral Clavulanate is a
clavulanate 500 mg competitive inhibitor
be recognised. Generalised symptoms include
(Augmentin) 8 hourly of the beta-lactamase
fever, malaise and loss of appetite. Local symp- 5–7 days enzyme produced by
toms include dysphagia, sore throat, neck stiff- bacteria to inhibit
ness, neck pain, trismus and voice changes. penicillin
Clinical signs include facial/neck swellings, intra- Metronidazole Oral 400 or Synergistic reactions
200 mg with medications
oral swellings and possible elevation of the floor 8 hourly
of the mouth. Airway signs include a ‘hot-potato’ 5–7 days
voice, dyspnoea, stridor and shortness of breath. IV 500 mg
History, physical examination and diagnostic 12 hourly
imaging should provide important clues when Clindamycin Oral Used in known
assessing a patient with a facial swelling. Initial 600 mg penicillin allergy
8 hourly Effective against
evaluation of the airway is a priority, and where 5–7 days Gram-positive
impending airway compromise or respiratory facultative
distress is evident, then immediate and aggres- microorganisms and
sive management is warranted with appropriate anaerobes
referral and hospital admission. Erythromycin Used in known penicillin allergy
Empirical antibiotic therapy should be admin- Not recommended for treatment of
endodontic infections due to poor
istered in all fascial space infections as an adjunct spectrum of activity and significant
to surgical intervention until culture and sensitivity gastrointestinal upset
results are available. Either penicillin (amoxicil- Dosages obtained from British Medical Association and
lin) or a β-lactamase-resistant antibiotic (flucloxa- the Royal Pharmaceutical Society of Great Britain. British
cillin) in combination with a drug that is highly National Formulary. 66th ed. UK: BMJ Publishing Group.
2013
effective against most Gram-negative anaerobes
(clindamycin or metronidazole) is recommended cases that respond to simple measures. In cases
for optimal coverage. Oral antibiotics will be the where hospitalisation is required and where a
first line of treatment within the dental office set- more aggressive approach has been preferred,
ting; however, intravenous administration may be removal of the source of infection may be neces-
warranted if the infection does not abate or where sary for a timely response in most cases.
potential airway compromise is anticipated.
Removal of the source of infection and surgi-
cal drainage is the first line of treatment for any 6.4 Intra-oral Incision
facial infection with either simple intra-oral and Drainage
drainage or extra-oral incision and drainage. A
drain may prevent the early closure of an incision Localised fluctuant soft tissue swellings are ideal
and should be removed when drainage has ceased candidates for incision and drainage procedures
or is minimal (Table 6.2). to reduce the swelling and render relief for the
Some patients may be inclined to try and con- patient. Where swellings are generally diffuse
tinue with endodontic therapy in an attempt to with suspected extension into fascial planes and
save the tooth, which is often reasonable in mild anatomical spaces, accompanied with associated
6.4 Intra-oral Incision and Drainage
a b
c d
Fig. 6.8 Diagram and clinical photographs demonstrat-
ing a fluctuant swelling and its management. Note (a) and
(b) fluctuant swelling overlying tooth 23 (c) and (d) inci-
sion using a disposable scalpel blade number 15 and (e)
fever and trismus, caution must be excised. A
decision with regard to referral and hospitalisa-
tion must be made with cellulitis of this nature
that can easily become life-threatening.
Appropriate antibiotic therapy, fluids and
analgesics administered intravenously with pos-
sible extra-oral drainage may be required particu-
larly if the airway is becoming compromised
(elevated tongue, marked trismus and difficulties
with breathing). The steps involved in intra-oral
incision and drainage comprise of:
1. Adequate anaesthesia is administered. A
block or infiltration is more than sufficient for
adequate anaesthesia of the area. Care should
be excised to infiltration around the area of
infection not directly into it. General anaes-
thesia may be indicated in cases of marked
trismus to facilitate mouth opening and access.
2. The area of maximum fluctuance is located.
3. Using a #15 or #11 blade, an incision is made
through the fluctuant mass perpendicular to
the underlying periosteum and bone. Caution
must be excised in areas of anatomical land-
marks such as the mental foramen and greater
palatine neurovascular bundle. Once the
85
e
post-operative following drainage. Note that the incision
in this case is made in the most fluctuant part of the swell-
ing (arrow) and the incision taken to bone. Care must be
taken when administering anaesthesia to the area
fluctuant area has been penetrated, adequate
drainage should follow unimpeded.
4. A small curved haemostat can be used to
bluntly explore the abscessed area and open
up any remaining pockets of pus and the
innermost aspects of the abscessed area.
5. The incised area can be lavaged using normal
sterile saline to ensure that any remaining
exudate, pus and clotted blood can be removed
prior to placement of a drain if applicable.
6. A drain can be selected (Penrose drain or
other suitable latex material) and inserted into
the abscess cavity using the haemostat and
secured using a 4.0 non-resorbable suture
material (such as silk). The drain is kept in
place for 24–48 h depending on the patient’s
response before considering removal.
7. The patient is encouraged to use saline
rinses until closure begins and drainage has
ceased.
8. The patient should be reviewed to ensure that
all symptoms have improved, the cause has
been established and a definitive treatment
plan formulated to ensure the problem does
not reoccur (Fig. 6.8).
86
Clinical Hints and Tips
• Soft tissue swellings of endodontic origin
should be incised for drainage. An intra-
oral drain can be sutured in place for
24–48 h to allow for adequate drainage.
• Determine severity of infection and
whether simple incision and drainage of
pus adjunctive use of oral antibiotics will
be sufficient to control infection.
• Effective treatment of endodontic infec-
tions will also include removal of the cause
by either endodontic treatment or tooth
extraction. Successful management of the
infected root canal system will require
chemo-mechanical debridement and place-
ment of a calcium hydroxide dressing with
appropriate sealing of the access opening.
• Consider leaving the canal open until the
next day if there is continuous drainage.
However leaving the tooth open for drain-
age for a longer time allows further con-
tamination with no benefit to the patient.
• Select appropriate antibiotics. Consider
oral penicillin and metronidazole in combi-
nation for at least 5 days. Patients should
have reduced swelling, discharge and mal-
aise within 48 h. If no response or symp-
toms getting worse, then prompt referral
will need to be considered.
• Consider prompt referral if rapid progres-
sion of swelling evident, trismus, elevation
of tongue or difficulty with speech or
swallowing.
References
1. Kakehashi S, Stanley HR, Fitzgerald RJ. The effects
of surgical exposures of dental pulps in germfree and
conventional laboratory rats. J South Calif Dent
Assoc. 1966;34:449–51.
2. Bergenholtz G. Microorganisms from necrotic pulps
of traumatized teeth. Odontol Revy. 1974;25:347–58.
3. Sudqvist G. Bacteriological studies of necrotic dental
pulps. Umea University Odontological Dissertation
No.7. Umea: University of Umea; 1976.
4. Haapasalo M, Udnaes T, Endal U. Persistent, recur-
rent and acquired infection of the root canal system
post-treatment. Endod Top. 2003;6:29–56.
6 Endodontic Emergencies
5. Fabricius L, Dahlen G, Holm SE, Moller AJ.
Influence of combinations of oral bacteria on peri-
apical tissues of monkeys. Scand J Dent Res. 1982;
90:200–6.
6. Fabricius L, Dahlen G, Ohman AE, Moller AJ.
Predominant indigenous oral bacteria isolated from
infected root canals after varied times of closure.
Scand J Dent Res. 1982;90:134–44.
7. Molander A, Reit C, Dahlen G, Kvist T.
Microbiological status of root filled teeth with apical
periodontitis. Int Endod J. 1998;31:1–7.
8. Stashenko P. Etiology and pathogenesis of pulpitis
and apical periodontitis. In: Essential endodontology.
Oxford: Blackwell Science; 1998. p. 42–67.
9. Grodinsky M, Holyoke EA. The fasciae and fascial
spaces of the head, neck, and adjacent regions. Am J
Anat. 1938;63:367–408.
10. Laskin DM. Anatomic considerations in diagnosis
and treatment of odontogenic infections. J Am Dent
Assoc. 1964;69:308–16.
11. Granite E. Anatomic considerations in infections of
the face and neck. Review of the literature. J Oral
Surg. 1976;34:34–44.
12. Christian JM. Odontogenic infections. In: Cummings
otolaryngology head & neck surgery. 5th ed.
Philadelphia: Mosby; 2010. p. 177–90.
13. Fielding AF, Cross S, Matise JL. Cavernous sinus
thrombosis: a report of a case. J Am Dent Assoc.
1983;106:342–5.
14. Allan BP, Egbert MA, Myall RW. Orbital abscess of
odontogenic origin. Case report and review of the
literature. Int J Oral Maxillofac Surg. 1991;20:
268–70.
15. Brady P, Bergin S, Cryan B, Flannigan O. Intracranial
abscess secondary to dental infection. J Ir Dent Assoc.
2014;60(1):32–4.
16. Bridgeman A, Wiesenfeld D, Newland S. Anatomical
considerations in the diagnosis and management of
acute maxillofacial bacterial infections. Aust Dent J.
1996;41(4):238–45.
17. Uluibau IC, Jaunay T, Goss AN. Severe odontogenic
infections. Aust Dent J Medications Suppl. 2005;
50(4):S74–81.
18. Osborn TM, Assael LA, Bell RB. Deep space neck
infections: principles of surgical management. Oral
Maxillofac Surg Clin North Am. 2008;20:
353–65.
19. Reynolds SC, Chow AW. Life threatening infections
of the peripharyngeal and deep fascial spaces of the
head and neck. Infect Dis Clin North Am.
2007;21:557–76.
20. Marcus BJ, Kaplan J, Collins KA. A case of Ludwigs
angina: a case report and review of the literature. Am J
Forensic Med Pathol. 2008;29(2):255–9.
21. Duprey K, Rose J, Fromm C. Ludwig’s angina. Int J
Emerg Med. 2010;3:201–2.
22. Olsen I, Van Winkelhoff AJ. Acute focal infections of
dental origin. Periodontol 2000. 2014;65:178–89.
 Infection Control
in the Endodontic Office 7

Summary
The adherence to strict infection control procedures helps to protect
practitioners, patients and the community. Implementation of univer-
sal cross-infection precautions and practices within a health-care set-
ting prevents transmission of HIV, HBV and HCV. Vaccination is an
important infection control strategy for HBV and HAV. All health-
care workers should be aware of their immune status and vaccinated
accordingly. Dental practitioners are aided in this process by the gen-
eration of rules, guidelines and recommendations by regulatory ser-
vices and professional organisations within their jurisdiction or
country of residence.

Clinical Relevance 7.1 Overview of Infection

Clinicians must adhere to universal cross-
infection procedures to prevent the risk of
transmission of pathogens to patients. Personal
hygiene practices including hand washing, use
of personal protective equipment, safe dispos-
able systems for sharps and contaminated waste,
adequate cleaning, disinfection and sterilisa-
tion procedures must be adhered to according to
strict guidelines outlined. Endodontic practice
and the adoption of single-use instruments have
been highlighted due to concerns with prion dis-
ease and the inability to adequately sterilise such
instruments.
Control and Standard
Precautions
The prevention of transmission of potentially
pathogenic microorganisms from all blood and
body substances necessitates the implantation of
vigorous infection control practices and policies.
Universal precautions in the dental setting ensure
a high level of protection against the transmission
of pathogenic organisms with minimal stigma
and discrimination to patients. The implemen-
tation of strict hand hygiene procedures, use of
personal protective equipment (gloves, masks,

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 87
DOI 10.1007/978-3-319-15591-3_7, © Springer International Publishing Switzerland 2015
88
clinical attire, protective eyewear), immuniza-
tions and standard recommended sterilisation and
disinfection procedures are applied to all patients
regardless of information or assumptions made
about a patient’s infection status [1].
Routine hand hygiene is essential in preventing
the spread of infection and is considered to be the
single most important infection prevention strategy
in health care and also the simplest. It must be per-
formed before and after every episode of patient
contact using alcohol-based hand rubs that contain
between 60 and 80 % v/v ethanol or equivalent.
Plain soaps act by mechanical removal with no anti-
microbial activity. They are sufficient for general
social contact and for cleaning very soiled hands.
Effective hand hygiene relies on an appropriate
technique as well as selection of the correct product.
Strict guidelines should be adhered to in relation to
cuts, abrasions, fingernails, nail polish and jewel-
lery [2–10].
Employers are responsible for providing appro-
priate personal protective equipment in the work-
place. A surgical mask and protective eyewear must
be worn during procedures that generate splash or
sprays with blood, body substances, secretions or
excretions into the face and eyes. Single-use gloves
are recommended for each invasive procedure and
must be changed between patients and after every
episode of individual patient care. Latex allergy is a
reaction to certain proteins in latex rubber, which
can cause sensitization in health-care workers.
Latex gloves should be non-powdered due to the
risks associated with aerosolisation and an increased
risk of latex allergies. Alternative non-latex gloves
should be available for the use of both health-care
workers and patients with known latex allergies.
Sterile gloves must be used for aseptic procedures
such as surgical endodontics. Suitable footwear
should be worn preferably designed with closed
toes to minimise the risk of injury from dropped
sharps. Uniforms should be recommended in areas
of clinical practice where there is a high risk of
repeated exposure to blood and other body sub-
stances and washed on a daily basis [11–18].
The use of sharps devices exposes health-care
workers to the risk of injury and potential expo-
sure to blood-borne infectious agents including
hepatitis B virus (HBV), hepatitis C virus (HCV)
7 Infection Control in the Endodontic Office
and human immunodeficiency virus (HIV).
All health-care workers should take standard
precautions to prevent injuries caused by needles,
scalpels and other sharps instruments or devices
during procedures, during disposal of used nee-
dles and when handling sharps instruments during
procedures and when cleaning used instruments.
Any person who has used a disposable sharps
instrument or equipment must be responsible for
its safe management and immediate disposal after
use. Sharps must not be passed directly from hand
to hand, and handling should be kept to a mini-
mum. Needles must not be recapped, bent or bro-
ken after use. Approved sharps containers must be
present, preferably at the point of use, and must
not be filled above the mark indicating that the bin
is three quarters full [19–26].
Vaccination is an important infection control
strategy for the prevention of transmission of
HBV, measles, mumps, rubella, pertussis, tuber-
culosis and chicken pox (varicella) within the
clinical setting. All health-care workers should
ensure that adequate levels of protection are
maintained by awareness of their immune status
and appropriate vaccination and booster immuni-
zations where necessary [13, 27–30].
Infectious agents can be widely found in the
health-care setting, and there is a body of clinical
evidence, derived from case reports and outbreak
investigations, suggesting an association between
poor environmental hygiene and the transmission
of infectious agents. Transmission of infectious
agents can occur directly through contaminated
clinical equipment or indirectly when touching
patients via hands that come into contact with con-
taminated equipment or the environment. Minimal
hand contact surfaces such as floors should be rou-
tinely cleaned when visibly soiled and immedi-
ately after any spillage has occurred. Frequently
touched surfaces within the clinical environment
(clinical contact surfaces) should be cleaned with
suitable detergent solution at least daily, when vis-
ibly soiled and after every known contamination.
Clean touched surfaces of shared clinical equip-
ment should be routinely cleaned between patients
using suitable detergent. Surface barriers are rec-
ommended to protect the clinical environment par-
ticularly where equipment is touched frequently
7.1 Overview of Infection Control and Standard Precautions
with gloved hands during patient care delivery,
surfaces that are likely to be contaminated with
blood or bodily substances or areas that are diffi-
cult to clean. Site decontamination after spillage of
blood or other potentially infectious materials is
recommended using suitable gloves and personal
protective equipment. The spillage should be con-
fined and contained and any visible matter cleaned
using absorbent disposable material that is dis-
carded appropriately after use. Detergent solution
should be used [31–36].
All contaminated instruments must be disin-
fected and sterilised according to the degree of
risk of infection involved in the use of these items
(critical, semi-critical and noncritical). Critical
items confer a high risk of infection if they are
contaminated with any microorganism and must
be sterile at time of reuse. Manual cleaning of
critical and semi-critical instruments, in order to
remove organic material, must always precede
high-level disinfection and sterilisation, thereby
increasing its effectiveness. Automated cleaners
such as ultrasonic cleaners and washer-
disinfectors reduce the handling of instruments
and are recommended. Manufacture recommen-
dations must be adhered to when selecting appro-
priate cleaning solutions for particular
instruments. Neutral pH or mildly alkaline solu-
tions generally provide the best material compat-
ibility compared to acidic solutions that may
damage instruments. Enzyme cleaners such as
proteases may be added to assist in removal of
organic material such as blood and pus. Lipases
(active on fats) and amylases (active on starches)
are also recommended. Specific test methods to
check the effectiveness and verify the cleaning
processes of manual and automated processes are
recommended. Visual inspection with magnifica-
tion where possible should be the minimum step
to ensure satisfactory cleaning prior to disinfec-
tion and sterilisation.
Disinfection is a process that inactivates non-
sporing infectious agents using either thermal
(moist or dry heat) or chemical (alcohols, chlo-
rine, formaldehyde, hydrogen peroxide, pheno-
lics and quaternary compounds) means. Items
need to be cleaned prior to disinfection and are
not a replacement for sterilisation.
89
Sterilisation destroys all microorganisms on
the surface of an instrument or device to prevent
disease transmission associated with that item.
Reprocessing of heat-resistant items is recom-
mended by steam sterilisation due to the safety
margin, reliability, validity and lethality. The user
must validate the sterilisation process, and all
records must be kept. All sterilised items must be
stored in a way that ensures that the level of repro-
cessing is maintained. Dry, sterile, packaged
instruments and equipment should be stored in a
clean, dry environment and protected from sharp
objects that may damage the packaging [37–40].
Dental unit water systems harbour bacterial
biofilms, which may serve as a haven for patho-
gens. The reservoir of bacteria within the dental
unit water lines (DUWL) carries the potential to
infect patients and dental workers alike.
Maintaining drinking water standard in the DUWL
by incorporating independent bottled sterile water,
automatic treatment systems, antibacterial filters,
antimicrobial tubing, anti-retraction valves and
chemical flushing of the units on a daily basis
should be an integral component of dental surgery
infection control and quality assurance. Sterile
water or saline should be used for all endodontic
surgical procedures [41–44].
After use, endodontic stainless steel files and
rotary instruments that are to be reused should be
kept in moist storage whilst awaiting the cleaning
process. Sequential combined mechanical (brush-
ing) and chemical-cleaning (ultrasonic bath and
sodium hypochlorite solution) procedures will
greatly reduce the organic debris located on the
flutes of instruments. The removal or organic
debris prior to heat sterilisation theoretically
reduces the bioburden and increases the assur-
ance that the sterility process is effective in mini-
mising cross-contamination and infection
[45–48].
The recognition of prions as infectious agents
in humans has caused significant concern
amongst the public and medical/dental profes-
sionals alike. Creutzfeldt–Jakob disease (CJD)
in humans has been shown to be transmissible
via several routes, including transplantation,
contaminated medical products and neurosur-
gery. Whilst the likelihood of transmission in
90 7 Infection Control in the Endodontic Office

dentistry is undoubtedly very low, this may be Table 7.1 Levels of hand hygiene
amplified considerably by unknown risk factors, Situation When?
such as disease prevalence (particularly in the Social hand Before starting work
UK) and the failure of routine recommended hygiene After leaving work
decontamination protocols currently used in Using computer
dental practice to inactivate prions adequately. Before touching patient
Cleaning, disinfection and steam sterilisation are After visiting the toilet
not recommended for reprocessing of items After removing gloves
potentially contaminated with prions such as Instrument decontamination
Hygienic hand Before all endodontic procedures
vCJD. Single-use items should be used wherever
hygiene After contact with blood or other
possible and subsequently destroyed by inciner- bodily fluids
ation. In light of these findings, the UK Surgical scrub All endodontic surgical procedures
Department of Health has advised dentists to
ensure that endodontic reamers and files are
treated as single use as a precaution, to reduce Table 7.2 The 5 moments of hand hygiene
any potential risk of vCJD transmission. In all Example in the Hand hygiene
patients suspected of CJD or those awaiting neu- Moment dental setting recommendation
rological diagnosis, the mandatory use of single- Before touching a Shaking hands Social
patient Helping the
use items and subsequent removal from service
patient move
and storage in a secure facility is standard proto- around
col. The application of universal precautions and Before a dental All dental Hygienic or
implementation of the use of single nonreusable procedure procedures surgical scrub
equipment would theoretically prevent cross- After a dental Gloves are Hygienic
contamination of all potential pathogens includ- procedure or body visibly soiled
fluid exposure risk
ing prions but financially would be unsustainable
After touching a Shaking hands Social
and impossible. Current guidelines continue to patient Helping the
recommend strict adherence to cross-infection patient moving
policy and practices adopting universal precau- around
tions for all patients to assure the best practice After touching the After contact Social
[49–60]. patient’s with dental
surroundings equipment
Adapted from WHO applied in the endodontic office

7.2 Hand Hygiene

Hand hygiene is one of the simplest methods in
preventing the spread of infection and is consid-
ered to be the single most important infection
prevention policy in health care. Microorganisms
are usually present on the hands most of the time
(resident flora) or acquired during the treatment
of patients (transient). The act of hand washing
using soap and water is typically acceptable as a
means of social hand hygiene. Within the clinical
setting the decontamination of hands using
antibacterial-based rubs or gels is categorised as
hygienic hand decontamination necessary to pre-
vent cross-transmission of infectious agents.
Surgical scrubbing including the decontamina-
tion of hands and forearms aims to remove both
resident and transient flora prior to any planned
surgical procedure (see Table 7.1).
Fingernails have the potential to harbour bac-
teria and should be neatly trimmed. Artificial
nails should not be worn, and fingernails should
be clean and free of polish. Watches, rings and
wrist jewellery should not be worn during clini-
cal sessions to ensure the effectiveness of hand
hygiene procedures and also prevent the risk of
tearing of gloves during treatment.
The ‘5 moments of hand hygiene’ developed
by the World Health Organization (see Table 7.2)
can be applied to the dental clinical setting to
ensure that adequate levels of hand hygiene are
performed to protect both patients and health-
care workers from acquiring infectious agents.
7.3 Personal Protective Equipment
a b
e f
i j
Fig. 7.1 Clinical photographs demonstrating hand
hygiene technique with soap and water. Note (a) wet
hands with water; (b) apply enough soap to cover all hand
surfaces; (c) foot controlled taps to prevent hand contami-
nation; (d) rub hands palm to palm; (e) right palm over left
dorsum with interlaced fingers and vice versa; (f) palm to
palm with fingers interlaced; (g) backs of fingers to oppos-
For general patient care, hygienic hand decon-
tamination should be carried out ensuring hands
are washed with an antimicrobial soap such as
4 % chlorhexidine when visibly soiled. If the
hands are not soiled, an alcohol-based hand rub
(70 %), which can be less irritant, is recom-
mended. Before performing surgical procedures
hands, wrists and forearms should be thoroughly
decontaminated using either a chlorhexidine or
iodine antiseptic soap. The six stages of hand
hygiene (see Fig. 7.1) ensure that a thorough
decontamination of the hands has been carried
out prior to donning gloves. A hands-free tap sys-
tem such as a foot-operated tap or elbow-operated
tap and a bin that does not require opening and
closing with hands are essential in preventing
recontamination following hand hygiene.
Disposable wall-mounted hand towels must be
used to thoroughly dry the hands after hand
hygiene procedures.
91
c d
g h
k l
ing palms with fingers interlocked; (h) rotational rubbing
of left thumb clasped in right palm and vice versa; (i) rota-
tional rubbing, backwards and forwards with clasped fin-
gers of right hand in left palm and vice versa; (j) rinse
hands with water; (k) dry hands thoroughly with single-
use towel; and (l) hands are now safe (Adapted from
WHO [2])
The use of water-based hand lotions can be used
to prevent dryness of hands, and the development
of irritant contact dermatitis is associated with reg-
ular use of hand hygiene products (Fig. 7.2).
7.3 Personal Protective
Equipment
Personal protective equipment refers to a variety
of barriers used alone or in combination to protect
mucous membranes, airways, skin and clothing
from cross-contamination of infectious agents.
Mask, eyewear and face shields
A properly fitted surgical mask and protective
eyewear shield the individual from the risks of
splattered or splashing of blood. Masks should not
be touched during the procedure of a patient and
preferably changed between patients. Protective
safety spectacles should also be provided to the
92
Fig. 7.2 Clinical
photograph demonstrating
(a) hand cream and (b–d)
alcohol-based rubs, gels
and antibacterial soaps
commonly used for hand
washing decontamination
a b
patient particularly in view of the irrigants and
medicaments routinely used during endodontic
procedures. Single-use or reusable face shields
may also be used in addition to surgical masks as
an alternative to protective eyewear. Face shields
extend from the chin to crown providing better
protection against splatter particularly in known
HCV patients.
Protective eyewear should be routinely
cleaned according to manufacturer’s instructions
using a suitable detergent solution to ensure no
cross-contamination can occur between patients.
Protective clothing
During endodontic procedures, the risk of
sprays and spills of either blood contaminants or
through the use of irrigants/medicaments warrants
the use of protective clothing. Single-use plastic
aprons or gowns prevent contamination of cloth-
ing with blood or bodily substances. Sterile gowns
are recommended during all surgical endodontic
procedures. Suitable footwear must be worn pref-
erably designed to minimise the risk of injury from
dropped sharps. Uniforms may be worn in addi-
tion to protective clothing and due to the inherent
risk of progressive contamination throughout the
day must be changed on a regular basis.
Gloves
Non-sterile single-use medical gloves are
available in a variety of materials, the most com-
mon being natural rubber latex and synthetic
7 Infection Control in the Endodontic Office
c d
materials (nitrile). Acceptable powder-free or
latex-free gloves should be available for individ-
uals with known allergies or when treating sensi-
tised patients. Gloves that fit well should be
selected and changed routinely in between
patients and during patient procedures when
breaches in glove integrity are evident (see
Fig. 7.3). Sterile gloves are selected when carry-
ing out aseptic endodontic surgical procedures.
7.4 Needlestick or Sharps Injury
Prevention
In endodontics several sharps devices are used
during any course of treatment including local
anaesthetic needles, various burs and endodontic
hand- and engine-driven instruments. The poten-
tial for risk of injury and exposure to blood-borne
infectious agents, including HBV, HCV and HIV,
is high for both clinician and nurse as well as any
individual involved with cleaning and sterilisa-
tion procedures. Injuries typically occur during
the use of a particular sharps instrument on a
patient after use but prior to disposal or during or
after inappropriate disposal.
Standard measures to avoid sharps injuries
include appropriate handling of sharps devices
and effective verbal communication when passing
sharps. Examples include the use of instruments
7.4 Needlestick or Sharps Injury Prevention
a b
d e
Fig. 7.3 Clinical photographs demonstrating how to
remove gloves. Note (a–c) remove the glove of one hand
by peeling it back with the fingers of the opposite hand,
a b
Fig. 7.4 Clinical photographs demonstrating (a) safe level indicated on the bin regarding where to fill to and (b) dis-
posed sharps used during endodontic procedures
to grasp needles, retract tissues and load/unload
needles and scalpels. The person using the
sharps instrument should be responsible for
immediate and safe disposal after use.
Appropriate sharps containers should be avail-
able (Fig. 7.4) at the point of use or in close
proximity to work sites to aid easy and immedi-
ate disposal. The container should never be used
if it is full (usually set at ¾ level).
In the event of a needlestick injury, the
dental health-care professional should stop the
93
c
f
(d, e) remove the other glove using the finger of the other
hand (f) and discard gloves. Perform hand hygiene after
glove removal according to guidelines
procedure. The wound should be gently cleansed
but not scrubbed for several minutes with soap
and water or iodine solution potentially lowering
any infectious pathogens that may be present at
the wound site. Downstream pressure should be
applied above the wound to induce bleeding from
the contaminated injury further extruding any
potential pathogen. The source patient should be
encouraged to be tested for the presence of blood-
borne pathogens. A risk assessment by a quali-
fied physician will need to be carried out, based
94
Table 7.3 Recommended Vaccine preventable
immunisation policy within disease
the endodontic office
Hepatitis B
Hepatitis C
Tuberculosis (TB)
Influenza
Measles, mumps,
rubella (MMR)
Pertussis
Chicken pox (varicella) Health-care workers considered immune if documented
on the patient’s medical history and any prior his-
tory of parenteral drug abuse, to determine the
need for postexposure prophylaxis.
The rate of infection following a needlestick
injury is greater for HBV (6–30 %) than for HCV
(0–7 %) or HIV (0.3 %). The risk of infection fol-
lowing exposure is determined by a number of
factors including the inoculum size (or how big a
dose of organism the person is exposed to), the
method of exposure (percutaneous needlestick
versus material splashed in the eye or mouth) and
the susceptibility of the host.
All health-care workers should have access to
infection control guidelines that advise about the
management of an occupational injury, including
clear written instructions on the appropriate
action to take in the event of a needlestick or
other blood/body substance exposure.
7.5 Vaccination
Immunisation is a successful intervention for the
prevention of disease by the use of vaccines.
Dental health-care workers can pose a risk with
the potential to expose both patients and/or other
health-care workers within the same practice to
vaccine preventable diseases. These include
diphtheria, pertussis, tetanus, influenza, measles,
mumps, rubella, hepatitis B and varicella.
7 Infection Control in the Endodontic Office
Vaccination notes
To be considered immune a blood test result (anti-HBs)
must be provided following three injections in a series
Anti-HBs >10 at any stage postvaccination indicates
lifelong immunity to hepatitis B
No effective vaccine exists
Tuberculin skin test prior to employment commencement.
Positive Mantoux test requires chest x-ray
Annual seasonal influenza vaccine available
Serology to confirm immunity to all three if uncertain
2-dose vaccine recommended from childhood
Within the last 10 years
Booster dose available
evidence of history of chicken pox or shingles
2-dose vaccine available
Vaccines act by stimulating the immune system
to produce a protective immune response without
the harmful consequences of the infection itself.
All staff members should be current with the rec-
ommended vaccination policy within the practice
(see Table 7.3).
For adults a full course of HBV vaccine con-
sists of three doses at 0-, 1- and 6-month inter-
vals. Postvaccination serological testing is
recommended after the third dose. If a person’s
anti-HBs level is <10 IU/mL, then he/she is clas-
sified as a nonresponder. A further dose of HBV
vaccine can be given either as a fourth double
dose or further three doses at monthly intervals.
Further serological testing is mandatory 4 weeks
later.
7.6 Cleaning, Disinfection
and Sterilisation
Environmental surfaces within the endodontic
office, contaminated by aerosols generated dur-
ing treatment, can be classified broadly into mini-
mal hand contact surfaces (floors and ceilings)
and clinical hand contact surfaces. Clinical con-
tact surfaces or surfaces in frequent skin contact
include light handles, dental chair switches, den-
tal light switches, endodontic microscope and
controls on dental chair or customised carts.
7.6 Cleaning, Disinfection and Sterilisation
a b
Fig. 7.5 Clinical photographs demonstrating surface bar-
riers commonly used in the endodontic office. Note (a)
dental cart with protective plastic sheets on hand-pieces,
3 in 1 and chair operating buttons, (b) plastic bags overly-
Minimal hand contact areas should be regularly
cleaned by cleaning service providers according
to the frequency deemed necessary to meet the
required standards set out by relevant regulatory
bodies. Frequently touched surfaces should be
cleaned using recommended detergent solution
in between each patient to prevent organism
transfer.
Surface barriers
Surface barriers (e.g. clear plastic wrap, bags,
sheets, tubing or other materials impervious to
moisture) should be used to protect clinical con-
tact surfaces. Any area that cannot be covered
with a barrier should be disinfected with a TGA-
registered hospital grade disinfectant (Fig. 7.5).
Disinfection
This is the process by which non-sporing
infectious agents are inactivated using either ther-
mal (moist or dry heat) or chemical means. Visible
blood and debris must be removed prior to disin-
fection using a suitable detergent since organic
debris will interfere with the actions of the disin-
fectant reducing its efficacy. Instrument cleaning,
disinfection and sterilisation should take place in
a predesignated central area. There should be a
specially designated ‘dirty’ and ‘clean’ area to
ensure that contaminated critical or semi-critical
instruments are kept away from each other.
Pre-sterilisation cleaning
This is the process of removal of foreign mate-
rial (e.g. organic material such as blood or pus)
using detergent solution. Cleaning of residual
proteinaceous material must always precede dis-
infection and sterilisation procedures to increase
95
c
ing dental operating microscope handles and knobs and
(c) dental chair light with appropriate coverings on
handles
their effectiveness. Cleaning can be carried out
either manually or using an automated device.
The former involves the use of a soft hand brush,
whereas the latter reduces the handling of the
instrument and risk of injury to the sterilisation
nurse. Ultrasonic cleaning devices work by sub-
jecting the instruments to high-frequency, high-
energy sound waves aiming to loosen and
dislodge dirt. Washer-disinfectors use detergent
solutions at high temperature to remove dirt and
debris from instruments (Figs. 7.6 and 7.7).
Steam sterilisation
The steam autoclave assures sterility provided
that the proper time and temperature settings have
been used. A typical autoclave setting involves a
temperature of 121 °C at a pressure of 15 lbs for a
period of 20 min. Overloading of the autoclave is
avoided and packaging material must permit pen-
etration of steam. Mechanical, biological and
chemical monitors should be used to assess the
effectiveness of the sterilisation process. Records
of sterilisation must also be kept to assure validity
of the process. The use of a biological spore test
should be carried out at least weekly to ensure that
equipment malfunction has not occurred. During
each cycle the simple use of colour-change auto-
clave tape may provide an early warning as to any
malfunctions (Figs. 7.8 and 7.9).
Instrument storage
Following effective cleaning, disinfection and
sterilisation, the instrument packs must be stored
in a clean, dry area. All packages should be dated
permitting retrieval should a positive spore test
arise.
96
a b
c d
Fig. 7.6 Clinical photographs showing manual cleaning
and selection of various brushes according to instrument
type prior to ultrasonic cleaning, disinfection and sterili-
sation procedures. Note (a) detergent applied to selected
Dental unit waterlines
Dental hand-pieces (high-speed drills), air and
water syringes and ultrasonic scalers are all con-
nected to dental units by a network of plastic tub-
ing through which water and air are propelled to
either activate or cool down the instruments. As a
result the inner tubing surface of these waterlines
can have tenacious biofilms that are adherent and
difficult to remove. The resident microorganisms
colonising the dental waterline can inadvertently
result in cross infection to both patient and
health-care workers.
A number of solutions have evolved to
reduce the risk of contaminated dental water-
lines and are adopted on a day-to-day basis
within the practice setting. Filters can be
7 Infection Control in the Endodontic Office
brush prior to cleaning instrument. Brush used varies
according to the instrument size and type selected. Note
(b–d) three different brushes used for day-to-day cleaning
purposes
installed to physically provide a barrier method
to the passage of microorganisms. Autoclavable
systems are available allowing components of
the dental unit waterlines to be sterilised. The
use of chemical disinfectants can help to
reduce the microbial counts to an acceptable
level similar to portable water. In general, dis-
infectants can be flushed through the dental
waterline, and this should be done on a regular
basis to effectively reduce the microbial bur-
den within the system. Effective flushing
should be done for several minutes at the
beginning of the working day.
Sterile water or saline solution should be used
for irrigation purposes when considering any
endodontic surgical procedure.
7.7 Single-Use Endodontic Instruments and Prion Disease
a b
d e
g h
Fig. 7.7 Clinical photographs demonstrating cleaning,
disinfection and sterilisation procedures for a reusable
instrument. Note (a) instrument to be reused and ‘dirty’
(b) placement of detergent and cold water in sink, (c, d)
manual cleaning of instrument under cold water/detergent
using suitable brush, (e, f) placement of instrument into
7.7 Single-Use Endodontic
Instruments and Prion
Disease
Endodontic files and reamers have been desig-
nated as single-use instruments (SUI) in some
dental jurisdictions. This action has arisen out of
concern for the difficulties encountered in their
cleaning and sterilisation after use and the possi-
bility that they may act as vehicle for disease
transmission when reused. Of particular concern
is the transmission of prion protein, which causes
acquired iatrogenic Creutzfeldt–Jakob disease
97
c
f
i
suitable device prior to placement in (g) automatic ultra-
sonic cleaner, (h) further washing in cold water following
ultrasonic agitation and (i) packaging into appropriate
pack ready for sterilisation. Note instrument is allowed to
dry completely prior to placement in pack
(iCJD). No current treatment or prophylaxis is
available for this disease, and its acquisition is
almost always fatal.
Current methods for cleaning and sterilisation
of endodontic instruments prior to reuse fall short
of consistently rendering instruments surgically
sterile. The threat of prion transmission associ-
ated with reuse of endodontic instruments has led
to the mandate that all such instruments be desig-
nated single-use instruments (SUI) in some
countries such as the UK.
There has never been a confirmed case of
iCJD transmitted through dental treatment. Much
98 7 Infection Control in the Endodontic Office

a b

Fig. 7.8 Clinical photographs showing (a) cleaned only (arrowed). (b) Indicator on sterile pack pink and
reused instruments packaged after manual cleaning with black (arrowed) confirming that contents of packet have
brush and detergent, ultrasonic agitation and pre-packed been adequately sterilised and are ready for reuse
after drying is complete. Note sterilisation indicator pink

a b

Fig. 7.9 Clinical photograph demonstrating (a) pre-sterilisation endodontic instrument tray with indicator strip green
and (b) post-sterilisation endodontic instrument tray with indicator strip purple

of the concern regarding its transmission through
dental treatment has arisen from the identifica-
tion of prion protein in dental and oral tissue of
animals that have been experimentally infected
with prions. The National Institute of
Neurological Disorders and Stroke and the World
Health Organization (WHO) have estimated the
worldwide incidence of CJD caused by all man-
ner of transmission to be 1 per 1,000,000
people.
Dental jurisdictions mandate that all endodon-
tic instruments be sterilised prior to reuse. This
References
a b
Fig. 7.10 Clinical photographs showing (a) symbol on packaging indicating single use and (b) blister pack of single-
use rotary endodontic files ready for use
includes mechanical and chemical removal of all
organic tissue from the instrument surface and
heat sterilisation by a device that destroys or
inactivates all microorganisms and their by-
products. These methods appear to be effective in
eliminating disease transmission caused by most
microorganisms found within the root canal sys-
tem but have shown to be not effective in elimi-
nating prion proteins (Fig. 7.10).
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 Treatment Planning
and the Decision-Making Process 8

Summary
The decision between tooth retention using endodontic treatment and
crown restoration and extraction and prosthodontic replacement is a com-
mon dilemma encountered in clinical practice. Correct treatment planning
involves establishing whether the tooth in question is restorable and peri-
odontally sound, the patient is able to tolerate the proposed treatment and
the clinician has the skills required to perform the necessary treatment.

Clinical Relevance including dentures, bridges or implants, are

In everyday practice the clinician along with the
patient must weigh up the option of saving teeth
against extraction and alternative prosthodontic
replacement options that may be more predict-
able. A compromised tooth troubled by a combi-
nation of endodontic, periodontal and restorative
problems must be carefully assessed from a risk/
benefit point of view not only in terms of out-
come but also costs involved.
8.1 Treatment Planning
and the Decision-Making
Process
The goal of endodontic treatment, re-treatment or
endodontic surgery is to preserve the tooth as a
functioning unit of dentition. Alternative prosth-
odontic replacement options following extraction,
selected for the same reasons and more often than
not when the tooth is compromised (Fig. 8.1).
Clinicians are often faced with the challenge of
informed decisions as to which option best serves
the patient. Judgements must be made not only
on clinical experience but also prognostic factors
that determine long-term success of the various
options. Careful evaluation of all factors must be
made, and occasionally a multidisciplinary
approach including the endodontist, prosthodon-
tist and/or periodontist may be required before
the final decision is reached.
Having taken a case history and carried out
all relevant diagnostic tests, the patient’s treat-
ment can then be planned. The type of endodon-
tic treatment chosen must take into account the
patient’s medical condition and general dental
status. Contraindications to treatment include
local factors such as an unrestorable tooth,

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 103
DOI 10.1007/978-3-319-15591-3_8, © Springer International Publishing Switzerland 2015
104
Fig. 8.1 Pre-operative parallel peri-apical radiograph of
tooth 36 which was referred for endodontic management.
Note moderate – severe periodontal disease (50–70 %
horizontal bone loss), furcation involvement (grade III)
and gross furcal caries associated with the tooth. This
tooth has a poor long term prognosis and is not a candi-
date for “herodontics”
insufficient periodontal support, nonstrategic
tooth, root fractures and extensive internal/exter-
nal root resorption [1].
The decision-making process to decide
whether the tooth is salvageable or whether
extraction is preferred should be based on a logi-
cal sequence of decision-making. As such the
endodontic treatment must be integrated into a
comprehensive treatment plan that includes
restorative and periodontal management. The dif-
ficulty of the case should be balanced with the
skill and experience of the dentist in deciding
whether to manage the case in general practice or
to refer the patient to an endodontist. The overall
treatment planning in endodontics should be in
agreement with the overall dental management of
the patient [2].
Overall success in root canal treatment has
often been based on a strict set of criteria defining
success as an asymptomatic tooth with normal
periodontal architecture at the peri-apex, bony
infill and the absence of infection [3]. Systematic
reviews using clinical and radiographic mea-
sures of peri-apical healing revealed that the esti-
mated weighted pooled success rates of primary
root canal treatment completed at least 1 year
prior to review ranged between 68 and 85 %
8 Treatment Planning and the Decision-Making Process
when strict criteria (complete absence of peri-
apical radiolucency) were used. The equivalent
estimated weighted pooled success rates of root
canal re-treatment ranged between 70 and 86 %.
The reported success rates for both treatments
had not improved over the last five decades. Four
conditions were found to be significantly asso-
ciated with better peri-apical healing following
treatment. These included the absence of a peri-
apical lesion, a root filling with no voids, a root
filling within 2 mm of the radiographic apex and
a satisfactory coronal restoration [4–6].
A further prospective study revealed that the
success rate of 1° root canal treatment with com-
plete healing occurred in 83 and 80 % after 2° root
canal re-treatments. Four preoperative factors (the
presence of a preoperative peri-apical lesion, the
size of peri-apical lesion, the presence of a preop-
erative sinus and the presence of a pre-existing
perforation), six intraoperative factors (patency at
apical foramen, apical extent of instrumentation,
additional use of chlorhexidine for irrigation,
additional use of EDTA as an irrigant, the occur-
rence of interappointment complications (swell-
ing or pain) and apical extent of root filling) and
one postoperative factor (quality of coronal resto-
ration) were found to be significant prognostic
indicators for the success of 1° root canal treat-
ment and 2° root canal re-treatments. Those roots
with a preoperative peri-apical lesion were sig-
nificantly associated with 49 % lower odds of suc-
cess than roots without a lesion. The odds of
success of treatment were found to decrease by
14 % for every 1 mm increase in the diameter of
the preoperative lesion. The presence of a preop-
erative sinus or root perforation significantly
reduced the odds of success by 48 and 56 %,
respectively. During treatment, achieving techni-
cal patency at the canal terminus significantly
increased the odds of success twofold, whereas
the odds of success were reduced by 12 % for
every 1 mm of the canal short of the terminus
remaining ‘un-instrumented’. In contrast, a long
root filling reduced the odds of success by 62 %.
The use of 0.2 % chlorhexidine in addition to
sodium hypochlorite solution for canal irrigation
did not improve but reduced the odds of success
8.1 Treatment Planning and the Decision-Making Process
by 53 %. Interestingly, the additional use of EDTA
solution for canal irrigation had no significant
effect on the success of 1°RCTx but significantly
increased the odds of success of 2°RCTx by two-
fold. The occurrence of inter-appointment com-
plications (swelling or pain) reduced the odds of
success by 47 %. Finally, a good-quality coronal
restoration significantly increased the odds of suc-
cess by 11-fold [7, 8].
Surgical endodontics is primarily indicated
and related to difficultly in access for conven-
tional nonsurgical treatment or retreatment or
where access to the peri-apical area is necessary
to aid diagnosis, for example, for biopsy or to
identify a possible root fracture/perforation.
Limited evidence suggests that although surgery
may offer a more favourable outcome in the short
term, nonsurgical retreatment appears to offer a
better long-term result. Nonsurgical retreatment
may provide a better opportunity to clean the
pulp space over a surgical approach and therefore
remains the preferred treatment option where
appropriate [9, 10].
Coupled with magnification through the use of
the surgical operating microscope, refined princi-
ples of soft and hard tissue management, the use
of tissue regenerative root-end filling materials
and enhanced principles of wound closure and
postoperative management, surgical endodontics
has emerged as a highly predictable and relatively
painless procedure with success rates of 94 %
compared to 59 % using traditional techniques
[11–14]. The outcome of repeat endodontic sur-
gery was less favourable than that of primary end-
odontic surgery for posttreatment disease [15].
The long-term prognosis of an endodontically
treated teeth and whether it is extracted depends on
the health of the periodontium. Periodontal diseases
are diagnosed on the basis of clinical signs, with
radiographs assisting in treatment planning decision.
The full diagnostic approach relies on periodontal
probing and the response to probing [16]. Careful
assessment and attempt to distinguish between true
periodontal lesions, a lesion of endodontic origin, a
combined periodontal-endodontic lesion or vertical
root fracture is essential from both a management
and prognostic point of view [17–19].
105
The completion of root canal treatment does
not signal the end of patient management. The
endodontically treated tooth needs to be restored
back to form, function and aesthetics. It is clear
from the literature that a well-constructed coro-
nal cuspal coverage restoration serves to protect
both the weakened tooth from catastrophic frac-
ture and also to prevent re-infection from the oral
microbiota. In one sample study of 280 patients
and 400 teeth, those that were not crowned after
root canal treatment were lost at a six times
greater rate than those that had been crowned. A
restorability assessment is therefore imperative
before embarking upon root canal therapy and a
clinical judgement must be made including
whether additional crown lengthening proce-
dures are indicated to attain a suitable ferrule [5,
8, 20–24].
A multitude of viable treatment options are
available to the clinician and patient following
the loss of a tooth. From a cost analysis point of
view following extraction the option of doing
nothing may be beneficial to the patient.
Nevertheless, the patient must be made aware of
the fact that failure to maintain the space may
result in tooth positional changes such as supra-
eruption, tilting, rotation and lateral movement of
the opposing tooth [25–27].
The decision to treat a tooth endodontically
or to extract and replace with either conventional
removal partial dentures or bridgework or to place
a single-tooth implant should be based on crite-
ria including prosthetic restorability of the tooth,
quality of bone, aesthetic demands, cost–ben-
efit ratio, systemic factors, potential for adverse
effects and patient preferences. Endodontic treat-
ment of teeth represents a feasible, practical and
economical way to preserve function in a vast
array of cases and dental implants serve as a good
alternative in selected cases in which the progno-
sis is poor [28–31].
Whilst treatment outcomes of root canal treat-
ment have been based upon strict criteria mani-
fested by clinical and radiographic signs of
healing, this has not been the case with implant
studies. Instead survival rates have often been
used not giving a true representation of the
106
failures inherent with implants [31]. Recent
advancement in implantology techniques has
brought about a useful option in the management
of severely compromised teeth troubled by a
combination of endodontic, periodontal and
restorative problems. Contraindications to
implant placement include psychosis, acute
infectious disease and pregnancy and cancer ther-
apy. The risk of bisphosphonate-induced osteo-
necrosis has been associated with patients on
systemic bisphosphonate therapy. Caution must
be taken in patients with diabetes and other co-
morbidities such as poor oral hygiene and smok-
ing. Implants should be only placed when cranial
growth is complete. In the anterior region single
tooth implants should only be considered after
the age of 25 [31–35].
Implant failure can occur as a result of the
implant’s failure to integrate with the bone or
bone loss subsequent to integration. Soft tissue
complications such as inflammation and/or pro-
liferation, soft tissue fenestration and/or dehis-
cence and fistulas have been reported. Mechanical
complications such as screw loosening, screw
fracture, prosthesis fracture and implant fracture
also can occur. Perimucositis and periimplantitis
are not uncommon following implant placement
and if left untreated will result in subsequent
bone loss and eventual failure [35, 36].
Patients now face a number of choices regard-
ing the treatment of individual teeth. A tooth can
be retained with root canal treatment and subse-
quent restoration or may be extracted and not
replaced, replaced with a bridge, a removable
denture or an implant. Dentists have a duty to
provide a comprehensive review of the benefits
and risks of each option and to ensure that the
patient’s needs are addressed with the goal of
improving oral and general health [37].
8.2 Peri-Apical Pathology
The presence of peri-apical pathology is
sometimes the first sign that pulpal disease has
occurred. The vast majority of teeth with peri-
apical infection are expected to heal following
routine nonsurgical root canal treatment or
8 Treatment Planning and the Decision-Making Process
re-treatment. Occasionally surgical exploration/
treatment may be indicated, but this is reserved
for those cases that do not respond to conven-
tional treatments (Fig. 8.2).
Evidence suggests that those teeth with peri-
radicular radiolucencies present preoperatively
have a poor prognosis compared to teeth with no
lesions in terms of success. The prognosis for
endodontic treatment of the tooth in question
must be taken into account in the treatment plan-
ning phase. Classical studies have shown end-
odontic success to be 95 % with a vital tooth,
85 % with a tooth with peri-apical pathology,
80 % with re-treatment cases and 65 % with con-
temporary surgery. Clinicians should be
reminded that studies reporting an overall suc-
cess rate may not be applicable to the same tooth
that you are treating and may be misleading to
the patient. Nevertheless, if the standard of care
for root canal treatment and subsequent coronal
restoration is carried out methodically, then suc-
cess should be achievable in the majority of
cases.
8.3 Periodontal Assessment
The health of the periodontium needs to be
assessed, and insufficient periodontal support
may be a contraindication to carrying out root
canal therapy (Fig. 8.3).
Current periodontal classification recognises
the following categories of destructive periodon-
tal diseases: chronic periodontitis, aggressive
periodontitis, periodontitis as a manifestation of
systemic disease, necrotising ulcerative gingivi-
tis/periodontitis, abscesses of the periodontium
(gingival, periodontal, pericoronal), combined
periodontic–endodontic lesions and developmen-
tal or acquired deformities and conditions.
A visual inspection of the marginal periodon-
tal tissues, plaque, calculus, overhangs, gingival
bleeding and bleeding on probing, basic peri-
odontal examination, probing depth and loss of
attachment measurements, furcation involve-
ment, mobility, suppuration, tooth drifting/migra-
tion and radiographic assessment are all necessary
in order to assist in treatment planning decisions
8.3 Periodontal Assessment
a b
Coronal restoration
Pulp horn
Pulp
Pdl space
d e
Fig. 8.2 Diagrams representing (a) extensive caries
involving the pulp. (b) Normal radiographic appearance –
intact periodontal ligament space. (c) Early apical
changes – widening of the radiolucent periodontal liga-
ment space. (d) Extensive destructive acute inflammation –
a b
d e
Fig. 8.3 Diagrams representing (a) healthy (b) localised
bilateral infrabony vertical defects – typically seen in
occlusal trauma, (c) localised vertical bone loss, (d) mild
107
c
f
diffuse, ill-defined area of radiolucency at the apex. (e)
Long-standing chronic inflammation – well-defined area
of radiolucency surrounded by dense sclerotic bone. (f)
Low-grade chronic inflammation – diffuse radiopaque
area at the apex (sclerosing condensing osteitis)
c
f
horizontal bone loss, (e) moderate horizontal bone loss
with early furcation involvement, (f) severe horizontal
bone loss
108
regarding root canal therapy on a prospective
tooth. Those cases where a questionable
prognosis is suspected may require specialist
referral prior to further determine long-term
prognosis. Certainly in cases where there is no
doubt as to an unfavourable (poor) periodontal
prognosis, then extraction will be the only option.
8.4 Restorative Assessment
It is generally accepted that root-filled teeth differ
from their vital counterparts. It would seem that
the main difference is due to the cumulative loss
of tooth structure as a result of previous restor-
ative and further endodontic procedures that are
carried out. Furthermore, loss of pulp tissue
means that the nonvital tooth has an impaired
ability to prevent mechanical overload, which in
turn may lead to cuspal fracture. The longevity of
root-filled teeth is therefore dependent on both
preservation of maximum coronal tooth structure
and cuspal coverage protection by a suitable
coronal cast restoration.
When assessing the restorability of an
individual tooth, it is important to remember
adopting a whole mouth approach to ensure that
a b
e f
Fig. 8.4 Clinical photographs demonstrating tooth
restorability assessment, (a, b) preoperative views of
tooth. Assessment is made under rubber dam. (c) All
existing restorative material is removed, (d) caries
removal carried out (black arrow), (e) MB pulp horn
8 Treatment Planning and the Decision-Making Process
a comprehensive treatment plan is formulated
taking into account alternative treatment options
if the tooth in question is of questionable
prognosis (Fig. 8.4).
Methodical clinical evaluation including
endodontic assessment, periodontal support,
occlusal scheme assessment, parafunction
assessment and intended function of the tooth
(e.g. single cast restoration, bridge or removal
partial denture abutment) are essential steps prior
to assessing restorability.
The first step when assessing a tooth’s restor-
ability is to ensure that all prior restorations have
been dismantled and the tooth is caries-free.
Restorability assessment will involve systematic
assessment of the remaining tooth structure
including the height, location and thickness of
remaining dentine walls. These aspects are
inspected to visualise whether the future planned
restoration is feasible and to assess the resistance
and retention form of the cavity itself.
An important design principle when consider-
ing cast cuspal coverage or post and core prepa-
rations is the incorporation of an adequate ferrule
into the design. This ‘ferrule effect’ is achieved
by parallel walls of dentine extending above the
finishing line of the preparation or by encircling a
c d
g h
exposed following caries removal (red arrow), (f–h)
access cavity preparation with minimal extension to allow
for adequate canal preparation with retention of maximum
coronal dentine
8.5 Crown Lengthening
a b
e f
Fig. 8.5 Clinical radiographs and photographs demon-
strating endodontic management of same tooth shown in
Fig. 8.4. (a, b). The patient presented with extensive car-
ies and fractured coronal restoration (c, d) initial and mas-
ter apical file preparation following access cavity
preparation, chemo-mechanical preparation and comple-
tion of cleaning and shaping. (e) Mid-fill obturation using
AH plus cement and gutta-percha using a warm vertical
band of metal as part of the crown or post and
core restoration. 1–2 mm of coronal dentine
above the finishing line provides additional pro-
tection by reducing stresses within a tooth thereby
increasing fracture resistance.
Crown lengthening may be indicated in those
cases where an adequate ferrule cannot be
provided due to limited remaining tooth structure
or subgingival or near crestal tooth structure that
would result in unfavourable or difficult to
prepare finishing lines at the crown preparation
stage (Fig. 8.5).
Further assessments regarding restorability
can be made following completion of access cav-
ity design, location of canals and cleaning and
shaping procedures. The root canals can be
assessed and inspected for suitability regarding
further retention by conservative means or addi-
tional retention using posts. The question of
whether a post is required for additional retention
is dependent on the remaining tooth structure.
In general terms where more than half of the
remaining coronal tooth structure is present, then
no post and core restoration is indicated. The
109
c d
g h
compaction technique (f, g) completed obturation of canal
with 3 mm of coronal pulp space left for further retention
by core material using the Nayyar core concept. (h)
Completed coronal temporary restoration of IRM and
glass ionomer cement. The patient was referred back to
her general dental practitioner for placement of a cast
restoration
coronal access cavity can be utilised as an
additional retention by placement of a Nayyar
amalgam core. Amalgam can be condensed
2–4 mm into the coronal root canal space and
undercuts within the pulp chamber avoiding the
risk of iatrogenic perforation that may occur
during post preparation.
8.5 Crown Lengthening
Periodontal crown lengthening can be used for
teeth with subgingival caries, fractures or both,
and this treatment can establish a biological
width and, if needed, a ferrule length facilitating
prosthetic management. Crown lengthening sur-
gery involves various techniques, including
gingivectomy or gingivoplasty or apically posi-
tioned flaps, which may include osseous resec-
tion. Authors of wound healing investigations
have reported that an average of 3 mm of suprag-
ingival soft tissue will rebound coronal to the
alveolar crest and can take a minimum of
3 months to complete vertical growth.
110
a b
c d
Fig. 8.6 Clinical radiographs showing (a) preoperative
view of tooth 36 with extensive distal tooth loss (yellow
arrow) and caries encroaching near crestal bone level (red
arrow) (b) endodontic assessment following chemo-
mechanical preparation of the tooth (prognosis deter-
mined to be favourable). At this stage the patient was
referred to a periodontist for consultation regarding
The indication for crown lengthening for a
tooth undergoing endodontic treatment is due to
insufficient remaining dentine to support the
definitive cast cuspal restoration. Provided the
patient has both the desire and is suitable to
undergo the surgical procedure, then a periodon-
tal referral can be made for assessment. The
length and taper of the root, the crown–root ratio
and the location of the furcation will need to be
assessed. The length of the root should be long
enough to allow for adequate bone removal
without compromising the crown–root ratio.
The taper of the root is important in terms of the
cervical embrasure space that will be created as a
result of the crown lengthening procedure. The
level of the furcation will dictate the amount of
8 Treatment Planning and the Decision-Making Process
whether crown lengthening was feasible (c) post-end-
odontic treatment completion. The patient was sent to the
periodontist who carried out crown lengthening. (d)
Following an interim 3-month healing period the patient
was seen for definitive cast restoration. Note supra-crestal
restorative margins (green arrow). Red arrow represents
crestal bone height
bone removal possible without compromising the
furcation (causing a furcal defect) (Fig. 8.6).
Initiation of final prosthetic treatment should
wait at least 3 months and possibly up to 6 months
for aesthetically important areas, as the free
gingival margin requires a minimum of 3 months
to establish its final vertical position.
8.6 Alternative Prosthodontic
Replacement Options
The decision by the clinician and patient to retain
or remove teeth should be based on a thorough
assessment of factors related to the risks and
benefits affecting the long-term prognosis for
8.6 Alternative Prosthodontic Replacement Options
a b
Fig. 8.7 Diagrammatic representation showing (a)
second premolar tooth with endodontic infection, (b)
subsequent endodontic treatment and satisfactory coro-
nal restoration resulting in (c) resolution of peri-apical
a b
Fig. 8.8 Diagrammatic representation showing (a) sec-
ond premolar tooth diagnosed with endodontic pathology.
A decision was made to (b) extract the tooth. Arrow is the
adjacent tooth moving mesially into the extraction site.
either endodontic or alternative prosthodontic
replacement options.
In cases where patient-related factors such as
systemic health preclude extraction or where tooth
and periodontium factors and treatment-related
factors are favourable, then the choice of retaining
the tooth is probably the first choice (Fig. 8.7).
Where the patient has made a conscious deci-
sion to not embark upon root canal therapy or
where patient-, tooth- and periodontium- or
treatment-related factors are potentially guarded
or poor, then extraction may be indicated.
Following extraction of the tooth, the first
option all patients have is to do nothing (Fig. 8.8).
The risk of doing nothing is changes in the occlusal
scheme whereby neighbouring teeth have migrated
into the edentulous space. The decision to replace
the tooth following this is markedly more difficult
111
c
pathosis. Note long-term success will be dependent on a
well-fitting cast restoration to prevent coronal leakage and
catastrophic tooth fracture
c
Note the risk of tooth movement with either (c) mesial
drifting of the adjacent tooth or overeruption of the oppos-
ing tooth is dependent on interocclusal factors
with the possibility of further orthodontic interven-
tion to try and remedy the situation.
Removable partial dentures (RPDs) remain a
mainstay of prosthodontic care for partially den-
tate patients and can be considered for the
replacement of a single tooth in some instances.
Appropriately designed, they can restore masti-
catory efficiency, improve aesthetics and speech
and help secure overall oral health. However,
challenges remain in providing such treatments,
including maintaining adequate plaque control,
achieving adequate retention and facilitating
patient tolerance (Fig. 8.9).
The replacement of a missing tooth with exten-
sive crowns and bridges is a common procedure for
many dental practitioners. When correctly planned
and executed, fixed prostheses will provide pre-
dictable restoration of function and aesthetics.
112
a b
Fig. 8.9 Diagrammatic representation showing (a) sec-
ond premolar tooth diagnosed with endodontic pathology.
A decision was made to (b) extract the tooth. (c)
Replacement with a partial denture. The inherent prob-
lems with this replacement option tend to be related to
increased plaque retention with the possibility of
When done poorly, they are more likely to fail
prematurely and lead to irreversible damage to
the abutment teeth and supporting structures
beneath. Furthermore, from a cost/benefit analy-
sis, the provision of extensive crowns poses a risk
of pulpal damage to the adjacent abutment teeth
requiring further remedial endodontic treatment
and possible replacement of crowns/bridge in the
future. This must be taken into consideration
with careful assessment of abutment teeth and a
comparison made to the feasibility of a single
unit implant as a suitable alternative.
The incidence of endodontic treatment
required after tooth preparation has ranged from
3 to 23 %. Fixed partial dentures and complex
prostheses had higher incidence rates than single
crowns. It has been assumed that the higher rates
are because of the greater tooth reduction some-
times required to align multiple teeth (Fig. 8.10).
The final option for replacement of a missing
tooth is the use of an osseointegrated dental
implant. Within the last 20 years, there has been
a tremendous surge in the use of this technology
by both general dentists and specialist
practitioners spurred on by multicentre studies
demonstrating high levels of success. Implant
failure can be divided into primary failures
(failure to establish osseointegration prior to
loading) and secondary failures (failure to main-
tain established osseointegration following load-
ing). The long-term failure rate of dental implants
8 Treatment Planning and the Decision-Making Process
c
periodontal disease or caries and patient discomfort
attributed to the bulkiness of the prosthesis and potential
for movement due to inadequate retention features. When
the patient has an existing partial denture or multiple
edentulous spaces, this option may be effective both from
a patient and cost–benefit perspective
is generally 5–10 %. A distinction has also been
made between failed implants, failing implants
and ailing implants or implant complications.
The designation of failed implants is assigned to
mobile or exfoliated implants. The ailing implant
term was put forward in the literature to refer to
clinically stable implants affected by bone loss
with pocketing. A failing implant displays fea-
tures similar to the ailing implant but is refractory
to therapy and continues to get worse.
Implant complications denote an increased
risk for implant failure and are either of only tem-
porary significance amenable to treatment or
results in failure (Fig. 8.11).
Most implant failures occur during the initial
healing period or following abutment connection
and initial loading. Longer-term complications are
associated with general wear and tear, inadequate
attention to oral hygiene, poorly controlled occlu-
sal forces, poor design of prostheses or use of an
inadequately tested implant system. Complications
include screw loosening and fracture, crown dece-
mentation, abutment loosening, soft tissue issues
including perimucositis and periimplantitis and
implant fracture. Maintenance requirements and
complications vary widely between patients,
depending on susceptibility to caries and peri-
odontal disease in the dentate patients; complexity
and type of implant supported prostheses, func-
tional demands and the patient’s ability to attain
an adequate standard of oral hygiene.
8.6 Alternative Prosthodontic Replacement Options 113

a b

c d

Fig. 8.10 Diagrammatic representation of replacement conventional fixed–fixed bridge could be constructed. (d)
of an (a) endodontically involved tooth. (b) Following Note the risk of endodontic failure in the abutments as a
extraction and assessment of abutment teeth, (c) a consequence of crown preparations
114
a b
c d
Fig. 8.11 Diagrammatic representation of (a) an end-
odontically treated tooth which has been (b) extracted and
(c) replaced with a single unit dental implant. (d) The dis-
tinction between failed, ailing and failing dental implants
has been discussed with only the loss of the dental implant
being considered as failed. Endodontic studies on the
other hand have been evaluated based on much stricter
guidelines where the differentiation between failure and
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 Endodontic Armamentarium
9

Summary
Endodontics, since its inception, has resulted in numerous concepts, strat-
egies and techniques for preparing canals. Over the decades, a staggering
array of files has emerged for negotiating and shaping canals principally
based on either stainless steel or nickel–titanium alloys. Manufacturers are
constantly developing file systems intended to improve on previous gen-
erations with proven performance features based on past and recent tech-
nological advancement. The clinician must be able to justify the use of
these systems based on scientifically proven evidence-based research and
clinical outcomes. Changing instrumentation techniques, particularly if it
is a radical departure from your usual technique, will require attendance
on hands-on courses and vigorous laboratory testing, preferably on
extracted teeth, followed by integration into daily practice following care-
ful case selection.

Clinical Relevance and clinically proven system that ensures predict-

The mechanical objectives of canal shaping are a
means to ensure that our biologically aimed
chemical preparation of canals is fulfilled.
Traditional techniques included the use of a com-
bination of a large number of stainless steel files
and Gates–Glidden burs, which were prone to
iatrogenic mishaps, particularly in curved canals.
Since the inception of nickel–titanium alloy and
its proven benefits, manufacturers have developed
numerous file systems with inherent advantages
and disadvantages depending on individual
design features. The clinician should be aware of
these features and be able to select a scientifically
able preparation with efficiency, simplicity and
safety in mind.
9.1 Overview of Endodontic
Instruments
Modern endodontics encompasses a multitude of
technologies that have allowed us to predictably
treat and prevent apical periodontitis, no more
so than the advent of the nickel–titanium revo-
lution. Yet despite this, some clinicians still fail
to understand the underlying principles of tooth

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 117
DOI 10.1007/978-3-319-15591-3_9, © Springer International Publishing Switzerland 2015
118
isolation, vision and irrigation, which together
allow us to successfully and effectively debride
those areas of untouched root canal anatomy
that our technologically advanced instruments
fail to reach. Endodontic armamentaria are con-
stantly evolving with newer instruments and
materials frequently marketed with the promise
of improving and simplifying a technique and
shortening the time taken and even claims of
superiority over existing products. Often these
promises are not fulfilled with many practi-
tioners quickly discarding these instruments
resigned to the back of a store cupboard collect-
ing dust. Recently, the introduction of single-
file systems aimed at predictably shortening the
time taken to shape the canal system only serves
to increase our chances of failure when negating
the principles fundamental to endodontics. The
astute clinician will always have in his mind’s
eye that the use of the multitude of endodontic
armamentaria available today is but one exten-
sion of the principles necessary to predictably
clean and shape the complexities of the canal
systems, allowing our patients the desired out-
come we seek to achieve.
In June 1976, the Council on Dental Materials
and Devices of the American Dental Association
approved specification #28 [1], which established
the International Standards Organization (ISO)
[2–4] classification, requisite physical properties
and procedures used for investigation, sampling
tests and preparation of root canal files and ream-
ers. In 1981, the specifications were revised,
including requirements for a uniform file taper of
0.02 mm per mm and a tolerance of + −0.02 mm
at each diameter inspection point [5]. Later, in
1989, a second revision was made on the design
of cutting blades, the geometry and the angle of
the tip [6].
This standardisation provided a coloured
numbering system that indicated the diameter of
the tip of the instrument at the first rake angle.
The coloured numbering is repeated every six
instruments with the exception of the first three in
the series (files 06, 08 and 10). This diameter at
the tip is termed D1, and the diameter at the end
of the cutting edge is termed D16. The difference
of the diameters D1 and D16 is always a constant
9 Endodontic Armamentarium
0.32 mm. This allowed for a consistent taper to
instruments of whatever size (e.g. taper 0.02
means the increment in diameter is 0.02 mm ×
each millimetre of length). The L1/L16 distance
is also constant (16 mm), so that the working por-
tion of the instruments is always the same, despite
the variability of the lengths of the available
instruments (21 mm short, 25 mm long and
31 mm extra long). The obturating materials were
also standardised, so that the manufacturers pro-
duce gutta-percha cones and paper points whose
size and taper corresponded to those of the instru-
ments [7, 8] (Fig. 9.1).
Despite attempts at developing standard speci-
fications, wide variations exist between the diam-
eters of instruments of the same nominal size
within or between different manufacturers. The
tolerance limit of + −0.02 mm for all diameters
has been identified as part of the problem [9, 10].
A number of endodontic files are commonly
used for cleaning and shaping the root canal sys-
tem. They can be manufactured from either stain-
less steel or nickel–titanium of either constant or
variable tapers depending on the file type.
Traditional standardised preparation techniques
employed either reamers or files, which are effec-
tive in both a linear filing motion and rotational.
Hedstroem files (H files) should only be used in a
linear filing motion [11].
The use of stainless steel files in curved canals
proved to be unpredictable with an increased risk
of iatrogenic damage and canal transportation (zip-
ping and ledging) which occurs in the apical 1/3 of
the canal due to their inherent inflexibility [12].
To overcome the inherent problems associ-
ated with inflexible stainless steel files and diffi-
culties negotiating tightly curved, fine canals,
the use of intermediate sizes (12.5, 17.5, 22.5,
etc.) has also been proposed (K-FlexoFiles
Golden Mediums) [13].
Modifications to the tip design of stainless
steel files have been marketed creating a rounded
tip that does not cut into the canal wall. The
Flex-R file designed by Roane (1985) was the
first to use a non-cutting tip to help avoid ledge
formation in curved canals. This design incorpo-
rated a guiding plane and removed the transition
angles inherent on the tip of standard K-type
9.1 Overview of Endodontic Instruments
Fig. 9.1 Standardised 2 % endodontic K-file instrument.
Note the diameter ‘D1’ is the diameter at the tip of the
instrument to the nearest 100 hundredths of a millimetre.
The diameter at the end of the cutting edge is D16. The
files. Lacking a sharp transition angle, the Flex-R
files will follow the canal, and they are prevented
from gouging into the walls. The tip design
causes a Flex-R file to hug the inside of a curve
and prevent the tip from engaging the external
wall of the curve. Other tip modifications include
the use of pyramidal file tips (such as the Flex-O
files) [14, 15].
C+ Files (Dentsply/Maillefer, Johnson City,
TN) modified with a pyramid-shaped tip facili-
tates insertion during negotiation and an overall
square cross section providing better resistance
to distortion and less buckling compared to con-
ventional K-files. These files allow easier loca-
tion of the canal orifices and easier access to the
apical third of the canal useful when negotiating
fine calcified canals [16].
The application of nickel–titanium in end-
odontics was first reported in 1988, and since its
introduction there has been a growing shift from
119
difference between D1 and D16 is 0.32 mm conferring a
consistent taper to instruments of whatever size tip (taper.
02: the increment in diameter is 0.02 mm × each millime-
tre in length)
manual hand instrumentation to rotary engine-
driven preparation. They have proven to be highly
flexible and elastic, reducing iatrogenic instru-
ment complications associated with the inherent
stiffness of stainless steel files. Instrument design
has changed considerably with progress being
made in the manufacturing process as well as
alloy processing. Nevertheless, all systems have
their own set of advantages and weaknesses
according to the type of alloy used, degree of
taper and cross-sectional design features [17–20]
(Table 9.1).
First-generation rotary Ni–Ti files include
Profiles 0.04 and 0.06 and orifice shapers [21,
22], LightSpeed instruments [23, 24] and Greater
Taper files [25, 26] designed with passive cutting
radial lands, fixed tapers over the length of their
working parts requiring a considerable number of
files to be used in order to achieve preparation
objectives.
120 9 Endodontic Armamentarium

Table 9.1 Design features of first- to fifth-generation K3 [28] and BioRaCe [29]. During this period,
rotary Ni–Ti file systems
manufacturers began to focus on methods to
Instrument Cross-sectional increase the resistance to file separation. One
system design Taper
process included electropolishing to remove sur-
1st generation
face irregularities caused from the traditional
Profile Triple U shape with Fixed 2, 4 and
Dentsply, radial lands 6%
grinding process. However, as proven clinically
Maillefer and scientifically, this process resulted in a file
LightSpeed Triple U shape with Specific surface that was less sharp. The perceived advan-
LightSpeed, radial lands instrument tages of electropolishing were counteracted by
San Antonio, Files have short sequences the more undesirable inward pressure required to
TX cutting portion
advance a file to length resulting in potential
GT Files Triple U shape with Fixed 4, 6, 8,
radial lands 10 and 12 % unwanted taper lock, screw effect and excessive
2nd generation torque on the file increasing the risk of file
ProTaper Convex triangular Variable taper separation.
Dentsply, shape, sharp cutting along length of Further improvements in metallurgy led to the
Maillefer edges with no radial instrument development of third-generation files whereby
lands
F3, F4 and F5 U the use of heat treatment (thermal processing) led
flutes increase to fatigue resistance of nickel–titanium and
flexibility improved safety when using Ni–Ti files in curved
K3 Positive rake angle Fixed 2, 4 and canals. Heat treatment serves to create a more
Sybron Endo for cutting 6% optimal phase transition point between martens-
efficiency
Three radial lands ite and austenite reducing cyclic fatigue and
Peripheral blade increasing overall clinical safety and perfor-
relief mance. Examples of file systems utilising heating
RaCe Triangular shape Fixed 2, 4, 6, 8 and cooling methods of Ni–Ti during manufac-
FKG, LaChaux except RaCe and 10 %
ture include Vortex Blue [30, 31] and Twisted
De Fonds, 15/0.02 and 20/0.02
Switzerland which have square Files [32, 33].
shape Fourth-generation files include the concept of
Two alternate single-file reciprocation. Reciprocation may be
cutting edges
defined as any repetitive back-and-forth or
No radial lands
3rd generation
up-and-down movement. Current reciprocating
Vortex Blue Triangular shape Fixed 4 and file systems utilise clockwise (CW) and counter-
Manufactured 6% clockwise (CCW) degrees of movement of
M-Wire unequal bidirectional rotation reducing the
No radial lands inward pressure required for file progression,
Twisted Files Triangular shape Fixed 4 and
examples of which include WaveOne [34] and
Manufactured 6%
R-phase wire Reciproc. WaveOne represented a merger of 2nd-
twisted not ground and 3rd-generation design features coupled with
4th generation a reciprocating motion in unequal bidirectional
WaveOne Convex triangular Taper 6 or 8 % angles. The CCW engagement angle is 5 times
shape the CW disengaging angle reducing the elastic
5th generation limit on the file with progression to length more
ProTaper Next
efficiently. The Self-Adjusting File represents a
new approach to file design and mode of opera-
Second-generation files were developed with tion. A hollow-designed cylinder comprising of
actively cutting edges without radial lands requir- thin-walled Ni–Ti lattice with a lightly abrasive
ing fewer instruments to be used in a preparation surface was developed and used in reciprocation,
sequence. File systems include ProTaper [27], with simultaneous irrigation. The manufacturer
9.2 Dental Magnification and Illumination
claimed that the SAF was capable of adapting
itself to the shape of the canal three dimension-
ally [35].
The most recent change has been the fifth-
generation shaping files designed so that the cen-
tre of mass and/or the centre of rotation is offset
resulting in a mechanical wave of motion that
travels the length of the file, minimising engage-
ment between file and dentine. ProTaper Next
[36] is the successor to the ProTaper Universal
featuring M-Wire technology, offset design creat-
ing a ‘swaggering’ effect reducing taper lock and
screw effect and minimising file contact, thereby
reducing the risk of file separation.
The creation of a glide path has been advo-
cated prior to instrumentation with Ni–Ti rotary
files to ensure a safe and predictable path for the
files to follow reducing the chance of instrument
separation. The uses of either traditional stainless
steel instruments or mechanically utilising Ni–Ti
rotary files have been used for this purpose. The
latter has been shown to be both safe and easy,
demonstrating better maintenance of the original
canal anatomy with less modification of canal
curvature and fewer canal aberrations compared
with manual preflaring performed with stainless
steel K-files [37–40].
The use of a torque-controlled motor set at
manufacturer-recommended speed of rotation
and set torque values for file systems is desirable
to prevent iatrogenic error such as instrument
separation. The use of a low-torque endodontic
motor operating below the limit of elasticity for
each instrument markedly reduces the risk of
instrument fracture [41].
One of the most important advancements in
endodontic armamentarium has been the use of
ultrasonics in conjunction with magnification and
illumination, which are essential prerequisites for
the ability to identify anatomical details found
within root canal systems that are impossible to
visualise using the naked human eye. The use of
the dental operating microscope has been a scien-
tifically researched and recognised method of
optimising root canal treatment improving
diagnostic and therapeutic accuracy both in non-
surgical and surgical treatment and re-treatment
cases. Ultrasonic instrumentation plays an
121
ever-increasing role in both chemo-mechanical
preparation and obturation techniques. The abil-
ity to conservatively remove root canal obstruc-
tions, the identification of missed and hidden
canals, ultrasonic irrigation and the possibility of
warm lateral compaction techniques have allowed
the discipline of endodontics to become a pre-
dictable outcome rather than a fortuitous discov-
ery [42–44].
New endodontic files are continually added to
the existing armamentarium used for root canal
preparation and will continue to do so as technol-
ogy advances. The choice of which file system to
select is an individual one based on experience
from attending hands-on courses, rigorous test-
ing on extracted teeth and endo-vu blocks and
ultimately making the transition into the clinical
setting within your practice. The system selected
must be based on optimal canal shaping ability,
maximum safety and simplicity. One must bear
in mind that all mechanical systems serve to
achieve the same goal in mind, which is to create
a shape that allows effective penetration of our
irrigants and subsequent obturating materials,
aimed at creating an environment conducive to
healing.
9.2 Dental Magnification
and Illumination
Successful negotiation of three-dimensional
canal anatomy is often perceived to be carried out
blindfolded with the operator’s ability to visual-
ise this path within their mind’s eye. With the
right tools, incorporating magnification and illu-
mination, this process has become much more
predictable, offering the operator unparalleled
views of canal anatomy that cannot be pictured
by tactile discrimination alone. The advantages
of magnification and illumination include
reduced operating time, improved posture during
treatment and reduced muscle, shoulder, neck
and back pain that can occur as you attempt to get
closer to an object without the aid of such devices.
The obvious disadvantages include the initial
learning curve requiring time and effort and the
inherent costs of such devices.
122
a b
d e
Fig. 9.2 Clinical photographs showing devices used to
enhance dental magnification and illumination including
(a) dental operating microscope (OPMI pico with MORA
Loupes
Magnifying loupes can be classified as single-
lens systems, Galilean and Prismatic (Keplerian)
loupes. Single-lens loupes are the simplest form
of magnification incorporating a magnifying lens
that attaches to either glasses or a headband.
They are the least expensive with limited magni-
fication (up to about 3X) and limited depth of
field of vision. Depth of field is the ability of the
lens system to focus on objects that are near or far
without having to change the position of the
loupe. As magnification increases, the depth of
field decreases (for a loupe of magnification 2x,
the depth of field is approximately 12.5 cm; for a
loupe of magnification 3.25x, it is 6 cm; for a
loupe of magnification 4.5x, it is 2.5 cm).
The Galilean and Keplerian systems are more
expensive than single-lens loupes, and although
the level of magnification is limited (2x to 6x
depending on the system), the depth of the field
of view and the resolution of the image are
improved with significant increased focal lengths
(distance between eyes and object), reducing
9 Endodontic Armamentarium
c
f
interface), (b) through the lens loupes x2.5 and (c) fibre
optic illumination light source. Note (d–f) 3.4x 5.1x and
13.6x magnification using the dental operating microscope
eyestrain and head and neck fatigue. Loupes can
be available as either ‘flip up’ or through the lens
(TTL) (Fig. 9.2). The former allows direct assess-
ment of the field of view but tends to be heavier
and bulkier.
Illumination
Resolution (the ability to distinguish two
objects close together separately as distinct
objects) is increased by the use of appropriate
light. The distance between the source of the
light and object observed determines light inten-
sity. If you halve the distance between the source
of light and the object, then the amount of light at
the object increases 4 times. The use of surgical
headlamps (Fig. 9.2) therefore increases the light
intensity and therefore resolution of objects
observed in comparison to conventional standard
dental lighting.
Dental operating microscope
The microscope has redefined the concept of
visualisation in dentistry and no more so than in
the field of endodontics, where it is now gener-
ally recognised as an essential element in the
9.3 Stainless Steel Instruments
endodontist’s daily armamentarium. In 1997, all
postgraduate endodontic residency programmes
in the USA would make microscopy training
mandatory and in accordance with the standards
set out by the Commission on Dental Accreditation
(CODA).
Dental operating microscopes offer ergonomi-
cally designed vision through Galilean optics
with either a manual- or power-assisted 3–5 step
magnification changer, dedicated illumination
along the same path as the optics and desired
focal lengths offering magnifications ranging
from 3x to 30x (Fig. 9.2). The microscope can be
free standing or wall or ceiling mounted.
Additional configurations can include assistant’s
scope and video or 35-mm camera adaptors,
which allow for documentation of cases treated.
Image clarity, resolution, illumination, depth of
field of vision, ideal focal length and ergonomics
allow for precise microsurgical and nonsurgical
treatments to be both observed and performed
with ease.
The efficient use of the operating microscope
within endodontics requires advanced training
with an initial steep learning curve. Many end-
odontic procedures are performed at the upper
limits of magnification (15x, 30x) requiring new
hand–eye skill co-ordination to be mastered.
Once accomplished, the use of anything but the
microscope will be deemed inferior and impracti-
cal in one’s day-to-day clinical endodontic
setting.
9.3 Stainless Steel Instruments
For many years, the standard cutting instruments
have been the K-type file and Hedstroem file.
These root canal preparation instruments have
been manufactured to a size and type advised by
the International Standards Organization (ISO).
For most standardised instruments, the number
refers to its diameter at the tip in one hundredth
of a millimetre; a number 10, for example, means
that it has a tip diameter of 0.10 mm. Colour
coding represents a sequence of sizes. All these
instruments have a standard 2 % taper over their
working length.
123
Fig. 9.3 Clinical photograph showing (a) stainless steel
K-files. The K-files are available in ISO diameters from
.06 to .140 mm and lengths from 21, 25 and 31 mm. The
six colours (white, yellow, red, blue, green and black are
repeated from size #15 to #140)
K-file
These instruments were originally made from
a square blank, machine twisted to form a tight
spiral. The angle of the blades or flutes is conse-
quently near a right angle to the shank, so that
either a reaming or a filing action may be used. In
cross section, the K-file has a durable quadrangu-
lar design, which increases its resistance to both
torsion and flexion, making it particularly useful
when negotiating the canal. The tip of the instru-
ment is aggressive with the ability to cut resulting
in the possibility of creating ledges when using
the less-flexible-sized instruments (#20 and
above) in curved canals. The K-files are available
in ISO diameters from 0.06 to 0.140 mm and
lengths from 21, 25 and 31 mm (Fig. 9.3).
The K-flex file
The K-Flex file is made from a rhomboid or
diamond-shaped blank. This hybrid file was man-
ufactured in an attempt to integrate the strength
and versatility of the K-file with the aggressive
cutting properties of the H file.
The K-FlexoFile
These files are manufactured by twisting a
steel wire with a triangular cross section. The
FlexoFile tip is rounded and has a transitional
angle that is blunted, making this instrument
safer during the shaping of curved canals. The
triangular section is less bulky than K-files,
increasing the flexibility of the FlexoFiles. The
FlexoFiles are only available in ISO diameters of
0.15–0.40 mm and lengths 21, 25 and 31 mm.
124
The K-FlexoFiles Golden Mediums
The K-FlexoFiles Golden Mediums are iden-
tical to the K-FlexoFiles except that the diame-
ters have intermediate values compared to those
of the ISO standard. The K-FlexoFiles Golden
Mediums are available in ISO diameters 12, 17,
22, 27, 32 and 37; the lengths remain the same as
conventional K-files of 21, 25 and 31 mm. Their
use is recommended for long and calcified or
curved canals where the passage from a 10 file to
a 15 file or from a 15 file to a 20 file proves to be
difficult. The use of intermediate diameters
enables the operator to reach the working length
easier and with less risk of iatrogenic
complications.
The Flex-R file
Developed by Roane, this hybrid-type file
attempts to incorporate characteristics of both
K-file- and H-file-type instruments. It is pro-
duced by a grinding process similar to H files
resulting in cross-sectional geometry similar to a
K-file with a non-cutting tip designed with a
compound angle of 70 and 35° without any active
cutting edges. The modified tip and greater flexi-
bility associated with these files allowed for a
balanced force technique to be applied to
mechanical preparation of curved canals with
less canal transportation, ledging and
perforation.
The C + files
The C + files are designed with a robust quad-
rangular which shows greater resistance to defor-
mation compared to corresponding K-files. They
are particularly useful in facilitating the location
of the canal orifices and the initial exploration of
calcified canals. The files are available in ISO
diameters 8, 10 and 15 with lengths of 18, 21 and
25 mm.
Hedstroem file
The Hedstroem file is machined from a round
tapered stainless steel blank, and the spiral flutes
are cut into the shank, producing a sharp blade.
Only a true filing action should be used with this
instrument because of the angle of the blade and
positive rake angle. Due to their inherent fragil-
ity, there is a strong possibility of fracture if a
reaming action is used and the blades are engaged
in the dentine. The H file is particularly useful for
9 Endodontic Armamentarium
K
H
C+
Fig. 9.4 Clinical photographs showing stainless steel
K-file (K), Hedstroem file (H) and C+ File (C+). The
K-file can be used in a reaming action. The H file should
be used in a push-pull action. The C+ file shows greater
resistance to deformation compared to the K-file due to its
robust cross-sectional file design. It is available in ISO
diameters 8, 10 and 15 with lengths of 18, 21 and 25 mm
and is particularly useful for calcified canals
removing gutta-percha root fillings or smoothing
dentinal walls or ledges (Fig. 9.4).
Barbed broach
This instrument is manufactured from a round
wire with smooth surfaces, which can be notched
to form barbs at angle to the long axis. The sharp
rasps pointing towards the handle may be used to
loosen or remove pulpal tissue remnants from
within the root canal. The barbed broach is care-
fully introduced deep in the canal, twisted a quar-
ter to a half turn and then withdrawn. Care must
be excised not to force the instrument apically
beyond the point at which it first binds since it
can fracture easily.
Gates–Glidden drills
The Gates–Glidden drills are steel instru-
ments used in a contra-angle slow hand-piece
characterised by a long shank and an elliptical
flame-shaped non-cutting tip. Gates–Glidden
drills are available in six sizes and marked with
corresponding circular notches. The #1 Gates–
Glidden drill has a maximum diameter of
0.50 mm, which increases 0.20 mm for each suc-
cessive size, until #6 which has a maximum
diameter of 1.50 mm. The Gates–Glidden drills
are designed with the weakest point at the start
of the shank, so that they are easier to remove in
case they fracture inside the root canal. It is very
important to remember that the Gates #1 and #2
9.4 Nickel–Titanium Alloy
Fig. 9.5 Clinical
a b
photographs of Gates–
Glidden drills 1–6. Note
(a) drill 1 has a maximum
diameter of 0.50 mm at the
tip, which increases to
1.50 mm for size #6. (b)
G–G Nos. 3 and 4 elliptical
flame-shaped tip is
non-cutting to be used on
withdrawal with a brushing
action
are very fragile and can fracture at the level of
the tip, especially if the recommended rotational
speed of 800 rpm is exceeded and if they are sub-
jected to overzealous bending stresses.
The Gates drills must be used passively on
withdrawal from the canal with a brush-like cir-
cumferential movement. Modification of the
Gates–Glidden drill has been utilised in creating
a staging platform when attempting to remove
separated instruments within the straight portion
of the canal (Fig. 9.5).
Spiral root canal fillers
Spiral root canal fillers are useful for the inser-
tion of calcium hydroxide or other intra-canal
medications in between appointments. It is essen-
tial to ensure that the size selected fits loosely and
passively to the required depth before the instru-
ment is rotated in the root canal since fracture is
otherwise likely.
9.4 Nickel–Titanium Alloy
Nickel–titanium alloy first developed by Buchler
and Wang for the US navy exhibits both super-
elastic behaviour and shape memory due to
atomic arrangements that differ from conven-
tional stainless steel. The atoms in stainless steel
125
can only move a small amount before plastic
deformation occurs, leading to permanent shape
change. By contrast, nickel–titanium exists
reversibly in two different temperature- or stress-
dependent crystal conformations known as mar-
tensite and austenite, which determine the
mechanical properties of the metal. Increasing
the resistance to file separation has been the main
goal of manufacturers in developing the latest
nickel–titanium rotary instruments. Innovative
design and new manufacturing processes have
been introduced, aiming to increase the safety of
new systems preventing instrument fracture.
The first- and second-generation nickel–tita-
nium files have an austenite structure at room
temperature which is quite strong and hard. To
improve the fracture resistance of nickel–titanium
files, manufacturers have introduced either new
alloys to manufacture nickel–titanium files or
developed new manufacturing processes. The
third-, fourth- and fifth-generation files have been
developed with the objective of producing nickel–
titanium wire blanks that contain more of the sta-
ble martensite phase under clinical conditions
resulting in a softer and ductile alloy that is easily
deformed. M-Wire technology has been intro-
duced by thermal processing (heat treatment)
resulting in a mixture of austenite and martensite
126
phases at body temperature, which adjusts the
transition temperatures of nickel–titanium alloys
resulting in greater fatigue resistance (Vortex
Blue). A novel thermal process was introduced to
allow twisting during a phase transformation simi-
lar to the twisting process used to produce the
majority of stainless steel K-files and reamers.
This produced a new R-phase transformation,
which confers good superelasticity and shape
memory with a higher fatigue resistance and
greater flexibility (TF files). Recently, a special
thermal process was introduced to the nickel–tita-
nium file after the grinding process was completed.
Post-machining heat treatment theoretically not
only improved the flexibility and strength of the
file but also modified the crystalline structure of
the alloy to accommodate some of the internal
stress caused by grinding. The manufacturer
claims that this process produces files with an
extraordinary new level of flexibility and resis-
tance to cyclic fatigue with the proprietary R-phase
technology (K3XF files).
9.5 Engine-Driven Instruments
The development of nickel–titanium alloy for
endodontic instruments has revolutionised the
concept of automated root canal preparation. The
flexibility inherent with this alloy, the use of
radial lands on the cutting flutes and non-end cut-
ting tips aimed at keeping the instrument centred
in the canal have allowed mechanised prepara-
tions to be completed with minimal risk of iatro-
genic damage and transportation common to
stainless steel files. New designs are constantly
evolving, and the clinician should ensure that
considerable experience with whichever system
is chosen has been obtained on extracted teeth,
before the instruments are introduced into the
clinical environment.
The first- and second-generation nickel–tita-
nium file systems utilised the traditional continu-
ous rotary motion when preparing root canals.
Recently, the notion of reciprocation with CW
and CCW movements has been introduced with
the purpose of further reducing instrumentation
stresses (WaveOne, Reciproc, Twisted File). This
9 Endodontic Armamentarium
has led to the development of the single-file con-
cept, whereby the instrument rotates in one direc-
tion (larger CW cutting angle) and following
engagement into the canal it disengages in the
opposite direction (usually smaller CCW angle)
resulting in reduced file stresses. One disadvan-
tage that has been reported is the extent of apical
debris that can accumulate increasing the risk of
post-operative pain following canal preparation.
Torque-controlled motors
A controlled high-torque, low-speed motor is
required for efficient use of the instruments. Most
manufacturers of endodontic instruments pro-
duce such a motor with recommended speed of
rotation, individual torque values assigned to
specific files and set CW and CCW angles for
files used in the reciprocating mode. Speed of
rotation refers to revolutions per minute (RPM),
and this varies according to the manufacturer’s
guidelines. The greater the speed, the greater the
cutting efficiency, although at higher speeds there
is loss of tactile sensation and less control that
can result in iatrogenic errors or file separation.
Torque is another parameter that might influ-
ence the occurrence of instrument locking, defor-
mation and potential separation. In low-torque
control motors, torque values set on the motor are
supposed to be less than the value of torque at
deformation and at separation of the rotary instru-
ments, whereas in high-torque control motors,
the torque values are relatively high compared to
the torque at deformation and at separation of the
rotary instruments. During root canal prepara-
tion, all the instruments are subjected to different
levels of torque. If the level of the torque is equal
or greater than the torque at deformation or at
separation, the instrument will either deform or
separate. Theoretically, with low-torque control
motors, the motor will stop rotating and can even
reverse the direction of rotation when the instru-
ment is subjected to torque levels equal to the
torque values set on the motor. Thus, instrument
failure could be avoided (Fig. 9.6).
Profile rotary system
The ProFiles rotary nickel–titanium instru-
ments, introduced by Dr. W. Ben Johnson in 1994,
are available in 0.02, 0.04 and 0.06 taper and in the
ISO diameters from 15 to 45 (0.02 taper) and from
9.5 Engine-Driven Instruments
Fig. 9.6 Clinical photograph showing (a) torque-
controlled X-Smart plus motor. Both torque and speed can
be adjusted from preprogrammed settings as to manufac-
turer’s recommendations
15 to 80 (0.04 and 0.06 taper) and in 21-, 25- and
30-mm lengths. ProFiles all present a working sur-
face of 16 mm and a round non-cutting tip. ISO
standard coloured rings are present on the handle,
allowing the user to easily identify both the diam-
eter and the taper (one small ring for the 0.02
series, two small rings for the 0.04 series and three
small rings for the 0.06 series).
ProFiles are obtained by micromachining a
nickel–titanium wire so that in cross section the
instrument has a design defined as a ‘triple U’
with bidirectional cutting edges characterised by
three flat cutting surfaces called ‘radial lands’.
The radial lands maintain the instrument centred
within the canal, whilst the cutting edges aim to
plane the walls smooth rather than cut, minimis-
ing canal transportation. The radial lands are
separated by three U-shaped flutes, which pro-
vide space for the accumulation of debris.
The files are used in a crown-down prepara-
tion sequence at 150–300 RPM. Several
127
instrumentation sequences have been described
for ProFile, including the variable taper sequence,
the variable tip sequence and a sequence that
alternates between 0.06 and 0.04 tapers.
LightSpeed
LightSpeed (LS) nickel–titanium rotary
instruments introduced by Drs. Senia and Wildley
are similar to the Gates–Glidden drills, with a
short cutting blade (0.25–2 mm in length) with a
non-cutting pilot tip and a smooth flexible shaft.
Instruments consist of ISO diameters from 20 to
100 and intermediate sizes such as 22.5, 27.5,
32.5 and 37.5. The long, thin shaft ensures that
the LightSpeed (LS) has increased flexibility
with a point of separation at 18 mm from the tip
in order to facilitate their removal in case of
instrument fracture. LS instruments are available
in 21-, 25-, 31- and 50-mm lengths.
The instruments are used from the smallest to
the largest in a step-back sequence with a peck-
ing movement (advancement in the apical direc-
tion followed by a light withdrawal). The
step-back sequence begins after having manually
pre-enlarging the canal up to K-file 15, ensuring
canal patency, achieving straight-line access and
determining working length (WL).
The original apical canal diameter is gauged
with LS instruments by hand. Gauging measures
the smallest diameter of a canal using an LS
instrument with moderate apical force. Begin
with a small instrument and test whether it goes
to WL. If it does, then it is smaller than the canal
diameter. The LS instrument that will bind before
WL is the first LS instrument size to bind (FLSB)
before reaching WL. Note that this size is used to
begin (not end) canal preparation. Mechanical
instrumentation is carried out with the FLSB. All
LS instruments are used the same way: with a
slow, continuous apical movement until the blade
binds and a momentary pause; then it is advanced
to WL with intermittent or ‘pecking’ motions (a
‘peck’ is a short inward and a slight withdrawal
motion). The number of pecks required to reach
WL will increase as instrument size increases
because more wall dentine is cut. The instrument
size that requires 12 pecks or more (‘12-peck
rule’) to advance from where it first binds (and
pecking begins) until reaching WL is called the
128
Master Apical Rotary (MAR). The MAR is the
‘correct’ instrument size for proper apical clean-
ing. Smaller sizes do not clean, whereas larger
sizes may cause over-enlargement and weaken-
ing of root structure.
The next larger size LS instrument is used to a
length that is 4 mm short of WL using a pecking
motion but without counting pecks. This com-
pletes cleaning and shaping the apical 5 mm of
the canal for obturation.
The middle third of the canal is instrumented
with sequentially larger full-size LS instruments
(there is no need to use the half-sizes). When an
instrument no longer advances easily with light
pecks, it is withdrawn from the canal and replaced
with the next larger full size. This sequence con-
tinues until reaching a size that does not easily
advance beyond the coronal third of the canal.
Mid-root is usually prepared with three or four
LS instruments.
Recapitulate to WL with the MAR. This
ensures a clear path for filling. The suggested
rotation speed for the LightSpeed instruments is
between 1,200 and 2,000 rpm using a low-torque-
controlled motor.
Greater Taper files (GT)
GT instruments devised by LS Buchanan are
available in four basic categories of sizing, the 20
Series, the 30 Series, the 40 Series and the 0.12
Accessory Series. The 20, 30 and 40 Series GT
files have the same range of tapers, 0.04, 0.06,
0.08 and 0.10 mm/mm in each file set, but vary
by their designated tip diameters. The 0.12
Accessory GT files vary by their tip diameters
and have a constant rate of taper within the file
set, namely, 0.35, 0.50, 0.70 and 0.90 mm – all
with a large 0.12 mm/mm taper.
GT files have been designed with limited
maximum flute diameters, passive rounded-tip
geometry, landed and variably pitched cutting
flutes. These features allow for a wide range of
tapered instruments to be safely taken to WL;
they have reduced ledging and maintenance of
canal curvatures with minimal risk of transporta-
tion. The variable pitched flutes allow for less
‘screwing-in’ effect and greater strength and
reduced torsional stresses in the smaller, more
fragile diameters.
9 Endodontic Armamentarium
GT instruments are also available in hand
form in sizes 20–0.06, 20–0.08, 20–0.10,
35–0.12, 50–0.12 and 70–0.12. GT hand instru-
ments have triangular cross-sectional blade
geometry and counterclockwise flute paths but
cut the same preparation shapes as GT rotary
instruments of the same size designation.
The GT instruments are identified by the num-
ber of black bands on the shank ends, times two,
equivalent to the taper of the file. The colour
bands on the shanks indicate the tip diameters in
the ISO convention.
The clinical objective of initial shaping is to
cut a shape that has a taper greater than 0.04 mm/
mm to the end of the root canal so that the termi-
nal diameter of the canal can be accurately
gauged or measured, a necessity prior to choos-
ing the final GT instruments appropriate for that
canal preparation. Initial shaping always begins
with the 20–0.10 GT instrument, regardless of
the root size or the morphology of the root canal
being prepared. Before shaping, it is essential
that the canal be negotiated to length up to a size
#15 K-file so that a glide path has been estab-
lished and straight-line access is achieved.
GT instruments are used at 300 RPM. It may
be necessary to use progressively smaller tapered
20 Series GT instruments, each cutting deeper,
until the root canal terminus is reached during
this first phase of shaping. As soon as one of the
GT instruments in the 20 Series has reached ter-
minal length in the canal, apical gauging is car-
ried out in preparation for creating the ideal final
shape. Apical gauging is defined as the measure-
ment of the terminal diameter of a canal and is
determined to see which size file will pass
through the terminus, which size binds at length
and how progressively larger instruments step
back from that position.
The ideal taper for a given canal must then be
decided upon with the root size, canal size and
curvature in mind. Roots can be divided into
small, medium and large classes and shaped to
0.04, 0.06 or 0.08 mm/mm tapers. Canals with
moderate to severe curvature or small roots that
are extremely thin are shaped to a 0.06 mm/mm
taper, MB2 canals being a good example of both
criteria. Canals with severe cervical curvatures or
9.5 Engine-Driven Instruments
SX S1 S2 F1 F2 F3 F4 F5
Fig. 9.7 The ProTaper Universal system is made up of
eight instruments, available in 21-, 25- and 31-mm lengths
that are divided into two groups of instruments each con-
sisting of shapers (with the marking SX, S1 and S2) and
finishers (with the marking F1, F2, F3, F4 and F5)
multi-planar bends may only be safely shaped to
a 0.04 mm/mm taper. Medium and large roots are
shaped to 0.10 or 0.12 mm/mm tapers with 0.10
being chosen unless it is a large root with an api-
cal diameter larger than 0.40 mm, in which case,
one of the 0.12 Accessory GT instruments would
be the selected instrument.
ProTaper Universal
The ProTaper Universal system is made up of
6 instruments, available in 21-, 25- and 31-mm
lengths that are divided into 2 groups of 3 instru-
ments, each consisting of shapers (with the mark-
ings SX, S1 and S2) and finishers (with the
markings F1, F2 and F3). The shapers are instru-
ments for eliminating interferences in the coronal
and middle third of the canal, creating a smooth
pathway for the finishing instruments, which pro-
vide a definitive taper and diameter to the canal.
Tip diameters for SX, S1, S2, F1, F2, F3, F4 and
F5 are 0.19, 0.17, 0.20, 0.20, 0.25, 0.30, 0.40 and
0.50 mm, respectively (Fig. 9.7).
The important structural characteristics of
these files include a robust triangular cross sec-
tion with convex sides, increasing the metal mass
of the central core, improving cutting efficiency
whilst maximising core strength. Variable helical
angles and variable pitch (the distance between
spirals) aimed at reducing the risk of screw in and
aid the removal of debris within the canal.
Variable tapers are present whereby there is an
increase in tapers towards the handle of the
129
shapers (so as to increase the flexibility in the
apical third) and decrease towards the handle in
the finishers (so as to enlarge the apical prepara-
tion without making the coronal third of the
instrument too rigid).
The ProTapers are used in increasing order
from the smallest to the largest after having
explored and pre-enlarged the canal at least to
number 20 K-file. The ProTapers have a lateral
cutting action, and therefore the shapers can be
used with a brushing action, which is very useful
for removing coronal interferences away from
the furcal danger areas. The finishers with their
greater taper and diameter must be used with a
rapid insertion and withdrawal with minimal
pressure. The recommended rotational speed for
all the ProTapers is 250–300 rpm. In the canals
that are extremely curved, it is possible to use the
ProTapers by hand. Lastly, it should be remem-
bered that it is preferable, as with all Ni–Ti rotary
instruments, to use the ProTapers in an endodon-
tic hand-piece with torque control and autorev-
erse features (Figs. 9.8 and 9.9).
RaCe
The RaCe (reamers with alternate cutting
edges) system is characterised by a square-
shaped cross section in the smaller instruments
(15/0.02 and 20/0.02) and triangular cross sec-
tions in the remaining instruments. Cutting
angles with twisted areas similar to conventional
files and alternating straight areas give rise to
large space for debris and the reduced tendency
to thread, reduced canal blockage and reduced
working torque of the instruments. The RaCe
instruments are subjected to an electrochemical
processing of the blade that serves to increase the
resistance against torsional stress and fatigue
resulting in a smoother surface compared to other
instruments.
The RaCe are available in 0.02 taper (#15–
#60), 0.04 taper (#25–35) and 0.06 taper (#20–
30). The Pre-RaCe are also available for coronal
preflaring in ISO diameters 40 with 0.10 and 0.06
taper, ISO 35 with 0.08 taper and ISO 30 with
0.06 taper. The RaCe instruments can be used
either in the crown-down or step-back sequence;
the recommended rotational speed is 600 rpm,
whilst the use of torque control has not been
130
a b
Fig. 9.8 (a, d) Clinical diagrams representing the use of
ProTaper shaping file S1 in a brushing action to aid
removal of coronal interferences that prevent straight-line
Fig. 9.9 Clinical photograph showing ProTaper hand
files SX, S1, S2, F1, F2 and F3
recommended considering its low tendency to
screw in.
K3
The K3s are engine-driven instruments in
nickel–titanium available in lengths of 21, 25 and
30 mm and with a taper of 0.02 to 0.12 with tip
sizing ranging from ISO #15 to #60. The set is
completed with two orifice openers with a taper
of 0.08 and 0.10.
The K3 has a cross section of three radial
lands, the first of which lends support to the blade
increasing resistance to torsional stress; the sec-
ond which is retracted reduces friction, providing
smoother operation against the canal walls; and
the third centres the instrument, keeping it stabi-
lised inside the canal avoiding threading itself
into the canal. Other features include a slightly
positive cutting angle, a non-cutting safe-ended
9 Endodontic Armamentarium
c d
access. A lateral cutting action on withdrawal is recom-
mended away from the danger area such as the furcation
tip, a variable helical flute angle, a variable pitch
with less blades on the coronal part to prevent the
threading in effect and a diameter of the core that
reduces in the coronal direction so as to keep the
flexibility of the instrument constant all along its
length. The K3 file handle and hand-piece afford
the operator easier access to the posterior region
of the mouth. They are 4 mm shorter than their
competitors, yet the working (fluted) length is the
same.
The sequence of using the K3 is in a crown-
down fashion based on decreasing diameter,
taper or on alternate decreasing of diameter and
taper. Like all rotary systems, exploring and pre-
flaring with hand instruments up to file size 15
must precede the use of the K3. The crown-down
sequence must be recapitulated without force
until a 25 or 30.06 can be brought to WL. With
the K3, it is recommended to use an endodontic
motor, speeds of 300–350 RPM with automatic
torque control and autoreverse features.
Vortex blue
Vortex Blue (VB) was introduced into the
market in 2009 manufactured from M-Wire
technology with a distinct ‘blue-colour’ titanium
surface oxide layer which improves the cutting
efficiency and wear resistance of the files. VB
instruments are available in 21-, 25- and 30-mm
lengths of either 0.4 (ISO #15–50) or 0.6 (ISO
#15–50) tapers. The major difference between
the Vortex and the classical ProFile files lies in
the non-landed cross section of the VB files. The
9.5 Engine-Driven Instruments
Fig. 9.10 Clinical photograph showing (a) selection of
0.4 taper 25 mm #15, 20 and 25 Vortex Blue rotary files.
Standard Ni–Ti files continually try to revert to their origi-
nal straight state. Note 0.4 #20 file has been pre-bent. The
proprietary processing of Vortex Blue rotary files reduces
shape memory
files consist of constant tapers with a triangular
cross section, variable helical angles and safe-
ended non-cutting tip. The variable helical angles
compensate for the non-landed files preventing
threading into the root canal (Fig. 9.10).
Like all rotary systems, the files are used fol-
lowing establishment of WL and glide path cre-
ation. A crown-down shaping technique is used
and the choice of the initial file depends on
whether the canal is deemed to be small (mesial/
buccals of molars, small premolars and lower
anteriors) or large (palatal/distal molars, large
premolars, upper anteriors). A 30.04 rotary file is
used in small canals taken to either resistance or
WL. If resistance is encountered, then a smaller
instrument is used. In larger canals, the recom-
mendation is to use the 40.04 file in a similar
manner. VB files are used at 500 RPM and differ-
ent torque settings according to file size.
Twisted files
In 2008, SybronEndo introduced Twisted
Files (TF), the first fluted Ni–Ti file using a man-
ufacturing process similar to the twisting process
that is used to produce the majority of conven-
tional stainless steel K-files and reamers. A pro-
prietary thermal processing of heating, cooling
and twisting is employed in the R-phase (rhom-
bohedral crystalline configuration which is an
intermediate phase between austenite phase at
rest and martensite phase during function). Other
Ni–Ti rotary instruments are manufactured from
either grinding or M-Wire. Grinding during
131
manufacture can result in microcracks that may
lead to increased propensity for file separation if
the file is subjected to excessive torsional loads
and cyclic fatigue.
Instruments are available in 23- and 27-mm
lengths of varying tapers including 0.04 (ISO
#25, 40 and 50), 0.06 (ISO #25, 30, 35), 0.08
(ISO #25), 0.10 (ISO #25) and 0.12 (ISO #25).
TF files are colour coded for ease of identifica-
tion. The top band shows the taper and the bot-
tom band the ISO tip size. The files have a
triangular cross section maximising flexibility
with a safe-ended tip and are used in a crown-
down fashion. The TF technique advocates using
a 0.08/25 file until it engages dentine. The file is
then removed and flutes cleaned. Following reca-
pitulation to WL, the same file is advanced until
WL is achieved. If resistance is met before WL,
then you should proceed with a 0.06/25 file using
the same steps. Next, a 0.06/30 file is advanced to
WL for final apical shaping. If the apical foramen
is deemed larger than ISO #30 at working length,
then 0.06/35 or 0.04/40 tip sizes can be used.
TF adaptive files have also been introduced
with file sizes available according to whether
canals are deemed small or medium/large. The
small pack consists of three files, colour coded
green, yellow and red (SM1 0.04 ISO #20, SM2
0.06 ISO #25 and SM3 0.04 ISO #35). The
medium/large pack consists of three files colour
coded green, yellow and red (ML1 0.08 ISO #25,
0.06 ISO #35 and 0.04 ISO #50). The colour-
coded system is based on traffic lights. The clini-
cian starts with the green, continue or stop with
the yellow and stop with the red. Green means
go. Yellow means continue or stop. Red means
stop. Straight-line access, glide path creation and
WL are determined prior to beginning the file
sequence. Canals are prepared with the colour-
coded files; ideally finishing on red is possible to
achieve ideal taper and apical preparation size to
maximise irrigation penetration.
By using an innovative patented motion, TF
adaptive instruments can either be used in a con-
tinuous rotary motion when not subjected to
stress within the canal or an interrupted recipro-
cating motion of CW–CCW angles when undue
stress is encountered. The CW–CCW angles vary
132
Fig. 9.11 Clinical photograph showing (a) WaveOne
rotary file system. Small file, primary file and large files
used in a reversed balanced force CW and CCW
directions
between 600-0 and 370-50 depending on the ana-
tomical complexities and intra-canal stresses
placed on the instruments. This ‘adaptive’ motion
is meant to reduce the risk of intra-canal file sep-
aration without affecting cutting efficiency.
WaveOne (Fig. 9.11)
These instruments, manufactured from
M-Wire technology, improve strength and resis-
tance to cyclic fatigue. Modified convex triangu-
lar cross section at the tip end and a convex
triangular cross section at the coronal end ensure
overall flexibility and allow canal curvatures to
be followed with improved safety over the length
of the instrument due to variable pitch flute
design. The files are specifically designed to
work in a ‘reversed’ balanced force action using a
preprogrammed motor moving the files in a CW
and CCW direction. At present, there are three
files in the WaveOne single-file reciprocating
system available in 21-, 25- and 31-mm lengths.
The WaveOne small file is used in fine canals.
The tip is ISO 21 with a continuous 6 % taper.
The WaveOne primary file used in the majority of
cases consists of a tip size ISO 25 with an apical
taper of 8 % that reduces towards the coronal
end. The WaveOne large file has a tip size ISO 40
with an apical taper of 8 % that reduces towards
the coronal end.
The instruments are designed for single use
only with the added advantages of reduced instru-
ment fatigue as well as reducing the risk of prion
disease cross-contamination that exists with
9 Endodontic Armamentarium
potential CJD-infected patients. The plastic
colour coding (yellow, red and black synony-
mous with small, primary and large WaveOne
files) in the handle becomes deformed once ster-
ilised, preventing the file being placed back into
the hand-piece.
The WaveOne instrument is selected follow-
ing straight-line access, WL determination and
glide path preparation. A progressive up-and-
down movement no more than three or four times
with minimal force is required. A brushing action
to create straight-line access and relocate canals
away from danger zones is possible.
ProTaper Next
There are five ProTaper Next (PTN) instru-
ments available in different lengths available for
shaping canals: X1, X2, X3, X4 and X5. The files
have yellow, red, blue, double black and double
yellow identification rings on their handles cor-
responding to sizes 17.04, 25.06, 30.07, 40.06
and 50.06. The X1 and X2 files have an increas-
ing and decreasing percentage taper on a single
file, whereas the X3, X4 and X5 have a fixed
taper from D1 to D5, then a decreasing taper over
the remaining active portions.
Instruments are used after creation of a repro-
ducible glide path by means of hand instruments
or rotary PathFiles. The PTN X1 is always fol-
lowed by the second instrument: the PTN X2.
The PTN X2 can be regarded as the first finishing
file in the system as it leaves the prepared root
canal with adequate shape and taper for optimal
irrigation and root canal obturation. The PTN X3,
PTN X4 and PTN X5 can be used to either create
more taper in a root canal or to prepare larger root
canal systems.
The progressively tapered instruments are
manufactured from M-Wire technology that con-
tributes towards greater flexibility resulting in
increased safety and protection against instrument
fracture. The instruments have a bilateral sym-
metrical rectangular cross section with an offset
from the central axis of rotation (except in the last
3 mm of the instrument, D0–D3) creating an
asymmetric rotary motion. The PTN X1 file,
which has a square cross section in the last 3 mm,
has a centred mass and axis of rotation from D1
to D3m, whereas it has an offset mass of rotation
9.6 Sonic and Ultrasonic Instruments
Fig. 9.12 Clinical photograph showing (a) ProTaper
Next rotary file systems X1, X2 and X3. The off-centred
rectangular cross section fives the file a snake-like ‘swag-
gering’ movement as it moves through the root canal
from D4 to D16. Starting at 4 %, the file has 10
progressive tapers from D1 to D11, whereas there
are decreasing tapers from D12 to D16. The
asymmetric rotary motion allows the instrument
to experience a rotational phenomenon known as
swagger. The benefits of these design characteris-
tics include reduced engagement between the
instrument and the dentine walls because only
two cutting points make contact with the canal
wall at any time. This contributes to a reduction
in taper lock, screw-in effect and stress on the
file. It also ensures that debris removal occurs in
a coronal direction because the off-centre cross
section allows for more space around the flutes of
the instrument, which leads to improved cutting
efficiency, as the blades will stay in contact with
the surrounding dentine walls. Root canal prepa-
ration is done in a very fast and effortless manner.
PTN files are used at 300 RPM and a torque set-
ting of 2–5.2Ncm (Fig. 9.12).
9.6 Sonic and Ultrasonic
Instruments
The production of mechanical vibration in the
ultrasound frequency range is known as the
piezoelectric effect, which can be transferred to
cutting tools or tips that produce micro-vibratory
movements. The term piezoelectric refers to
‘electricity by pressure’, a phenomenon of gener-
ating an electric charge from the application of
133
mechanical or strain energy onto a crystalline
piezoelectric material. Ultrasonic frequency
range used in dentistry range between 25 and
42 kHz. By comparison, the sonic frequency
range is 6–9 kHz. Magnetostriction, on the other
hand, converts electromagnetic energy into
mechanical oscillation when an alternating mag-
netic field is applied to a ferromagnetic material.
The physical dimension of the material changes
(lengthwise), causing the ultrasonic tip to vibrate.
Magnetostrictive units operate between 18 and
45 kHz.
Various ultrasonic applications in endodontics
include cavity preparation, passive ultrasonic
irrigation, root canal instrumentation, root-end
preparation, re-treatment procedures such as
gutta-percha/sealer removal and obturation
(warm lateral condensation using energised
spreading technique).
Many commercially available piezoelectric
ultrasonic dental devices are available including
the ProUltra Piezo (Dentsply Tulsa) and P5 series
of ultrasonics (Acteon). ProUltra or Satelec
hand-pieces are available and compatible with
ProUltra or Satelec ultrasonic tips. Several tips
are available with differing designs (length,
diameters, angles) according to use manufac-
tured from a range of metal alloys (stainless steel,
titanium alloy) and can be coated with an abra-
sive material such as diamond or zirconium to
increase the cutting efficiency, with our without
water ports. Tips intended for endodontic use
have incorporated a contra-angle bend that allows
unobstructed views when used in conjunction
with the surgical operating microscope. Tips can
be interchangeable between different devices, but
the thread patterns must be checked for compati-
bility. Currently two different thread patterns are
used (E and S thread). The various tips have been
designed specifically for virtually every step of
endodontic treatment procedures and are used in
the recommended power settings according to
the manufacturer’s instructions.
One example of a commercially available kit
for use in endodontics is the Start-X tips (Dentsply
Maillefer) comprising of five ultrasonic tips. The
Start-X tips have a cutting surface characterised
by longitudinal rounded micro-blades (increase
134
efficiency) separated by grooves (facilitate cool-
ing and removal of debris). Each tip has a water
port that allows for effective cooling of the den-
tine when used. The Start-X tips are robust with
minimal tendency to breakage and deformation.
Tips are used on a medium setting and activated
with a light touch with intermittent dispersion of
water for removal of dentine dust to ensure maxi-
mum cutting efficiency. A 110° angle is incorpo-
rated between the shaft and cutting surface to
optimise visibility during clinical use with the
operating dental microscope.
Start-X tip #1
The diameter at the tip is 0.8 mm with a maxi-
mum diameter of the active portion at 1.6 mm and a
distance D1–D2 (blade length) of 12 mm. The
rounded non-cutting end minimises the risk of alter-
ing the morphology of the pulp chamber floor. The
main indication for use is refinement of access cavity
walls. Following opening of the pulp chamber, the
tip can be used to remove restorations, filling materi-
als, caries and dentine interferences that would pre-
vent direct access to the root canal orifices.
Start-X tip #2
The diameter at the tip is 1.0 mm with a maxi-
mum diameter of the active portion of 1.54 mm
and distance D1–D2 (blade length) of 8 mm. The
micro-blades extend to the rounded end of the tip
increasing its cutting efficiency at the tip. Its use is
intended for removal of dentine on the pulp cham-
ber floor when trying to locate the MB2 canal.
Start-X tip #3
A sharp acuminated end characterises this tip.
The micro-blades stop approximately 1 mm short
of this tip. The diameter at the tip where the
micro-blades end is 0.64 mm with a maximum
diameter of the active portion of 0.9 mm and a
distance D1–D2 (blade length) of 8 mm. Its main
purpose is for removal of calcifications from the
pulp chamber floor or coronal 1/3 of the root
canal. The tip is aggressive and should always be
used with a light touch.
Start-X tip#4
The tip has a tapered conical shape with a
diameter that progressively reduces from 1.24 to
0.8 mm. However, at 1.5 mm from the distal end,
the diameter increases again and the shape
changes into a convex triangular shape with a
9 Endodontic Armamentarium
Fig. 9.13 Clinical photographs showing (a) Start-X
ultrasonic tips 1–5
maximum diameter of 1.4 mm and a length of
1.5 mm. Its main use is intended for removal of
both screw and cast metal posts. The most active
distal end of the ultrasonic tip is kept in intimate
contact with the post to maximise energy transfer,
promoting cement/bond failure. The tip should be
circumferentially moved along the exposed length
of post with intermittent water activation to mini-
mise heat transfer to the surrounding tooth and
bone. In cases of cast metal posts, the core should
be reduced with a high-speed diamond bur to
facilitate and optimise transmission of ultrasonic
energy transferred from tip to post.
Start-X tip#5
This tip is characterised by parallel sides with
the active length of 10 mm and a diameter of
1.0 mm. A characteristic concave shape is evi-
dent at the tip end, which follows the convexity
of the floor of the pulp chamber of molar teeth
facilitating calcification removal without altera-
tion of pulp floor morphology. The tip is used for
removal of pulpal floor calcifications enabling
developmental lines to be seen which help local-
ise the root canal orifices. The tips have also been
advocated for use in re-treatment cases and the
removal of obturation and/or restorative materi-
als that may be present (Fig. 9.13).
9.7 Microsurgical Instruments
Most practitioners will have an established prefer-
ence for a particular type of surgical instrument
that he/she may use. For all surgical procedures,
9.8 Burs
a b
d e
Fig. 9.14 Clinical photographs showing typical arma-
mentarium of burs used for access preparations, (a) dia-
mond grit tapered bur, (b) tungsten carbide bur, (c)
instruments should be set out, preferably in the
order in which they will be used. Traditional
endodontic surgery encompassed resection of the
root apex, followed by placement of a root-end
filling material to seal the apex using round burs
attached to a straight hand-piece and amalgam
retrograde fillings. Advances over the last 20
years have led to not only refinement in the mate-
rials used but also the techniques and instruments
available. These advances are centred on the use
of a surgical operating microscope and microsur-
gical instruments which allow for small osteot-
omy (approximately 3–4 mm in diameter, 3-mm
root tip resection, no resection bevel angle,
inspection of resected root surfaces, ultrasonic
preparation of resected roots and biocompatible
root-end filling material placement (using MTA).
Instruments specific to this end include burnishers,
135
c
f
non-end cutting Endo Z bur, (d) long shank diamond, (e)
diamond grit round diamond and (f) parallel tapered short
diamond bur
condensers, microsurgical mirrors, microsurgical
blades, smaller sutures (5.0) and Castroviejo nee-
dle holders (microsurgical) to name but a few (the
reader is advised to refer to Chap. 13 Microsurgical
endodontics In Treatment, Re-Treatment and
Surgery, Mastering clinical endodontics for a
more comprehensive review).
9.8 Burs
Several types of bur may be required for root
canal treatment. Some of these are described
below and shown in Fig. 9.14.
Cutting an access cavity
High-speed burs should be used to gain access
and shape the cavity. A diamond or tungsten
carbide tapered fissure bur can be used for initial
136 9 Endodontic Armamentarium

penetration of the roof of the pulp chamber. A 9.9 Instrument Packs

tapered safe-ended diamond or tungsten carbide
bur is then used to remove the roof of the pulp A basic pack of instruments must be available spe-
chamber without damaging the floor. cifically for endodontic consultation (Fig. 9.16),
Location of canal routine root canal procedures (Fig. 9.17) and obtu-
Burs should only be used as a last resort to ration appointments (Fig. 9.18).
locate a sclerosed canal because of the danger of A front surface reflecting mouth mirror is use-
iatrogenic perforation. It is deemed much safer to ful to prevent the double image of the fine detail
use specially designed ultrasonic tips in order to in an access cavity that occurs with a conven-
remove secondary dentine and assist in the iden- tional mirror. A larger mouth mirror is particu-
tification of canal orifices and in shaping the larly useful when taking intra-oral clinical
canal orifice during preparation. Specifically photographs of cases for records. The use of
designed tips are available for troughing and
chasing sclerosed canals, refining access cavity
walls and line angles, removing obstructions
(pulp stones) and cutting around posts. It is gen-
erally wise to use them with a low-power setting
and to ensure that they are in contact with dentine
before activating the piezoelectric unit. As with
all instruments, it is advisable to follow manufac-
turer instructions as to the recommended settings
to avoid instrument fracture.
Canal preparation
The use of Gates–Glidden drills were useful in
the past when using a crown-down approach
although their use has now been superseded with
nickel–titanium rotary file systems which have
corresponding tapered files that can do the job Fig. 9.15 Clinical radiograph demonstrating the use of
Gates–Glidden drills used to prepare mesial root of tooth
with much less risk of iatrogenic damage and 26. Note the excessive overpreparation with risk of iatro-
overzealous preparation which may lead to root genic perforation during preparation or potential root frac-
fracture (Fig. 9.15). ture in the future

Fig. 9.16 Clinical D

photograph showing tray
setup for new patient E
consultations containing
(a) Fractfinder, (b) college F
tweezers, (c) small
excavator, (d) flat plastic,
(e) mouth mirror and (f)
periodontal probe
9.9 Instrument Packs 137

M
B

C D E F G H I K L
P

Fig. 9.17 Clinical photograph showing typical tray setup
for root canal treatment and re-treatment cases including
(a) rotary files; (b) re-treatment files; (c) ruler; (d) straight
probe; (e) DG16 endodontic probe; (f) small excavator;
(g) flat plastic; (h) large excavator; (i) locking tweezers;
(k) periodontal probe; (l) dental mouth mirror; (m) K-files
sizes 06–40; (n) access burs including Endo Z, endoac-
cess, tungsten carbide, spiral filler and Gates–Glidden I;
(o) topical anaesthetic; and (p) pre-sterilised cotton wool
pledgets

A D G L N

E K

B F O P

M
C I J
H

Fig. 9.18 Clinical photograph showing basic instrument
setup including (a) gauze; (b) paper points (pre-sterile
packs); (c) glass mixing slab; (d) interim IRM restoration;
(e) orthodontic bands; (f) articulating paper; (g) Ledermix/
calcium hydroxide 50:50 mix; (h) sodium hypochlorite
solution; (i) EDTA; (j) chlorhexidine solution; (k) caulk-
ing; (l) Endo V block holder; (m) rubber dam, rubber dam
frame, clamp and forceps; (n) apex locator file attach-
ment; (o) glass ionomer restorative capsule and handler;
and (p) local anaesthetic needle and syringe
138
B C D E F G
Fig. 9.19 Clinical photograph showing typical obtura-
tion tray setup containing (a) sterilised file holder, (b) fast
hand-piece, (c) metal ruler, (d) Buchanan plugger, (e)
locking tweezers x2, (f) plugger, (g) flat plastic, (h) small
endolocking tweezers ensures small items are
gripped safely allowing safe instrument transfer
between nurse and operator. A DG16 endodontic
probe is useful for the detection of canal orifices.
The excavator is long shanked, with a small blade
to allow access into the pulp chamber. The
pocket-measuring probe such as a routine CPITN
probe with clearly visible gradations is ideal
when assessing the periodontal status of the
tooth. A furcation probe is useful when confirm-
ing the presence of furcation involvement and
recording the degree of severity.
Other items usually included are a flat plastic,
sterile cotton wool rolls, sterile cotton wool pled-
gets and a metal ruler or other measuring device
that may be easily sterilised. A clean-stand or
other device such as the endo-ring is required to
hold the endodontic instruments and minimise
the risk of a sharps injury to both operator and
nurse. Paper points are also required, and the
simplest method of storage and use is to purchase
pre-sterilised packs.
9 Endodontic Armamentarium
H I J K
excavator, (i) periodontal probe, (j) dental mouth mirror,
(k) sterile cotton wool pledgets, (l) topical anaesthesia and
(m) sterile burs
Trays for various treatment stages can be cus-
tomised according to the clinician’s preference of
techniques employed and instrument require-
ment thereof. Pre-sterilised radiographic equip-
ment (see Chap. 12) and a basic rubber dam kit
should be available (see Chap. 14). As mentioned
previously, any instrument placed in the root
canal should be sterile to prevent cross-
contamination to the patient and introduction of
extraneous microorganisms, which may
compromise treatment (for further reading, see
Chap. 7) (Fig. 9.19).
References
1. Council on Dental Materials and Devices. The
American Dental Association, specification no 28 for
endodontic files and reamers. J Am Dent Assoc.
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2. ISO 3630–1. Dentistry – root-canal instrument – part
1: general requirements and test methods. Geneva:
International Organization for Standardization; 2008.
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3. ISO 3630–2. Dentistry – endodontic instruments –
part 2: enlargers. Geneva: International Organization
for Standardization; 2013.
4. ISO 3630–3. Dental root canal instruments – part 3:
condensers, pluggers and spreaders. Geneva:
International Organization for Standardization;
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5. Council on Dental Materials, Instruments, and
Equipment. Revised American National Standards
Institute. American Dental Association specification
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J Am Dent Assoc 1982:104(4):506.
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7. Cohen S, Burns RC. Pathways of the pulp. 6th ed. St
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9. Serene T, Loadholt C. Variations in same size end-
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10. Stenman E, Spandberg LS. Root canal instruments are
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11. Vessey RA. The effect of filing vs reaming on the
shape of the prepared root canal. Oral Surg Oral Med
Oral Pathol. 1969;27(4):543–7.
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tion techniques on the original canal shape and its api-
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13. Gutmann JL, Dumsha TC, Lovdahl PE, Hovland
EJ. Problem solving in endodontics. 3rd ed. Mosby:
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CPlusFiles. Accessed 28 July 2014.
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instruments: from past to future. Endo Topics. 2013;
29:3–17.
19. Young GR, Parashos P, Messer HH. The principles of
techniques for cleaning root canals. Aust Dent
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ments alloys used in dentistry. Int Endod J. 2000;33:
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21. Thompson SA, Dummer PMH. Shaping ability of
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22. Hsu Y-Y. The ProFile system. Dent Clin North Am.
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23. Thompson SA, Dummer PMH. Shaping ability of
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mentation technique. Endod Top. 2005;10(1):148–50.
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aration – Part 1. Concepts for variably tapered shap-
ing instruments. Int Endod J. 2000;33(6):516–29.
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ment system. Endod Top. 2005;10(1):179–82.
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edges – concept and clinical application. Endod Top.
2005;10(1):176–8.
30. Gao Y, Shotton V, Wilkinson K, Phillips G, Ben
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card.pdf. Accessed on 1 Aug 2014.
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West J. The WaveOne single-file reciprocating sys-
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Solomanov M. The self-adjusting file system.
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189–210.
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TIPcard_2-24-10_1.sflb.ashx. Accessed on 1 Aug
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40. Berutti E, Cantatore G, Castellucci A, Chiandussi G,
Pera F, Migliaretti G, Pasqualini D. Use of nickel-
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41. Gambarini G. Rationale for the use of low torque end- 44. Eliyas S, Vere J, Ali Z, Harris I. Micro-surgical end-
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Dent Clin N Am. 2004;48(1):11–8.
 Antibiotics Use in Endodontics
10

Summary
Antibiotics are prescribed by dentists routinely for the treatment as well as
prevention of infection. Indications for the use of systemic antibiotics in end-
odontics are limited, since most intra-canal poly-microbial endodontic infec-
tions are best managed by nonsurgical endodontic treatments. Overprescribing
should be avoided in light of increasing antibiotic resistance and risk of drug
hypersensitivity in those cases where antibiotics are not warranted.

Clinical Relevance the greatest advances in modern medicine and for

Therapeutic use of antibiotics should be used as
an adjunct to either nonsurgical or surgical end-
odontic techniques when there is pyrexia and/
or local swellings. Primary measures includ-
ing pulpotomy, pulpectomy and/or incision and
drainage are first-line treatment modalities that
are proven when dealing with local infections.
Prophylactic use of antibiotics may be indicated
in certain patients who are susceptible to seri-
ous infections. Prophylactic antibiotic regimes
are discussed in light of recent changes. Local
uses of antimicrobial agents commonly used in
endodontics are discussed and the clinical impli-
cations and merits are also discussed.
10.1 The Role of Antibiotics
in Endodontics
In 1928 Alexander Fleming’s chance discovery of
Penicillium notatum growing on a discarded petri
dish of Staphylococcus colonies has led to one of
the benefit of mankind [1]. Antibiotics are com-
monly prescribed in dentistry and often for the
management of endodontic infections. Arguably
the greatest risk of hubris to human health comes
in the form of antibiotic-resistant bacteria. We
live in a bacterial world where we will never be
able to stay ahead of the mutation curve [2]. The
overprescribing of antibiotics in medicine and
dentistry has selected for antibiotic-resistant bac-
teria. When bacteria become resistant to antibiot-
ics, they gain the ability to exchange this
resistance, making them nonsusceptible to antibi-
otics commonly prescribed [3]. Inappropriate use
of antibiotics not only drives antibiotic resistance,
but it increases the risk of potentially fatal ana-
phylactic reactions and exposes patients to unnec-
essary side effects [4]. Furthermore, antibiotic
prescribing for common medical problems has
been shown to increase expectations for antibiot-
ics, whereby patients expect this as the standard
of care and anything less is an indication that the
clinician is somehow providing a disservice to

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 141
DOI 10.1007/978-3-319-15591-3_10, © Springer International Publishing Switzerland 2015
142
the patient. This, in turn, leads to a vicious cycle
of increased prescribing in order to meet patient
expectations [5]. Several surveys over the last
18 years of both general dentists and endodon-
tists have demonstrated the continued inappropri-
ate prescribing habits when managing endodontic
infections [6–9].
Endodontic pain is the result of an inflamma-
tory process. Reversible pulpitis, resulting from a
mild to moderate injury, has the potential for
recovery provided the insult to the pulp is
removed. Irreversible pulpitis, on the other hand,
due to persistent or extensive damage will result
in irreversible levels of inflammation within the
pulpal tissues leading to necrosis and bacterial
colonisation of the root canal system. Irreversible
pulpitis, which is characterised by acute and
intense pain, is one of the most frequent reasons
that patients attend for emergency dental care.
Apart from the removal of the tooth, the custom-
ary way of relieving the pain of irreversible pul-
pitis is by drilling into the tooth, removing the
inflamed pulp (nerve) and cleaning the root canal.
However, a significant minority of dentists con-
tinue to prescribe antibiotics to stop the pain of
irreversible pulpitis [10]. A prospective, double-
blind, placebo-controlled study was carried out to
determine the effect of penicillin on pain in
untreated teeth, diagnosed with moderate to
severe irreversible pulpitis. The study showed
without doubt that antibiotics gave the same
response as an inert placebo tablet confirming
that antibiotics are not indicated in pulpitis [11].
Systemic antibiotics may be indicated as an
adjunct in patients with acute dentoalveolar
infection resulting in a diffuse, spreading infec-
tion or evidence of systemic involvement
(pyrexia, malaise, extra-oral swelling, fascial
space involvement, submandibular or cervical
lymphadenopathy, muscle trismus and pain dur-
ing swallowing) [12–14]. A spreading infection
of endodontic origin may be painful due to
increasing pressure within the tissues.
Interventions to reduce the inflammatory pro-
cess, by either direct elimination of the microbial
irritants within the root canal system (chemo-
10 Antibiotics Use in Endodontics
mechanical preparation), incision and drainage
or extraction of an un-restorable tooth, are effec-
tive at reducing the pain by eliminating the
inflammatory process [15]. Rarely patients may
present with life-threatening Ludwig’s angina, a
rapidly progressing poly-microbial cellulitis of
the sublingual and submandibular spaces. These
cases require urgent referral to the local oral
maxillofacial unit for admission, extra-oral drain-
age if indicated and intravenous systemic antibi-
otics [16]. There is no question as to the necessity
of antibiotics and their benefits in managing
cases where systemic involvement is evident.
On the other hand, the effectiveness of antibi-
otics in the routine treatment of endodontic infec-
tions without systemic involvement is
questionable. The systemic administration of
antibiotics relies on patient compliance with the
dosing regimens followed by absorption through
the gastrointestinal tract and distribution via the
circulatory system to bring the drug to the
infected site. Hence, the infected area requires a
normal intact blood supply, which is no longer
the case for teeth with necrotic pulps and for
teeth without vital pulp tissue [17].
A placebo-controlled, prospective, ran-
domised, double-blind study was carried out to
assess whether the routine administration of pre-
operative antibiotics was warranted for endodon-
tic surgical procedures. The results showed that
clindamycin had no effect on post-operative
infections and as such did not warrant routine
prophylaxis [18].
Prophylactic antibiotics, taken prior to end-
odontic procedures, have been advocated to
reduce the likelihood of serious systemic compli-
cations like infective endocarditis (IE). Recent
changes to guidelines from the British Society for
Antimicrobial Chemotherapy, and the American
Heart Association, recommend that only patients
in the high-risk category require antibiotic cover-
age. This recommendation is based on a number
of findings including the fact that there is no con-
sistent association between having an interven-
tion, dental or non-dental, and the development of
IE. Regular tooth brushing/flossing and chewing
10.1 The Role of Antibiotics in Endodontics
almost certainly presents a greater risk of IE than
a single dental procedure because of repetitive
exposure to bacteraemia with oral flora. The clini-
cal effectiveness of antibiotic prophylaxis is not
proven. Antibiotic prophylaxis against IE for den-
tal procedures may lead to a greater number of
deaths through fatal anaphylaxis than would a
strategy of no antibiotic prophylaxis. Finally anti-
biotic prophylaxis against IE is not cost-effective.
Treatment decisions should be made in light of all
circumstances presented by the patient.
Treatments and procedures applicable to the indi-
vidual patient rely on mutual communication
between patient, physician, dentist and other
healthcare practitioners [19–21].
Immunocompromised patients may not be
able to tolerate a transient bacteraemia follow-
ing invasive dental procedures. Consultation
with the patient’s physician is recommended for
nonsurgical and surgical endodontic treatments.
Discussion of antibiotic prophylaxis for patients
undergoing chemotherapy, irradiation, and hema-
topoietic cell transplantation is essential to pre-
vent possible septicaemia [22].
Often in the past, prosthetic implants, such as
total knee replacements, have resulted in dental pro-
phylaxis being commonly recommended. Recent
guidelines have suggested that the practitioner
might consider discontinuing the practice of rou-
tinely prescribing prophylactic antibiotics for
patients with hip and knee prosthetic joint implants
undergoing dental procedures. Physicians, dentists
and patients should work collaboratively to custom-
ise a treatment plan that is based on the evidence,
clinical judgement and patient preferences [23].
There is limited evidence on the use of sys-
temic antibiotics in the management of luxation
injuries, and no evidence that antibiotic coverage
improves outcomes for root fractured teeth,
avulsed teeth and splinting. Antibiotic use
remains at the discretion of the clinician as trau-
matic dental injuries are often accompanied by
soft tissue and other associated injuries, which
may require other surgical intervention. In addi-
tion, the patient’s medical status may warrant
antibiotic coverage [24–28].
143
According to the BNF, amoxicillin is
recommended for dental infections in doses rang-
ing from 250 to 500 mg, every 8 h. The use of 3 g
amoxicillin repeated after 8 h is also mentioned,
as a short course of oral therapy. Another antibi-
otic that is also recommended by the BNF is co-
amoxiclav, which can be used in doses ranging
from 375 to 625 mg every 8 h. In patients allergic
to penicillin, clindamycin can be used in doses
ranging from 150 to 450 mg every 6 h. Another
option for penicillin-allergic patients (as recom-
mended by the BNF) is metronidazole, which can
be used in a dose of 200–400 mg every 8 h for
3–7 days [29–31].
Whilst systemic antibiotics appear to be clini-
cally effective as an adjunct in certain surgical and
nonsurgical endodontic cases, their routine use in
endodontics is not justified. On the other hand,
local application of antibiotics in endodontics
has been an effective mode of delivery. The first
reported local use of an antibiotic in endodontic
treatment was in 1951 when Grossman used a
poly-antibiotic paste known as PBSC. This con-
tained penicillin to target Gram-positive organ-
isms, bacitracin for penicillin-resistant strains,
streptomycin for Gram-negative organisms and
sodium caprylate to target yeasts. The compounds
were all suspended in a silicone vehicle. Although
clinical evaluation suggested that the paste con-
ferred a therapeutic effect, the composition was
ineffective against anaerobic species, which are
now appreciated as being the dominant organisms
responsible for endodontic diseases [32].
Numerous inter-appointment antimicrobial
medications have been used to further eliminate
bacteria or bacterial products from within the root
canal system locally as a topical application. The
two most common antibiotic-containing com-
mercial paste preparations currently available
are Ledermix paste (Lederle Pharmaceuticals,
Wolfratshausen, Germany) and Septomixine Fort
paste (Septodont, Saint-Maur, France). Both of
these preparations also contain corticosteroids as
anti-inflammatory agents. Ledermix paste remains
a combination of the same tetracycline antibiotic,
demeclocycline HCl (at a concentration of 3.2 %)
144
and a corticosteroid, triamcinolone acetonide
(concentration 1 %), in a polyethylene glycol base.
Septomixine Forte contains two antibiotics, neo-
mycin and polymyxin B sulphate [33, 34].
A 50:50 mixture of Ledermix paste with cal-
cium hydroxide was advocated as an intra-canal
dressing in cases of infected root canals, pulp
necrosis and infection with incomplete root for-
mation (as an initial dressing prior to using cal-
cium hydroxide alone for apexification),
perforations, inflammatory root resorption and
inflammatory peri-apical bone resorption and for
the treatment of large peri-apical radiolucent
lesions [13].
Clindamycin, which is effective against many
commonly found endodontic pathogens, was
found to offer no additional antimicrobial advan-
tage over conventional root canal medicaments
such as calcium hydroxide, and therefore, it has
not been recommended for routine use in end-
odontic therapy [35].
Tetracyclines including tetracycline hydro-
chloride, minocycline, demeclocycline, and dox-
ycycline are a group of broad-spectrum antibiotics
that are effective against a wide range of bacteria.
Tetracycline has been used in combination as an
intra-canal antibacterial paste (Ledermix) or as a
final irrigating solution (BioPure MTAD and
Tetraclean) [36, 37].
A recent resurgence of using a triple antibiotic
paste of ciprofloxacin, metronidazole and mino-
cycline in regenerative case reports has demon-
strated a favourable outcome provided careful
case selection has been carried out. Due to the
complexity of root canal infections, it is unlikely
that any single antibiotic could result in effective
and predictable complete disinfection of the
canal. More likely, a combination would be
needed to address the diverse flora encountered.
A combination of antibiotics would also decrease
the likelihood of the development of resistant
bacterial strains.
The presence of antibiotic resistance genes in
endodontic microorganisms has been investi-
gated and proven. The question remains whether
routine antibiotic prophylaxis is accounting for
this and also brings to question how effective
intra-canal medicaments containing antibiotics
10 Antibiotics Use in Endodontics
are in reality. If the existing endodontic flora
within the confines of the root canal contains
many of these resistant genes, are we simply cre-
ating further resistance and possible emergence
of persistent strains that may be responsible for
disease that does not respond to conventional
therapy or re-treatment strategies? [38–41].
10.2 Systemic Antibiotics
Prophylactic systemic antibiotics have been
guided by recommendations and indicated in
individuals susceptible to cardiac infection such
as endocarditis, in patients who have undergone
prosthetic joint replacements and in immuno-
compromised patients. The routine use and effi-
cacy of systemic antibiotics in treating
asymptomatic teeth with pulpal necrosis and
peri-apical pathosis have been proven to be inef-
fective. Systemic administration of potent drugs
should be reserved for endodontic cases where
systemic involvement exists and in conjunction
with local measures such as incision and drain-
age or pulpectomy. As with any drug, the benefits
of treatment must be outweighed with the risks of
side effects commonly found. The most impor-
tant side effect from a global health perspective is
the introduction of resistant bacterial strains,
which do not respond to commonly, produced
antibiotics. In the field of endodontics and par-
ticularly re-treatment cases, which have failed, an
emergence of drug-resistant bacteria such as
enterococci has been reported. Routine use of
antibiotics in endodontic cases where there is no
indication will only serve to create a multi-drug-
resistant flora within the confines of the tooth,
which are not amenable to routine-proven local
medications. These unnecessary, unscientific
and ineffective treatment strategies may satisfy
the patients’ expectations in the short term but
certainly may also be a fast-track strategy lead-
ing to the demise of the tooth.
Amoxicillin is an analogue of penicillin that is
rapidly absorbed and has a longer half-life. This
is reflected in higher and more sustained serum
levels than penicillin VK. Because of these traits,
amoxicillin is often used for antibiotic prophylaxis
10.2 Systemic Antibiotics
of patients that are medically compromised. Side
effects commonly associated with penicillin
include hypersensitivity reactions such as ana-
phylaxis and delayed type II hypersensitivity
reactions. Amoxicillin may be used for serious
odontogenic infections and is recommended for
dental infections in doses ranging from 250 mg to
500 mg, every 8 h. The use of 3 g amoxicillin
repeated after 8 h is also mentioned as a short
course of oral therapy. Antibiotic prophylaxis
consists of the following drugs:
Augmentin is the combination of amoxicillin
with clavulanate (a competitive inhibitor of the
beta-lactamase enzyme produced by bacteria to
inactivate penicillin). The usual oral dosage
ranges from 375 mg to 625 mg every 8 h.
Clindamycin is an effective antimicrobial
against Gram-positive facultative microorgan-
isms and anaerobes. It binds to the 50S ribosomal
subunit and interferes with protein synthesis.
Clindamycin is a good choice if a patient is aller-
gic to penicillin or a change in antibiotic is indi-
cated. Penicillin and clindamycin have been
shown to produce good results in treating odonto-
genic infections. Systemic use of this drug is
associated with occasional diarrhoea and the
uncommon occurrence of pseudomonas colitis
(due to overgrowth of Clostridium difficile). In
adult patients allergic to penicillin, clindamycin
can be used in doses ranging from 150 mg to
450 mg every 6 h.
Metronidazole is a synthetic antimicrobial
agent that is bactericidal and has activity against
anaerobes, but lacks activity against aerobes and
facultative anaerobes. It is therefore important
that the patient continue to take in combination
oral dosages of penicillin or clindamycin, which
are effective against the facultative bacteria and
those resistant to metronidazole. The usual oral
dosage for metronidazole is a 200–400 mg every
8 h for 3–7 days.
Erythromycin is a macrolide, which is bacte-
riostatic and exerts its action by interfering with
bacterial protein synthesis by binding to the 50S
ribosomal subunit. It has traditionally been pre-
scribed for patients allergic to penicillin; how-
ever, it is not effective against anaerobic
bacteria. Erythromycin is no longer recom-
145
mended for treatment of endodontic infections
because of this poor spectrum of activity and
significant gastrointestinal upset. Clarithromycin
and azithromycin are macrolides that have a
spectrum of activity that includes some anaer-
obes involved in endodontic infection and offers
improved pharmacokinetics. Food slows down
but does not affect the bioavailability of clar-
ithromycin. Food and heavy metals may inhibit
the absorption of azithromycin. Macrolides are
associated with nausea and vomiting and gastro-
intestinal distress in some patients. The oral
dosage for clarithromycin is a 500-mg loading
dose followed by 250 mg every 12 h for
5–7 days. The oral dosage for azithromycin is a
500-mg loading dose followed by 250 mg once
a day for 5–7 days.
Cephalosporins are usually not indicated for
the treatment of endodontic infections. First-
generation cephalosporins do not have activity
against the anaerobes usually involved in end-
odontic infections. Second-generation cephalo-
sporins have some efficacy for anaerobes;
however, there is a possibility of cross-
allergenicity of cephalosporins with penicillin.
Tetracycline is another group of bacteriostatic
antibiotics, which bind to the 30S ribosomal sub-
unit of bacteria, specifically inhibiting the bind-
ing of aminoacyl-tRNA synthetases to the
ribosomal receptor site. An interesting advantage
of these drugs in relation to endodontic infections
is the ability to inhibit the expression and produc-
tion of host metalloproteinases (MMPs) that are
upregulated during inflammation responsible for
tissue destruction. Tetracyclines also inhibit
osteoclast activity reducing bone resorption.
Both tetracycline and doxycycline occasionally
may be indicated when the above antibiotics are
contraindicated. However, many strains of bacte-
ria have become resistant to the tetracyclines, and
their systemic use is not usually indicated in the
management of endodontic infections.
Ciprofloxacin is a quinolone antibiotic that
is not effective against anaerobic bacteria usu-
ally found in endodontic infections. With per-
sistent infection, it may be indicated if culture
and sensitivity tests demonstrate the presence of
susceptible organisms.
146
10.3 Local Adjunctive Antibiotics
Ledermix
Ledermix paste has been used as a glucocorti-
costeroid–antibiotic compound which can be
used to reduce external inflammatory root resorp-
tion and external inflammatory replacement
resorption and as an intra-canal inter-appointment
pulpal dressing during routine endodontics.
Ledermix paste is a combination of the same tet-
racycline antibiotic, demeclocycline HCl (con-
centration of 3.2 %), and a corticosteroid,
triamcinolone acetonide (concentration 1 %), in a
polyethylene glycol base.
Ledermix/calcium hydroxide
Using a 50:50 mixture of Lederman paste and
calcium hydroxide has been advocated in incom-
plete root formation (as an initial dressing prior
to using calcium hydroxide alone for apexifica-
tion), perforations, inflammatory root resorption
and inflammatory peri-apical bone resorption and
for the treatment of large peri-apical radiolucent
lesions.
Triple antibiotic paste
Several case reports have been published
describing regenerative endodontic procedures
involving immature necrotic permanent teeth. All
the cases involved a non-instrumentation tech-
nique whereby the canal was disinfected using
sodium hypochlorite solution, calcium hydroxide
dressings or a triple antibiotic paste. The latter
consists of (1) antibiotics containing equal
amounts of ciprofloxacin 200 mg, metronidazole
500 mg and minocycline 100 mg (3Mix used in a
1:1:1 ratio). (2) A carrier of equal amounts of
macrogol ointment and propylene glycol are
mixed together resulting in an opaque mix (MP
used in a 1:1 ratio). Either a 1:5 MP: 3Mix
(creamy consistency) or 1:7 MP: 3Mix (standard
mix) can be prepared. The antibiotic paste is left
in the tooth for a period of 4 weeks to allow com-
plete disinfection of any necrotic tissue. After a
month, the tooth is re-entered and the antibiotic
paste washed out. This period ensures that the
tooth remains bacteria-free similar to an avulsed
tooth prior to creating a scaffold with a blood clot
10 Antibiotics Use in Endodontics
to the level of the cement–enamel junction. The
tooth is sealed with mineral trioxide aggregate
and reviewed to assess whether continued root
development continues indicating success.
Clinical Hints and Tips
• A regimen of antibiotics is not recom-
mended in an otherwise healthy patient for
a small localised swelling without systemic
signs and symptoms of infection or spread
of infection.
• Swellings increasing in size or associated
with cellulitis should be incised for drainage
followed by adjunctive use of antibiotics.
• Indications for adjunctive antibiotics
include fever (>100 °F), malaise, lymph-
adenopathy, trismus, increasing swelling
and cellulitis.
• Painful endodontic conditions such as irre-
versible pulpitis and acute apical periodonti-
tis without signs and symptoms of infection
do not require adjunctive antibiotics.
• Teeth with necrotic pulps and a peri-apical
radiolucency do not require adjunctive
antibiotics.
• Teeth with a draining sinus tract (chronic
apical periodontitis with suppuration) do
not require adjunctive antibiotics.
• Localised fluctuant swellings which are
amenable to incision and drainage of pus
do not require adjunctive antibiotics.
• Penicillin is the drug of choice for peri-
radicular infections. Amoxicillin may be
used for serious odontogenic infections
with a usual oral dosage of 1,000-mg load-
ing dose followed by 500 mg every 8 hours
for 5–7 days.
• Clindamycin is a good choice if the patient
is allergic to penicillin. The oral adult dose
for a serious odontogenic infection is a
600-mg loading dose followed by 300 mg
every 6 hours for 5–7 days.
• Metronidazole may be used in combination
with penicillin or clindamycin. The usual
loading dose is 400 mg followed by 200 mg
every 6–8 hours for 5–7 days.
References 147

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 Examination and Diagnosis
11

Summary
The challenge when assessing the dental pulp status is complicated since no
single diagnostic pulp testing technique can reliably diagnose all pulp condi-
tions. An assessment of the patient history with respect to the problem tooth,
careful clinical examination including diagnostic tests and appropriate radio-
graphs will enable the clinician to arrive at the best probable diagnosis.

Clinical Relevance when determining whether the pulp is vital or not.

Assessment of the dental pulp status is undertaken
using a combination of diagnostic tests including
thermal and electrical tests that indicate the func-
tioning of Aδ nerve fibres only. For many teeth the
tests are quick and often reliable but on occasion
these tests are inconclusive and do not represent
the true status of the pulp in disease. The clinician
must be aware of the shortcomings of these diag-
nostic tests and be able to interpret results with
confidence thereby serving the patient in their best
interests. Alternative methods to assess pulpal sta-
tus of teeth include physiometric testing such as
laser Doppler flowmetry, which although prove
valuable have yet to become established in our
common practising lives.
11.1 Overview of Endodontic
Diagnosis
Vitality testing is an important tool in the diagno-
sis of pulp disease and apical periodontitis. Several
devices or procedures are available to the clinician
Commonly used diagnostic procedures include a
detailed pain history, thermal testing (hot and
cold), electronic pulp testing, assessment of the
tooth for presence of mechanical allodynia and
radiographic detection of peri-apical disease. If the
pulp is deemed to be unhealthy based on diagnos-
tic tests, then endodontic treatment is indicated.
Pulp vitality testing has been recommended when
assessing traumatised teeth over an extended
period to monitor their vitality following the trau-
matic incident. Traumatised teeth, which may ini-
tially not respond to testing, may well do so after a
period of weeks or months. It is also important to
assess pulp vitality prior to undertaking extensive
tooth preparation in order to improve the prognosis
of the restoration. Vitality testing may also be indi-
cated for the periodic assessment of continued
pulp vitality in teeth that have undergone pulp
preservation procedures (such as indirect or direct
pulp capping). Patients typically attend our surger-
ies on a daily basis with pulpal complaints such as
extended thermal sensitivity associated with irre-
versible pulpitis. Vitality testing is a prerequisite in

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 149
DOI 10.1007/978-3-319-15591-3_11, © Springer International Publishing Switzerland 2015
150
the diagnosis of the offending tooth in such cases
where one needs to clearly identify the source of
the complaint and reproduce the symptoms to con-
firm suspected diagnosis [1–4].
As dentists we are involved in diagnosing dis-
ease as part of our everyday clinical practice. A
range of tests, systems, guides and equipment,
which can be generally referred to as diagnostic
procedures, are available to aid in diagnostic
decision-making. It is well known that the avail-
able diagnostic procedures, used to assess pulp
vitality, are not completely reliable, specific or
sensitive in determining the true nature of the
pulp status [5–10].
Clinical studies have demonstrated that there
is no direct correlation between signs and
symptoms of the pulp and histological diagno-
sis [11–13]. From a clinical standpoint the cli-
nician is only able to indicate the probable
status of the pulp. It is therefore recommended
that any pulpal diagnosis made should be based
on all the information readily available not reli-
ant on any one test in particular.
Current vitality testing is assessing the integ-
rity of the Aδ fibres present in the pulp–dentine
complex by application of thermal or electric
stimulus. The tests indicate that the nerve fibres
are conducting but do not give any indication as
to the blood flow within the tooth and whether
there is any damage. In general when there is a
diminished blood supply within the tooth, the
anoxic effects result in irreversible damage to the
Aδ fibres and loss of function. Hence a nonvital
tooth will not respond to thermal or electrical
pulp testing. A positive response would usually
indicate a healthy tooth. A negative response
could indicate the possibility that the tooth is
necrotic. A prolonged response to thermal stimu-
lus may indicate an irreversibly damaged pulp.
Often multi-rooted teeth may give rise to false-
positive or false-negative results depending on
the differing pulp status within the individual
canals. The tests themselves may also be unreli-
able giving false-positive or false-negative results
depending on how the test has been carried out,
11 Examination and Diagnosis
the age of the patient and the presence of a calci-
fied canal system with diminished pulp volume
and history of trauma. Since the responses to
these tests are subjective in nature, patient inter-
pretation may influence the clinicians’ determi-
nation as to whether the test result is normal or
not [4, 14–19].
Application of a cold stimulus causes a rapid
movement of dentinal fluid resulting in ‘hydrody-
namic forces’ acting on the Aδ nerve mechanore-
ceptors within the pulp–dentine complex leading to
a sharp sensation lasting for the duration of the ther-
mal test (see Chap. 1). The notion that the prolonged
application of cold stimulus to teeth resulting in
irreversible pulp damage is unfounded [20]. Cold
tests should be applied until the patient definitely
responds to the stimulus or for a maximum of 15 s,
whichevercomesfirst[20].Dichlorodifluoromethane
(DDM) and carbon dioxide (CO2) snow are more
reliable compared to ethyl chloride [21–24]. The
cold test is particularly useful when assessing teeth
with full coverage restorations [25].
Application of a hot stimulus to provoke a
pulpal response can be carried out using a num-
ber of methods including heated gutta-percha,
hot water applied by a syringe and direct applica-
tion of heat source (system B). The disadvantage
of using heated gutta-percha is that prolonged
heating could result in pulp damage. Application
of heat should be for no more than 5 s [26].
Electric pulp testing (EPT) stimulates intact
AD nerve fibres within the tooth on electrical
stimulation. The readout is not a quantitative
measurement whereby indicating how healthy or
to what degree the pulp is inflamed. The tech-
nique is sensitive and many variables will affect
the response given. The tooth to be assessed
should be sufficiently dry and a contact medium
should be used. The position of the electrode on
the tooth influences the response, and it should be
placed near to the pulp horns of the tooth where
the nerve density is greatest. In anterior teeth this
means that placing the electrode on the incisal
edge gives the least amount of electrical current.
A recent study has revealed that the optimum site
11.2 Examination
Table 11.1 Causes of false-positive and false-negative
responses to pulp testing
False-positive responses
Anxious patients
Pulp liquefaction necrosis (multi-rooted teeth)
Contact with metal restorations
Contact with gingivae or periodontium
Vital tissue still present in a partially necrotic canal
Vital tissue present in a multi-rooted tooth
False-negative responses
Incomplete root development
Recently traumatised teeth
Calcific metamorphosis (sclerosed canals)
Recent orthodontic treatment
Patients with psychotic disorders
for tester electrode placement on molars is the tip
of the mesiobuccal cusp [27–31].
There has been controversy in the past as to
the use of electric pulp testers and patients with
cardiac pacemakers. An in vivo study simulated
EPT use on 27 patients with implanted cardiac
pacemakers or cardioverter/defibrillators. The
report found that EPTs did not produce any inter-
ference effects [32].
It has been well documented in the literature the
possibility of false-positive (indicating a nonvital
tooth responding positively) and false-negative
readings (vital teeth responding negatively) obtained
from common pulp vitality diagnostic tests [33]
(Table 11.1). The clinician must be aware of these
confounding variables, which can influence the
result of the tests and take these into account when
assessing probable pulp status of any given tooth.
Traumatic injuries to teeth present problems
with respect to vitality. Teeth that temporarily or
permanently lose their sensory function will not
respond to EPT and are described as ‘concussed’.
These teeth, however, may have intact vascula-
ture and it is recommended that for traumatised
teeth pulps should be considered vital until
proved otherwise. The EPT is often unreliable in
testing immature permanent teeth, as full
development of the plexus of Raschkow does not
occur until 5 years after tooth eruption. The cold
151
thermal test is a more reliable one for these types
of teeth [34].
Physiometric testing has been reported in the lit-
erature as a means to overcome some of the inherent
problems of reliability associated with thermal and
electric pulp testing. These tests are aimed at mea-
suring or quantifying whether a healthy blood sup-
ply is present as opposed to a neurogenic response.
A modified technique involving pulse oximetry as a
non-invasive technique used to measure the oxygen
saturation levels within the tooth has been demon-
strated with some success [35]. Laser Doppler flow-
metry has been used to assess the vitality of the
tooth based on an intact blood flow. A modified
fibre-optic probe is attached to the tooth surface
whereby a laser light can be emitted directly to the
pulp. The light emitted is absorbed by red blood
cells within the intact pulpal circulatory system
resulting in a Doppler shift. By virtue of the Doppler
principle, light absorbed by stationary objects do
not undergo a shift in frequency (i.e. when the tooth
is nonvital, the blood flow is disrupted and absent).
Any frequency-shifted light can be detected by a
photodetector, which emits a signal. This technique
has been shown to be much more reliable and sensi-
tive in determining the pulp status of the tooth.
Unfortunately the technique is very treatment sensi-
tive, requiring a modified probe and expensive med-
ical grade equipment making it not suitable for
day-to-day clinical use at the present time [36–40].
11.2 Examination
Clinical examination of the patient is carried out
to reproduce the patient’s symptoms (defined as
any bodily changes perceptible to the patient) if
possible and confirm the presence of any signs
(defined as any bodily changes which are
perceptible to a trained observer) of disease. The
examination process can be categorised into three
main elements, namely, the general observation
of the patient’s health and appearance, extra-oral
examination of the head and neck and examination
of the intra-oral tissues. The examination must be
152
a thorough systematic approach ensuring all
areas are examined. Few patients have died as a
result of pulpitis, but many have died as a result
of a late diagnosis of a malignancy. Occasionally
malignant lesions can present as endodontic
lesions and careful examination with a methodi-
cal approach at each step will at least ensure to
some degree that we do not fall short of our clini-
cal duty to the patient.
Extra-oral examination
Head, face and neck
The face and neck is visually examined from
the front looking for any obvious lumps, skin
blemishes, moles, facial asymmetry or signs of
facial palsy. When examining the neck, the
patient is asked to tilt the head back slightly to
allow for any swelling or abnormality to be
clearly seen.
Eyes
The eyes are inspected for any signs of limita-
tion of ocular movement or strabismus, which
may indicate a fractured zygoma. Enophthalmos,
exophthalmos, subconjunctival haemorrhage,
colour of the sclera and dry eyes may all indicate
presence of underlying pathology.
Lips
Visual examination is carried out inspecting
for any drooping of the commissures or inability
to purse the lips. Any changes in colour, texture,
ulceration, patches, lumps or raised lesions may
require further investigations.
Lymph nodes
In normal health lymph nodes are not palpable
and any palpable nodes should alert the clinician
to some underlying pathology. Lymph nodes in
the outer circle group consist of the submental
(lies behind the chin, underlying the mylohyoid
muscle), submandibular (between the mandible
and submandibular gland), buccal (lies on the
buccinators muscle anterior to the insertion of
the masseter muscle), mastoid (on the mastoid
process), parotid (pre-auricular region in front of
the tragus of the ear) and occipital (around the
occipital artery). Lymph nodes of the cervical
group consist of the superficial cervical nodes
(distributed around the external and anterior jug-
ular veins), the deep cervical chain (distributed
along the internal jugular vein), jugulo-digas-
11 Examination and Diagnosis
tric (between the angle of the mandible and
the anterior border of the sternocleidomastoid
muscle) and jugulo-omohyoid (just behind the
internal jugular vein, above the inferior belly of
omohyoid).
Lymph node examination is carried out extra-
orally with bimanual palpation from behind the
patient. The patient is asked to expose the neck
by loosening relevant clothing. Asking the patient
to tip their head forwards and then trying to roll
the node against the inner aspect of the mandible
enable examination of the submental node. The
submandibular nodes are examined by asking the
patient to tip their head to the side being
examined.
The site, size, texture (soft, rubber hard), ten-
derness, number and whether the nodes are fixed
or mobile is recorded. Note acute infection will
often result in nodes that are large, soft, painful
and mobile. Chronic infection may result in large,
firm, less tender, mobile nodes on palpation.
Metastatic cancer will result in stony hard nodes,
which are fixed to underlying tissues and often
painless. If a non-dental cause is suspected, then
urgent referral to a specialist for further investi-
gations may be warranted.
Salivary glands
The parotid gland is located mainly distal to
the ascending ramus of the mandible. The
gland is viewed from the front and then pal-
pated for any enlargement or tenderness. The
submandibular gland is bimanually palpated
using the index finger and middle finger of one
hand intra-orally and the same fingers of the
other hand extra-orally. The gland is palpated
both above and below the mylohyoid, and the
ducts are checked for the presence of any
calculi.
Articulatory system and muscles of mastication
The temporomandibular joint is examined for
range of movement, tenderness on palpation, joint
sounds, locking, muscle tenderness, evidence of
bruxism, associated headache, neck ache and any
occlusal discrepancies (see Chap. 1).
Intra-oral examination
Lining mucosa
The site, shape and size of any lesions detected
are noted. The lesion is palpated to determine
11.3 Percussion and Palpation
whether it is soft or hard in texture, whether the
edges are well defined or diffuse and whether the
lesion is fixed or mobile. The colour of the lesion
is noted. Lesions can be described as ulcers, ves-
icles, erosions, bulla, plaques, papules, macules
or pustules.
A draining sinus indicates a blind-ended epi-
thelial lined track. A sinus should be tracked with
a probe or gutta-percha cone to reveal its origin.
Tongue
The dorsum of the tongue is inspected both at
rest and in the protruded position. The lateral
borders of the tongue are examined using gauze
to hold the tip and moved to one side.
The floor of mouth and ventral surface of
tongue are also carefully inspected. This area
known as the ‘gutter’ is a common site for oral
cancer to present. Asking the patient to raise the
tip of their tongue to the palate should allow for
inspection of the floor of the mouth.
Hard and soft palate
The tongue is depressed using a wooden spat-
ula and the hard palate examined and palpated.
The mobility of the soft palate and throat is
examined by asking the patient to say ‘ah’.
Salivary flow
The quality, viscosity and quantity of saliva
are noted. Adhesion of the mirror to the buccal
mucosa may indicate a reduced salivary flow.
Periodontium
The gingival colour, texture and any bleeding
are noted. Unhealthy gingivae may be red, swol-
len and occasionally ulcerated. Spontaneous
bleeding or bleeding on probing may also indicate
underlying disease. A Basic periodontal examina-
tion is carried out using a Williams’s probe.
Tooth mobility is assessed using either two
instrument handles or an instrument handle and a
finger against the corresponding tooth. Miller’s
classification is used to assess mobility. Class I
indicates normal physiological mobility. Class II
indicates up to 1 mm transverse movement. Class
III indicates more than 1 mm in any transverse
direction or any non-physiological mobility on
depression or rotation of the tooth.
Furcation defects are classified in accordance
with the amount of periodontal tissue destruction
in the inter-radicular area. Furcation involvement
153
should be recorded affecting the long-term prog-
nosis for the tooth and requiring further treatment
and maintenance with a periodontist.
Teeth
The dental chart is a medicolegal requirement,
which accurately represents the oral condition of
the patient. A routine must be established starting
in the same place and following the same
sequence. The FDI numbering system can be
used. Absent teeth are noted. Teeth must be
cleaned, isolated and dried in order to detect
overhangs, caries and ditched and fractured res-
torations. Good lighting is essential with magni-
fication using dental loupes. Tooth surface loss
(attrition, abrasion and erosion) is noted.
Suspected fractured cusps or cracked tooth syn-
drome is assessed (Chap. 17).
Occlusal examination is carried out with par-
ticular reference to posterior and anterior guid-
ance, centric occlusion, centric relation and
working side and nonworking side interferences.
Denture examination is carried out and classi-
fied accordingly (Kennedy classification Fig. 11.1)
with particular attention made if the tooth in ques-
tion is a denture abutment tooth or a strategic
tooth that is to be incorporated in the design of a
new removable partial denture.
11.3 Percussion and Palpation
Percussion
This test is a good indicator of periodontal
ligament inflammation. A positive test indicates
inflammation of the peri-radicular tissues.
However, a negative percussion test does not rule
out the presence of inflammation. A positive per-
cussion test in a tooth that tests vital to sensitivity
tests indicates the possibility of severe and prob-
ably irreversible inflammation in the pulp.
Care must be taken when interpreting the
result of percussion tests when the cause may be
traumatic periodontitis. This is particularly diffi-
cult in cases of irreversible pulpitis, which
respond positive to vitality testing.
Percussion is carried out in both an apico-
coronal direction and bucco-lingual direction
(Fig. 11.2). A control tooth should be percussed
154 11 Examination and Diagnosis

a b

c d

Fig. 11.1 Clinical diagrams representing Kennedy clas- posterior edentulous area, (c) Class III unilateral or bilat-
sification for partial denture design. Note (a) Class I bilat- eral edentulous area(s) bounded by teeth and (d) Class IV
eral posterior edentulous area, (b) Class II unilateral anterior bounded saddle

a b

Fig. 11.2 Clinical photographs demonstrating examina- selected so that both the clinician and patient can perceive
tion of (a) percussion and (b) palpation tenderness on a ‘normal’ sensation
tooth 11. Note prior to testing a control tooth should be
11.4 Thermal Testing
a b
Fig. 11.3 Clinical photographs demonstrating applica-
tion of thermal stimulus (cold) using (a) dichlorodifluoro-
methane (DDM) (boiling point −50 °C), (b) DDM sprayed
to demonstrate to the patient what is normal
before attempting to test the tooth in question.
This allows the patient and clinician to equate
their response to what is normal.
Pain on biting/release
Pain on biting is a good indicator of inflamma-
tion in the surrounding periodontal ligament
space, which may be due to a necrotic pulp. Pain
on release is particularly useful when diagnosing
cracked teeth and confirming the cusp responsi-
ble. A tooth sleuth is used routinely for this pur-
pose (see chapter).
Palpation
This test is used to detect inflammation in the
surrounding mucoperiosteum of the tooth
(Fig. 11.2). Negative results to palpation do not
mean that inflammation is absent. Again palpa-
tion of the opposite tooth in question should be
routinely carried before the area of concern so
that the patient can establish and differentiate
normal with abnormal.
11.4 Thermal Testing
There are several different types of cold thermal
tests available to the clinician, which vary in the
degree of cold being applied.
Simple ice sticks can be made in the dental
surgery by freezing water in non-contaminated or
disinfected local anaesthetic needle sheaths. The
155
c
on cotton wool pledget and (c) carbon dioxide gas cylin-
der used for creating carbon dioxide snow
ice stick can be removed from the freezer when
required, run under water to separate from the
sheath and applied directly to the tooth using
gauze.
Ethyl chloride (Fig. 11.3) (boiling point
−4 °C) can be sprayed on to a cotton pledget
resulting in the formation of ice crystals; it is then
applied to the tooth. Dichlorodifluoromethane
(DDM) (boiling point –50 °C) is a compressed
refrigerant spray, which can similarly be sprayed
on to a cotton pledget and applied to the tooth
under investigation (Fig. 11.3).
Another effective method of applying cold is
using carbon dioxide (CO2) snow (boiling point
-72 °C), which is particularly useful when
attempting to assess teeth with full gold coverage
metal restorations. The CO2 gas is released from a
gas cylinder into a plastic plunger mechanism
(Fig. 11.3) and compressed to produce a stick of
CO2. By using a special applicator, it may then be
applied to the tooth under investigation (Fig. 11.4).
Frictional heat may be generated by using a rub-
ber cup intended for prophylaxis (without paste)
against the buccal aspect of a tooth (Fig.11.5).
A gutta-percha stick may be heated with a
naked flame or an electric heater until it becomes
soft and glistens. This can then be applied to the
tooth under investigation, which has been coated
with Vaseline (Fig. 11.5). A specialised system B
tip can also be directly applied to the tooth under
investigation.
156 11 Examination and Diagnosis

a b

Fig. 11.4 Clinical photographs demonstrating application of thermal stimulus (cold) using carbon dioxide gas (boiling
point −72 °C). (a) Compressed stick of CO2 ice and (b) application to tooth under investigation

a b

Fig. 11.5 Clinical photographs demonstrating application of thermal stimulus (heat) using (a) slow hand-piece and a
rubber cup to create frictional heat and (b) a heated gutta-percha stick placed on the tooth in question

The tooth under investigation may be isolated
with rubber dam and submerged with hot water
from a syringe. This is an effective method of
testing the entire crown instead of just one aspect
(Fig. 11.6).
11.5 Electric Pulp Testing
Two widely used battery-operated electric pulp
testers (EPT) are the Analytic Technology pulp
tester and the Vitality Scanner (Analytic Sybron
Dental Specialities, Orange, CA, USA)
(Fig. 11.7). These monopolar pulp testers involve
only one electrode, which is applied to the tooth.
The patient completes the electric circuit by hold-
ing the metallic handle of the EPT, or a lip clip,
which is applied to the patient’s lower lip
(Fig. 11.7).
They function by producing a pulsating elec-
trical stimulus. The intensity automatically
begins from a very low value to prevent unneces-
sarily excessive stimulation and discomfort. The
intensity of the electrical stimulus steadily
11.5 Electric Pulp Testing
increases at a predetermined rate selected by the
clinician. A note is made of the reading on the
digital display when the patient acknowledges a
warm or tingling sensation.
The clinician should consider a response or no
response as being the important finding, rather
than the digital reading on the tester.
Fig. 11.6 Clinical photographs demonstrating applica-
tion of thermal stimulus (heat) using hot water in s
syringe. The tooth in question is isolated. Note care must
be taken to avoid spillage of hot water and the possibility
of burning the patient
a b
Fig. 11.7 Clinical photographs demonstrating (a) appli-
cation of electric pulp testing (EPT) using the Analytical
Technology pulp tester. (b) A lip clip is provided which
157
The use of an electric pulp tester may be
frightening to patients (particularly the young)
and are sometimes painful. They are not recom-
mended for use on crowned teeth or in patients
wearing orthodontic bands since a false-positive
response may be caused by conduction of the
current to the gingival or periodontal tissues and
adjacent teeth through contacting metallic resto-
rations or orthodontic appliances. Crowned teeth
may be tested using a small electrode tip onto
root structure and with the tooth isolated with
plastic strips interproximally.
Tests require tooth isolation and conducting
media. Tooth isolation using rubber dam during
EPT is essential to prevent gingival conduction.
Electric current can also be transferred between
adjacent teeth through contacting metallic
restorations. In these cases drying the enamel
and the placement of a plastic strip interproxi-
mally and use of rubber dam can prevent electri-
cal impulses from spreading across the surface
of the tooth and to adjacent teeth. A conducting
medium should be used to ensure that maximum
current passes from the electrode to the tooth
surface.
the patient can hold or alternatively place in the inner
aspect of the lip to complete the circuit
158
Clinical Hints and Tips
The use of EPT in combination with one of the
commonly used cold pulp tests will provide
more accurate results for the evaluation of
pulp vitality rather than using one of these
methods alone.
• A response to EPT does not provide any
information about the health status of the
pulp, its integrity or circulation. It only
indicates that some sensory fibres are pres-
ent within the pulp tissue that are capable
of responding to stimulus.
• In immature teeth EPT is not reliable
because the myelinated fibres entering the
pulp may not reach their maximum number
until 5 years after tooth eruption, there is a
lack of development of the plexus of
Raschkow at the pulpodentinal junction,
large pulps cause impedance to electrical
currents and children may be apprehensive.
• Use of EPT for full or partial coverage
crowns may be difficult due to accuracy of
tip placement. Cold testing is preferable in
these situations. Accurate responses require
correct placement of EPT probe tip (incisal
or coronal 2/3rd of the crown) and use of an
appropriate conducting medium
(toothpaste).
• There are no contraindications when using
EPT and cardiac pacemaker patients.
• Traumatised teeth can often suffer from
paraesthesia, which can take up to 9 months
to fully recover. Pulp vitality testing alone
cannot determine whether the tooth is
necrotic. Further evaluation including
mobility, percussion, palpation testing and
radiographic examination is needed to help
determine the overall status of the pulp and
whether endodontic treatment is indicated.
• Cold testing using CO2 snow is safe for the
pulp tissue and enamel and has been shown
to be one of the most accurate and reliable
vitality tests.
• Heat testing using gutta-percha, hot water
bathing following rubber dam isolation and
electrically controlled heating devices must
be used with caution. Prolonged applica-
tion can cause pulpal damage.
11 Examination and Diagnosis
• Pulp testing in older patients or teeth that
have pulp canal obliteration may not
respond. Endodontic treatment cannot be
justified on the basis of these tests alone.
The clinician must take into consideration
other clinical and radiographic signs and
symptoms which together with pulp vitality
testing may correlate the true pulpal status.
• Currently no vitality test has been proven to
be superior, and therefore a combination of
testing devices may give the clinician the
most ‘probable’ pulp status diagnosis.
• Test cavities have been advocated as a ‘last
resort’ form of pulp testing, but this proce-
dure cannot be justified because of their
invasive and irreversible nature.
References
1. Chambers IG. The role and methods of pulp testing in
oral diagnosis: a review. Int Endod J. 1982;15:1–5.
2. Rowe AHR, Pitt-Ford TR. The assessment of pulpal
vitality. Int Endod J. 1990;23(2):77–83.
3. Cohen S. Diagnostic procedures in pathways of the
pulp. Mosby-Year Book, 6th ed. 1994; Chapter 1.
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4. Pitt-Ford TR, Patel S. Technical equipment for the assess-
ment of dental pulp status. Endod Top. 2004;7:2–13.
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11. Seltzer S, Bender I, Zionitz M. The dynamics of pulp
inflammation, correlations between diagnostic data
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12. Dummer PMH, Hicks R, Huws D. Clinical signs and
symptoms in pulp disease. Int Endod J. 1980;13:27–35.
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G. Evaluation of the ability of thermal and electrical
tests to register pulp vitality. Endod Dent Traumatol.
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14. Fulling HJ, Andreasen JO. Influence of the maturation
status and tooth type upon electrometric and thermal
pulp testing. Scand J Dent Res. 1976;84:291–6.
15. Smith JW. Calcific metamorphosis. A treatment dilemma.
Oral Surg Oral Med Oral Pathol. 1982;54(4):441–4.
16. Jacobsen I, Kerekes K. Long term prognosis of trau-
matized permanent anterior teeth showing calcifying
processes in the pulp cavity. Scand J Dent Res.
1977;85:588–98.
17. Nitzan DW, Mitchell V, Weinrab M, Azaz B. The
effect of aging on tooth morphology. A study of
impacted teeth. Oral Surg Oral Med Oral Pathol.
1986;61:54–60.
18. Michaelson PL, Holland GR. Is pulpitis painful? Int
Endod J. 2002;35:829–32.
19. Peters DD, Baumgartner JC, Adult LL, Diagnosis P. 1.
Evaluation of the positive and negative responses to cold
and electric pulp tests. J Endod. 1994;20(10):506–11.
20. Ingram TA, Peters DD. Evaluation of the effects of
carbon dioxide used as a pulpal test. Part 2. In vivo
effect on canine enamel and pulpal tissues. J Endod.
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Assessment of reliability of electrical and thermal
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22. Augsburger RA, Peters DD. In vitro effects of ice,
skin refrigerant, and CO2 snow on intrapulpal tem-
perature. J Endod. 1981;7:110–6.
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fluoromethane. J Endod. 1993;19(6):312–4.
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JM. Cold testing through full coverage restorations. J
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27. Bender IB, Landau MA, Fonsecca S, Trowbridge
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 Endodontic Radiology
12

Summary
Accurate diagnostic information leads to better clinical outcomes.
Radiographic examinations will always form the backbone of a diag-
nostic workup confirming clinical signs and symptoms. Conventional
plain film radiography and digital radiography have been proved to be
invaluable tools in the modern endodontic practice. The technology of
cone-beam computed tomography has evolved in recent times with
previous astronomical costs no longer prohibiting the purchase of
machines for the modern endodontic practice. The technology has
been embraced by endodontists to aid in the diagnosis of endodontic
pathosis and canal morphology, assessment of root and alveolar frac-
ture, resorptive defect analysis, identification of non-endodontic
pathology and pre-surgical assessment. The question still remains
regarding possible medicolegal issues pertaining to the acquisition and
interpretation of CBCT data. An alternative arrangement is to refer the
patient to an imaging centre where the CBCT scan can be reported by
a radiologist preventing the possibility of missing any additional
pathology or life-threatening lesions.

Clinical Relevance proposed as a viable alternative to overcome

Endodontic diagnosis, treatment planning and
outcome assessment are dependent on radio-
graphic examinations. Peri-apical radiographs
captured on conventional plain films or digital
sensors provide limited information due to
their two-dimensional nature and distortion
from surrounding anatomical noise. Recently
cone-beam computed tomography has been
the disadvantages of conventional peri-apical
radiography in the dental surgery. The clini-
cian should be aware of not only the advan-
tages and disadvantages of all techniques but
also the radiological principle of doses as low
as reasonably achievable (ALARA), thereby
minimising any risk of ionising radiation to
the patient.

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 161
DOI 10.1007/978-3-319-15591-3_12, © Springer International Publishing Switzerland 2015
162
12.1 Overview of Radiology
and Endodontics
Professor Wilhelm Conrad Röntgen was a German
physicist, who, on 8 November 1895, produced
and detected electromagnetic radiation in a wave-
length range [1]. This discovery has led to the use
of x-rays that is an integral and essential tool used
in modern endodontics. In 1899 Dr. Charles
Edmund Kells was one of the first dentists to use
x-rays and a lead wire placed in a fractured upper
central incisor to determine the working length
[2]. Radiography has provided useful information
about the presence, location and extent of the
peri-radicular lesion, anatomy of root canals,
proximity of adjacent anatomical structures and
determination of working length that enable
cleaning, shaping and filling procedures to be car-
ried out with a degree of certainty, simplicity and
accuracy. Conventional intra-oral radiography,
captured on x-ray films or digital sensors, has pro-
vided clinicians with a high-resolution imaging
modality that has been used for many years [3].
Recently there has been considerable debate as to
whether newer imaging techniques such as cone-
beam computed tomography (CBCT) should be
the new standard of care [4, 5]. The major concern
regarding standard preoperative CBCT relates to
the additional ionising radiation. The effective
radiation dose to patients when using CBCT com-
pared to conventional radiography is much higher,
and the benefit to the patient must be outweighed
by any potential risks in order to be justified.
Radiation dose should be kept as low as reason-
ably achievable (ALARA) [6].
Conventional two-dimensional (2D) radio-
graphs provide a cost-effective, high-resolution
image, which continues to be the most popular
method of imaging today [6]. According to the
consensus report of the European Society of
Endodontology, appropriate root canal treatment
includes a radiographical control showing a pre-
pared root canal tapered from crown to apex and
filled completely without space between canal
filling and canal walls [7]. However, the diagnos-
tic potential of peri-apical radiographs is limited.
Information may be difficult to interpret, espe-
cially when the anatomy and background pattern
12 Endodontic Radiology
are complex [8]. Radiographic interpretation is
limited since three-dimensional (3D) anatomy is
interpreted on a two-dimensional view. The sag-
ittal plane (bucco-lingual) is not observed [3].
Furthermore, when considering surgery, 2D
radiographs do not give an accurate spatial rela-
tionship of the intended roots to treated and adja-
cent structures such as the inferior alveolar nerve,
mental foramen or maxillary sinus [9].
Lesions of endodontic origin associated with
peri-apices of teeth may not be demonstrated on
conventional 2D films unless the cortical plate
has been breached. If the lesion is confined to the
cancellous bone, then it may not even be detected
[10–12].
The long-cone paralleling technique is the
technique of choice during endodontics minimis-
ing any distortions and enabling much greater
reproducibility. A further x-ray taken at a differ-
ent angle (mesial or distal parallax tube shift)
may provide additional anatomical information
limited by the conventional zero-degree projec-
tion of the 2D image [11, 13, 14].
The fastest available films consistent with sat-
isfactory diagnostic results should be used when
using plain film radiography. Intra-oral films of
ISO speed group E, or faster, are preferred. The
use of ‘instant process films’ should be limited to
specific essential situations (e.g. during surgery or
endodontics). In situations where ‘rapid images’
are routinely required, conventional film with
rapid-processing chemistry will generally give
better results than instant process films. Strict
attention should be paid to correct and consistent
film processing so as to produce good quality
radiographs and avoid the necessity for examina-
tions to be repeated. Where automatic processing
is used, the processor should be properly cleaned
and maintained. In the case of manual processing,
the temperature of the developer should be
checked prior to film processing and the develop-
ment time adjusted in accordance with the film
manufacturer’s instructions. The developer should
be changed at regular intervals in accordance with
the manufacturer’s instructions [15, 16].
In order to extract full diagnostic information
from the films, it is essential to have dedicated
viewing facilities. A specially designed light box
12.1 Overview of Radiology and Endodontics
should be installed in an area where the ambient
lighting can be adjusted to appropriate levels.
Suitable film masking should be used to optimise
the viewing conditions by cutting out stray light.
For viewing dense areas of a radiograph, the incor-
poration of a high intensity light source in the light
box is recommended. The provision of magnifica-
tion by a factor of two would be beneficial [15, 16].
Whenever practicable, techniques using film
holders incorporating beam-aiming devices should
be adopted for bitewing and peri-apical radiogra-
phy. If rectangular collimation is being used, a
beam-aiming device is essential for accurate align-
ment with the intra-oral film. Attention is drawn to
the probable need for additional operator training
in the use of film holders when moving from circu-
lar to rectangular collimation [15, 16].
Digital radiography has been available in
dentistry for more than 25 years but has not com-
pletely replaced conventional film-based radiog-
raphy. The main reasons cited for this appear to
be due to the financial investment required [17].
The advantages of using a digital system include
the ability to manipulate images allowing for
better interpretation and correction of under- or
overexposures optimising the image for the diag-
nostic purpose. Manufacturers often cite that the
radiation dose the patient receives is reduced.
However, the dose reduction is not as large as
often quoted due to an increase in the number of
radiographs taken due to the ease of remakes
akin to digital systems [18].
In selecting digital equipment, it is necessary
to ensure that the chosen system offers the sensor
sizes that are clinically required. Sensor sizes
should be available in a range that is comparable
with dental film [15].
The sensitivity of the detector system has to be
compatible with the x-ray set(s) for which it is to
be used. Ideally the x-ray set should have an
effectively constant operating potential with the
ability to select sufficiently low exposure settings
to enable the full extent of available dose savings
to be realised [15].
Cone-beam computed tomography (CBCT)
has been introduced to dental offices recently due
to reduced costs and the size of the machines to
produce undistorted 3D information of the maxil-
163
lofacial skeleton with a substantially lower
radiation dose compared to conventional CT [3].
3D imaging software enables the CBCT scans to
be viewed by the clinician in axial, coronal and
sagittal 2D sections not seen with conventional
peri-apical radiography. The software also allows
3D reconstruction of areas of interest further opti-
mising the true clinical picture. A limited CBCT is
often utilised for endodontic purposes with a lim-
ited field of view ranging from 40 to 100 mm [19].
The applications of CBCT and its obvious
advantages over conventional plain film radiogra-
phy in endodontics include the diagnosis of peri-
apical disease [4, 20–23], assessment of internal
and external resorption lesions [24–28], identifi-
cation of perforations, root fractures and injuries
sustained from dental trauma [29–32] and pre-
surgical treatment planning [9, 33–37].
CBCT holds great promise for both patients
and dentists, but it comes with potential pitfalls.
Medicolegal issues pertaining to the acquisition
and interpretation of CBCT data have been high-
lighted with questions being raised as to the neces-
sity of a qualified radiologist being responsible for
this. With careful planning and the use of appro-
priately qualified individuals to aid in interpreta-
tion, dentists can enhance their practice and best
serve the interests of their patients [19, 38, 39].
However, its routine use is not recommended due
to the higher radiation dose required equivalent to
4–15 panoramic radiographs in some cases [40].
Observation of healing after completion of
endodontic therapy is by interpretation of periodic
recall radiographs. The time frame of this healing
process is poorly understood, but observational
follow-up studies and clinical experience have
shown that the majority of treated cases with
chronic apical periodontitis show signs of healing
within 1 year. Standard follow-up of 4 years has
been recommended, and in some clinical cases,
healing has been demonstrated several years
beyond this [7, 41–43]. Success and failure of
endodontic treatment are based on strict criteria.
Interpretation of radiographic findings related
to the stage and extent of chronic apical peri-
odontitis, both preoperatively and postoperatively,
during the course of follow-up has been shown to
have great variability amongst observers. This
164
observer variability exists within and amongst dif-
ferent observers when trying to radiographically
diagnose the presence of lesions in bone [44–49].
Several factors have been proposed for this varia-
tion including individual attitudes to treatment
and the hypothesis that dentists’ behaviour is
assumed to operate along a health continuum.
Furthermore, general dentists and endodontists
differ greatly in their treatment decisions and also
the assessment of the probabilities of disease and
future complications [50, 51].
Although radiographs are an indispensable
diagnostic tool, the increased effective doses of
common intra-oral and extra-oral imaging tech-
niques are high enough to warrant reconsidera-
tion of means to reduce patients’ exposure [52].
Alternative imaging techniques have been inves-
tigated for their potential in detecting and diag-
nosing peri-apical lesions, including ultrasound
real-time imaging [53] and magnetic resonance
imaging [54], where the side effects of radiation
are irrelevant. Nevertheless, conventional radio-
graphic imaging techniques remain the gold stan-
dard at this time, and close adherence to
recommended guidelines ensures that patients
are protected, limiting adverse health outcomes.
Every radiation dose of any magnitude can pro-
duce some level of detrimental effect that may
include an increased risk to genetic mutations
and cancers. With this in mind, ALARA (As Low
As Reasonably Achievable) is a safety principle
designed to minimize radiation doses, thereby
protecting both staff and patients [55].
12.2 Standard Equipment
X-ray source
Intra-oral x-ray units can be used for both con-
ventional radiography using plain film and digital
radiography.
Film selection
For conventional intra-oral radiography, film
speeds available are D-speed, E-speed and
F-speed, with F-speed being the fastest. The use
of a faster film results in up to a 50 % decrease in
exposure to the patient without compromising
diagnostic quality. Film speeds slower than
E-speed should not be used for dental radio-
12 Endodontic Radiology
graphs. Digital radiography consists of image
plates or sensors, which are available in exactly
the same sizes as conventional film.
Collimation
Collimation limits the amount of radiation,
both primary and scattered, to which the patient
is exposed. A rectangular collimator decreases
the radiation dose by up to fivefold as compared
to a circular one, so radiographic equipment
should provide rectangular collimation for expo-
sure of peri-apical and bitewing radiographs. The
use of a long source-to-skin distance up to 40 cm,
rather than shorter distances of 20 cm, decreases
exposure to the patient by 10–25 %.
Beam filtration
The operating potential of x-ray machines
affects the radiation dose and backscatter radia-
tion. Higher voltages produce lower contrast
images that allow for better separation of objects
with differing densities. The operating potential
of dental x-ray machines should range between
60 and 80 kVp.
Patient protection equipment
Lead aprons are patient protective equipment
that minimises exposure of scattered radiation. If all
radiation protection recommendations are imple-
mented, then theoretically a lead apron should not
be used. To prevent cracks from occurring in the
leaded shield, practitioners should ensure that all
leaded aprons are hung and not folded.
Film holders
Film holders that align the film precisely with
the collimated beam are recommended for both
peri-apical and bitewing radiographs reducing geo-
metric distortion. Heat-sterilisable film-holding
devices are recommended for optimal infection
control. Dental practitioners should not hold the
beam-aiming device during exposure. By eliminat-
ing the patient’s finger from the x-ray field and any
potential for displacement of the film, these devices
help to minimise retakes, reduce radiation expo-
sure and make it easier for both the patient and cli-
nician to properly position the film (see Fig. 12.1).
A number of commercial devices are available
that position the film parallel and at various dis-
tances from the teeth including the Dunvale Snapex
System, the EndoRay II endodontic film holder, the
Uni-Bite film holder, the Snap-A-Ray film holder
and the Snapex System film holder with aiming
12.2 Standard Equipment
a b
Fig. 12.1 Photographs demonstrating parallel film holder
devices available commercially. Note (a) posterior
(yellow), anterior (blue) and the endo-ray film holder
a b
DW F
d e
Fig. 12.2 Clinical photographs demonstrating film pro-
cessing procedure using conventional plain film radiogra-
phy. Note (a, b) manual chair-side film processing box
with ruby red filter to ensure x-rays are developed under
normal light safely. Plastic-covered cups hold developer,
device. The EndoRay has been designed to help the
clinician secure parallel working films with the
rubber dam clamp in place. Generally these holders
all have an x-ray beam-guiding device for proper
beam/film relationship and a modified bite block
and film holder for proper positioning over or
around the rubber dam clamp.
Film exposure and processing
Exposure settings and film processing proce-
dures affect the quality of the radiographic image.
165
(brown and green). (b) The XCP-ORA One ring and arm
positioning system convenient for anterior (blue), poste-
rior (yellow) and bitewing (red) radiographs
c
f
fixer and water inside (D, W, F). (c–f) Film processing
procedure carried out according to time/temperature
method. Manual film processing according consists of
development, rinsing, fixing, washing and drying
The operator must set the amperage and time set-
tings for exposure of dental radiographs for optimal
quality. The darkness of the resulting image (den-
sity) depends on the quantity and quality of radia-
tion delivered, the size of the subject (thickness) and
the developing and processing procedures.
Conventional plain film radiography requires
strict processing according to manufacturer’s
instructions regarding time, temperature and chem-
istry (developer and fixer solutions) (see Fig. 12.2).
166
For the sake of expediency in the production of
working films in endodontics, rapid-processing
methods are available to produce relatively good
films in less than 1–2 min. The contrast (degree of
density) in using rapid-processing chemicals is
lower than that achieved using conventional tech-
niques; the radiographs have sufficient diagnostic
quality to be used for treatment films that are
obtained in less time. Rapid-processing solutions
are available commercially, but they tend to vary in
shelf life, in tank life and in the production of films
of permanent quality.
It is recommended that after an image has been
evaluated, it be returned to the fixer for 10 min
more and then washed for 20 min and dried. This
is to ensure that all radiographs taken during the
course of endodontic treatment are preserved as a
part of the patient’s permanent record.
Both lead foil from the film packet and film
processing solutions (fixer solution) may contain
hazardous waste, which must be disposed of
appropriately.
Infection control
Universal standardised infection control poli-
cies must be adhered to when exposing dental
radiographs. Prior to exposing the film, all equip-
ment should be set out and the patient adjusted
according to ideal chair and head position. During
exposure of the film and handling of contami-
nated items, gloves should be worn at all times.
Barrier-protected film and heat-sterilisable film
holders should be used at all times. Digital sen-
sors or plates should be covered with appropriate
barrier protection. The film packet should be dried
after exposure of the film. The protective barrier
used in either conventional or digital radiography
should be removed carefully to avoid further
cross-contamination. The uncontaminated con-
tents of the film packet or film sensor can then be
handled without gloves or other precautions.
Image viewing
Clinicians should view the radiographs under
suitable viewing conditions. An illuminated
viewer is recommended for optimisation of high-
and low-density areas on a conventional plain
film radiograph. Magnification is recommended
when needed.
Additional equipment in relation to digital
radiography
12 Endodontic Radiology
A computer and high-resolution monitor are
necessary to process and view digital images
acquired. Often software bundled with the digital
radiography system installed has basic image
processing tools to allow for adjustment as well
as annotation and measuring tools. It is recom-
mended to ensure that the digital radiography
software is compatible with the in-house practice
management software used and whether integra-
tion of the radiographic images is feasible with-
out causing network conflicts.
It may be necessary to purchase additional
image receptor holders or positioning devices
that have been adapted for a particular brand of
digital image sensor used. For phosphor plate
systems, conventional film-positioning devices
such as Rinn XCP film-holding devices (Dentsply
Rinn, Elgin) may be used. Devices such as the
Snap-A-Ray film holder (Dentsply) or haemo-
stats may damage the plates resulting in further
expense and replacement.
12.3 Plain Film Radiography
Radiographs are an integral component to all
phases of endodontic therapy. They aid in the
diagnosis and the various treatment phases and
help evaluate whether the treatment provided has
been successful or failed. Root canal treatment
relies on the clinical ability to obtain accurate
radiographs; it is therefore necessary to master
radiographic techniques that produce films that
yield maximum diagnostic quality. Expertise in
radiographic interpretation is obligatory for
understanding both the limitations inherent with
specific techniques and for the recognition of
deviations from the norm, specifically non-
odontogenic pathology that may mimic an end-
odontic lesion.
Conventional intra-oral radiographic film
detects, stores and displays the radiographic
image representing the x-ray shadow of patients’
internal structures. This is based on the interac-
tion of x-ray photons with electrons of silver bro-
mide crystals in the film emulsion. When the film
has been exposed to x-ray photons, the silver
halide crystals are sensitised producing a latent
image. During the developing phase, the sensi-
12.3 Plain Film Radiography
tised silver halide crystals are rendered black
transforming the latent image into a visible one.
The radiographic film produced may have a con-
tinuous density distribution, limited by the maxi-
mum and minimum values of density (black and
white). Each optical density in between the maxi-
mum and minimum is related to the amount of
light that passes through the film at a certain site.
Based on this continuous density scale, conven-
tional radiographic film-based images are known
as analogue images.
Peri-apical radiography
Peri-apical radiography describes intra-oral
techniques to show individual teeth and the sur-
rounding structures around the apices and has
been considered the primary radiograph of choice
when carrying out endodontics. The paralleling
and bisecting angle are two techniques commonly
employed when using peri-apical radiography.
The former is the preferred method of choice pro-
viding less image distortion, ensuring a high
degree of reproducibility and reducing excess radi-
ation to the patient and should always be attempted
first. The latter can be reserved for patients unable
to accommodate the positioning required for a true
paralleling technique including patients with low
palatal vaults and children. This technique is prone
to image distortion and excessive radiation due to
increased angulations resulting in unnecessary
exposure of adjacent head and neck structures
such as the eyes and thyroid gland.
Bitewing radiography
Parallel bitewing radiographs are also a useful
adjunct in the initial endodontic workup provid-
ing additional information depicting the crowns
of teeth, interproximal contacts and the height
and relationship of the alveolar crest. Further
diagnostic information such as the status of resto-
rations, extent of caries, presence of pulp calcifi-
cations, external cervical root resorptive defects
and coronal pulp chamber anatomy can be
revealed. This information is helpful in not only
determining the pre-endodontic assessment of
the tooth and overall restorability but also aiding
any future planning and correcting execution of
any proposed root canal procedure (see Fig. 12.3).
Paralleling technique
From an endodontic prospective, the paral-
leling technique produces the most accurate
167
peri-radicular radiograph. Also known as the
long-cone or right-angle technique, it produces
improved images. The technique, developed
by Gordon M. Fitzgerald, is named because
the object (tooth), receptor (film packet) and
film-positioning device are all kept on parallel
planes. This technique permits a more accurate
reproduction of the tooth’s dimensions, enhanc-
ing the determination of the tooth’s length and
relationship to surrounding anatomic structures.
In addition, the paralleling technique reduces the
possibility of anatomical noise such as superim-
posing the zygomatic processes over the apices
of maxillary molars. A more angulated film, such
as those produced by means of the bisecting-
angle technique, is more likely to result in both
distortion and superimposition. If properly used,
the paralleling technique will provide the clini-
cian with films with the least distortion, mini-
mal superimposition and utmost clarity (see
Figs. 12.3 and 12.4).
1. The film packet (plain film or digital sensor) is
placed in a holder and positioned in the mouth
parallel to the long axis of the tooth under
investigation.
2. For incisors and canines (maxillary and man-
dibular), an anterior film holder should be
selected with a small film packet (22 × 35 mm).
For posterior premolar and molar teeth (max-
illary and mandibular), a posterior holder (left
or right) is selected using a large film packet
(31 × 41 mm).
3. Positioning of the film packet depends on the
tooth under investigation. For maxillary inci-
sors and canines, the film is positioned suffi-
ciently posteriorly to enable its height to be
accommodated by the vault of the palate.
Mandibular incisors and canines require the
film packet to be positioned in the floor of the
mouth, approximately in line with the lower
canines or first premolars. For maxillary pre-
molars and molars the position of the film is in
the midline of the palate accommodating the
vault of the palate. Mandibular posterior teeth
require the film to be placed in the lingual sul-
cus adjacent to the appropriate tooth.
4. The x-ray tube head is then aimed at right
angles (vertically and horizontally) to both the
tooth and film packet.
168
a b
c d
Fig. 12.3 Conventional radiographic views showing (a)
bisecting-angle view with elongation (provided by refer-
ring dentist), (b) preoperative parallel view taken by
myself, (c) preoperative bitewing radiograph and (d) post-
operative parallel view of completed endodontic case.
5. By using a film holder with fixed film packet
and x-ray tube head positions, the technique is
highly reproducible.
Bisecting-angle technique
A bisecting-angle technique may be used
when there may be no alternative because of dif-
ficult anatomic configurations or patient manage-
ment problems. The basis of this technique is to
place the film directly against the teeth without
deforming the film. Due to the inherent nature of
teeth when a film is placed in this position, an
obvious angle exists between the plane of the
film and the long axis of the teeth. This results in
distortion, because the tooth is not parallel to the
film. If the x-ray beam is directed at a right angle
to the film, the image on the film will be shorter
than the actual tooth (e.g. foreshortened). If the
12 Endodontic Radiology
Note parallelism throughout ensures accuracy when
assessing preoperative and post-operative films for com-
parison and future review appointments to assess healing
of peri-apical lesions
beam is directed perpendicularly to the long axis
of the teeth, the image will be much longer than
the tooth (e.g. elongated). Thus, by directing the
central beam perpendicular to an imaginary line
that bisects the angle between tooth and film, the
length of the tooth’s image on the film should be
the same as the actual length of the tooth.
Although the projected length of the tooth
may be correct, the image will show distortion
because the film and object are not parallel and
the x-ray beam is not directed at right angles to
both. This distortion increases along the image
towards its apical extent. The technique produces
additional error potential, because the clinician
must imagine the line bisecting the angle (an
angle that, in itself, is difficult to assess). In addi-
tion lack of reproducibility makes it difficult for
12.3 Plain Film Radiography 169

a b

c d

e f

g h

Fig. 12.4 Clinical diagrams and photographs demon- parallel image with minimal distortion which is important
strating film aiming device for both (a–d) posterior (yel- in endodontics from working length determination to
low) and (e–h) anterior (blue) teeth to achieve a true future follow-up and image comparison
170
the clinician to reproduce radiographs at similar
angulations to assess radiographic controls dur-
ing endodontic treatment phases and healing
after completion.
One major limitation of intra-oral radiographs is
their inability to detect bone destruction or pathosis
when it is limited to the cancellous bone. Studies
have proved that radiolucencies usually do not
become apparent on an x-ray film unless there has
been erosion of the cortical plate. This factor must be
considered in evaluating teeth that become symp-
tomatic but show no obvious radiographic changes.
12.4 Digital Radiography
In digital radiography an image sensor replaces the
conventional radiographic film. Dental digital
radiography sensors can be divided into storage
phosphor plates (SPP), also called photo-
stimulable phosphor plates (PSP), and silicon
devices such as the charge-coupled devices (CCD).
Phosphor plates are similar in size and thick-
ness to conventional radiographic film. For
a c
Fig. 12.5 Photographs demonstrating (a, b) conventional small and large film packets, (c) storage phosphor plates
(SSP) and (d) charge-coupled device (CCD) using a sensor attached to a cable lead directly to the computer
12 Endodontic Radiology
infection control purposes, the plate is placed in
a plastic pouch, which is sealed, preventing con-
tact with oral fluids. When an x-ray is taken, the
phosphor plate stores the latent image in the
phosphor crystals. The plate can be removed
from the patient’s mouth, the plastic pouch is
discarded and the plate is placed in a laser scan-
ner. A laser beam sequentially scans the plate
and the stored electrons are released as visible
light, which is quantified. The analogue signal is
then converted to a digital image, which can be
viewed on a computer monitor. The major disad-
vantage of this system is a delay in image acqui-
sition due to the scanning procedure. The other
main drawback is that the phosphor plates them-
selves can be prone to damage easily resulting in
artefacts on any images taken using the damaged
plate (Fig. 12.5).
Charge-coupled devices (CCD) include a sen-
sor attached to a cable lead, which is connected
directly to a computer. The sensor, which can be
quite bulky compared to both conventional film
and PSP, is placed in the patient’s mouth ready
for exposure using conventional x-rays. The CCD
d
12.4 Digital Radiography
a b
d e
Fig. 12.6 Clinical radiographs obtained with phosphor
plates. Dedicated software allows for image manipulation.
Note (a) preoperative unaltered view, (b) image-enhanced
includes a pixel array (electron wells) on a silicon
chip. The x-ray energy is converted to a propor-
tional number of electrons, which are deposited
in the electron wells. The electrons are trans-
ferred to a readout amplifier (charge coupling) as
an analogue signal, which is converted to a digi-
tal signal. This digital signal is converted to an
image, almost instantaneously on the computer
monitor, which is seen as an advantage. The
major drawbacks of this system are the bulky
sensors, which may not be tolerated well by
patients, and the risk of damage to the cable. The
cost of sensor or cable replacement is significant
compared to the cost of phosphor plates.
A digital image is comprised of a set of cells
that are ordered in rows and columns. Three
numbers (x-coordinate, y-coordinate and grey
value) characterises each cell. The grey value is a
number that corresponds with the x-ray intensity
at that location during a particular exposure of
the sensor. Individual cells are known as ‘picture
elements’ which has been shortened to ‘pixels’.
Each pixel is assigned a number, which is stored
in an image file on the computer. As a result
images stored on file can be manipulated by
171
c
f
view, sharpened (c) positive view, (d) application of
colour, (e) flashlight view and (f) measurement tools
mathematical operations to alter individual pixel
values that can have a desired effect on the image.
Dedicated software is available for the
practitioner to alter images adjusting brightness
and contrast, which can allow for corrections to
an overexposed or underexposed film (see
Fig. 12.6). Adjustments made to contrast and
density may allow for further manipulation ren-
dering structures more visible in some instances.
Other image processing tools available include
the ability to measure accurately root canal
lengths and set distances such as the crown of the
tooth to the cement–enamel junction. Other use-
ful tools include the possibility of inversion of the
grey scale resulting in a negative image, edge
enhancement and the ability to zoom in on any
part of an image.
Digital subtraction radiography is a sensitive
method for detecting changes in radiographic den-
sity over time. In endodontics, digital subtraction
radiography may be especially useful for evaluat-
ing osseous healing after completion of treatment.
By definition, subtraction radiography requires that
two images have nearly identical image geometry.
Specialised positioning devices and bite
172
registrations aid in matching the images. The sub-
tracted image is a composite of the images, repre-
senting their variations in density. By subtracting
all anatomic structures that have not changed
between radiographic examinations, changes in
diagnostic information become easier to interpret.
12.5 Cone-Beam Computed
Tomography
Cone-beam computed tomography (CBCT) is a
relatively new extra-oral imaging system which
was specifically developed to produce 3D undis-
torted images of the maxillofacial skeleton with
considerably lower doses of radiation compared
to conventional CT. The entire 3D volume of data
that is acquired for CBCT is done so by a single
sweep of the scanner using a simple direct rela-
tionship between scanner and source, which can
rotate around the patient’s head. The x-ray beam
is cone shaped capturing a cylindrical or spheri-
cal volume of data identified as the field of view.
These modern CBCT machines are specifically
b c
Fig. 12.7 Cone-beam CT scan images highlighting one
of the many advantages a 3D scan has to offer compared
to conventional plain film radiography. (a) This particular
patient had an external cervical root resorption lesion
associated with tooth 21. (b–e) The exact extent and posi-
12 Endodontic Radiology
designed to suit dental practices in terms of space
required occupying the same space or even smaller
compared to panoramic machines of the past.
Typical images can be displayed in axial, sag-
ittal or coronal planes and simultaneously if
desired. An accurate 3D view of the tooth or sur-
rounding area of interest can be viewed after the
volumes of data are reconstructed using appro-
priate software (see Figs. 12.7 and 12.8). Slices
can be selected according to anatomical noise
present (superimposition of anatomical struc-
tures, alveolar bone, adjacent roots) and the abil-
ity to avoid its selection accordingly.
The resolution of current generation CBCT
machines is still not the same compared to con-
ventional radiography. The resolution of a CBCT
image is measured in terms of ‘voxel’ sizes. A
voxel is a series of 3D pixels, which comprise the
volume image. Unlike pixels, voxels are isotropic
enabling objects within volumes to be accurately
measured in the different planes. Voxel size
determines both the quality and scanning times
required for CBCT volumes (the smaller the
voxel size the greater the detail seen).
d e
tion of the lesion in three dimensions can be visualised
aiding preoperative assessment and whether a surgical
approach is amenable. Note evidence of an incomplete
root fracture that was also demonstrated (yellow arrow)
12.6 The Tube Shift Technique
a c
Fig. 12.8 (a) Cone-beam CT scan demonstrating an
extensive lesion occupying the left maxillary sinus. (b–c)
Note axial views demonstrating slices at various points
confirming extent of the lesion. This type of scan enables
12.6 The Tube Shift Technique
In endodontic therapy, the ability for the clini-
cian to recognise the spatial or bucco-lingual
relationship of an object within the tooth or alve-
olus can be advantageous. The technique used to
identify the spatial relation of an object is called
the tube shift technique. Other names synony-
mous with this procedure are the buccal object
rule or SLOB (same lingual, opposite buccal)
rule. Correct application of the technique allows
the clinician to locate additional canals or roots,
to distinguish between objects that have been
superimposed and to distinguish between vari-
ous types of resorption. It also helps the clinician
to determine the bucco-lingual position of frac-
tures and perforation defects, to identify the pre-
cise location of foreign objects and to locate
anatomic landmarks in relation to the root apex,
such as the mandibular canal or mental foramen
(Fig. 12.9).
The buccal object rule relates to the manner in
which the relative position of radiographic
images of two separate objects changes when the
projection angle at which the images were made
is changed. The principle states that the object
closest to the buccal surface appears to move in
173
any surgical approach to be undertaken with greater confi-
dence when determining the true extent of the lesion and
what anatomical structures may be involved
the direction opposite to the movement of the
cone or tube head, when compared with a second
film. Objects closest to the lingual surface appear
to move (on a film) in the same direction that the
cone moved, thus the ‘same lingual, opposite
buccal’ rule.
Figure 12.10 shows the position of the
mesial root apex of the mandibular second
molar and how implementation of the buccal
object rules allows differentiation of the mesio-
buccal and mesio-lingual roots. The first radio-
graph shows superimposition of the two mesial
roots; in this case the tube head was positioned
for a straight-on view. In the second radiograph,
the tube head was shifted mesially, and the
beam was directed at the tooth from a more
mesial angulation. In this case the mesio-lin-
gual root (yellow) moved mesially with respect
to the first radiograph, and the mesio-buccal
root moved distally with respect to the tooth
(see Fig. 12.10).
These radiographic relations confirm that the
lingual object (mesio-lingual canal) moves in the
same direction with respect to the tube head and
that the buccal object (mesio-buccal canal) moves
in the opposite direction of the radiograph tube.
Thus, according to the rule, the object farthest
174 12 Endodontic Radiology

B L B L B
L

B B B
Mesial Mesial Mesial

L L L

X- ray beam X- ray beam X- ray beam

mesial shift 20° straight distal shift 20°

Fig. 12.9 Diagrams representing the buccal object rule.
When the x-ray beam is directed in a straight line over the
paths of both the buccal and lingual canals, the canals
appear superimposed and as one. When the angulation of
the x-ray machine is adjusted either mesially or distally,
the two canals cease to be superimposed. When the angu-
lation of the x-ray machine is known, the lingual object
(the one farthest from the radiograph) is displaced in the
same direction as the x-rays. B buccal, L lingual

a b c

d e f

Fig. 12.10 Clinical cases demonstrating tube shift with the lingual canal can be seen (red arrow). (d–f) Upper left
respect to distinguishing anatomy. Note (a–c) lower second maxillary second molar demonstrating mesial tube shift dis-
permanent molar. When the tube is shifted in a mesial direction, tinguished additional MB2 canal (yellow arrow)

(i.e. most buccal) from the film moves farthest on
the film with respect to a change in horizontal
angulation of the radiograph cone.
1. A straight-on diagnostic long-cone paralleling
technique should be taken such that the x-ray
cone is aimed perpendicular to both the facial
and long axes of the tooth (see Fig. 12.11).
2. A second mesially angulated image can be
obtained by horizontally aiming the x-ray
beam up to 30° mesial to the straight-on angle
12.7 Differential Diagnosis of Radiolucent and Radiopaque Lesions of the Jaw
a b
d e
Fig. 12.11 (a–e) Clinical photographs demonstrating placement of parallel film holder using CCD device and tube
shifts to enable differentiation of anatomical objects on the radiograph
and perpendicular to the long axis of the tooth
(see Fig. 12.11).
3. As the x-ray tube head is moved from poste-
rior to anterior, objects imaged on the film
which are on the lingual aspects (palatal roots
or mesial lingual roots or distal lingual roots)
will be positioned mesially in the radiograph
(the same position as the head tube)
12.7 Differential Diagnosis
of Radiolucent
and Radiopaque Lesions
of the Jaw
Many anatomic structures and osteolytic lesions
can be mistaken for peri-radicular pathoses.
Amongst the more commonly misinterpreted ana-
tomic structures are the mental foramen and the
incisive foramen. These radiolucencies can be dif-
ferentiated from pathologic conditions by expo-
sures at different angulations and by pulp-testing
procedures. Radiolucencies not associated with
the root apex will be projected away from the apex
by varying the angulation. Radiolucent areas
resulting from sparse trabeculation can also simu-
late radiolucent lesions. In such cases these areas
175
c
f
must be differentiated from the lamina dura and
periodontal ligament space.
A commonly misinterpreted osteolytic lesion
is peri-apical cemental dysplasia or cementoma.
The use of pulp-testing procedures and follow-up
radiographic examinations will avoid the poten-
tial mistake of diagnosing this as a peri-radicular
pathosis. The development of this lesion can be
followed radiographically from its early, more
radiolucent stage through to its mature or more
radiopaque stage.
Other anatomic radiolucencies that must be dif-
ferentiated from peri-radicular pathoses are the
maxillary sinus, nutrient canals, nasal fossa and
lateral or submandibular fossa. Many systemic
conditions can mimic or affect the radiographic
appearance of the alveolar process. A discussion
of these conditions is beyond the scope of this
chapter, but the reader is encouraged to read fur-
ther in any oral pathology textbook.
Clinical Hints and Tips
• Gagging patients – placement of the sensor/
film towards the midline away from the soft
palate will reduce the tendency to gag.
Distraction strategies such as breathing
through the nose, salt on the tongue and lifting
176
one leg up in the air can be useful. Local anaes-
thetic may be beneficial. Organisation prior to
taking the radiograph will be essential in terms
of presetting the exposure setting, pre-align-
ment of the positioning device and being quick.
• Patients with tori – consider using bisecting-
angle technique instead of paralleling tech-
nique. Placement of the sensor/film behind
mandibular tori. Ensure maxillary tori are
between the teeth and sensor/film.
• Shallow palatal vaults – consider placement
of the sensor/film towards the midline.
Consider using the bisecting-angle technique.
• Narrow dental arch – placement of the recep-
tor as far lingually as possible. Use smallest
size sensor/film available.
• Edentulous situations – place the sensor/film
towards the midline. Use cotton wool on a bite
block to replace missing teeth.
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 Anatomy and Root Canal
Morphology 13

Summary
The majority of endodontic failures can often be attributed to the inability
of localising and treating all the canals of the root canal system. Root canal
systems are commonly complex with the teeth often having lateral
ramifications, extra roots or additional canals. Molar and premolar teeth
can present with the highest incidence of aberrant morphology. A thorough
knowledge of expected anatomy and variations from the norm are essen-
tial when undertaking root canal therapy to ensure success.

Clinical Relevance 13.1 Overview of Root

The clinical impact of missed anatomy may result
in failure and the necessity to carry out costly
root canal re-treatment. Prevention of missed
anatomy begins with a thorough knowledge of
common tooth morphology. The clinician must
be aware of the complexities of the root canal
system and anatomical variations of the norm
that may be encountered according to tooth type.
The human dental pulp manifests multiple con-
figurations and shapes which can vary from one
individual to another. Careful interpretation of
preoperative angled radiographs, correct access
extension and a detailed exploration of the inte-
rior of the tooth using magnification and illumi-
nation are key steps for achieving clinical and
radiographic success.
Canal Anatomy
In 1925 Hess and Zurcher first published a study
showing us how the teeth had complicated root
canal systems rather than the simplified canals
that had been previously described [1]. For the
first time we were able to see the intricate com-
plexities of the internal root canal anatomy using
vulcanised Indian rubber following dissolution
of the surrounding tooth using 50 % hydrochlo-
ric acid. Even roots with a single canal will have
lateral (an accessory canal located in the coro-
nal or middle third of the root, usually extending
horizontally from the main canal) and accessory
canals leaving the main canal and communi-
cating with the external surface of the root [2].

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 179
DOI 10.1007/978-3-319-15591-3_13, © Springer International Publishing Switzerland 2015
180
I II
Fig. 13.1 Schematic diagrams representing Weine’s
classification of root canal configurations. Type I - single
canal from pulp chamber to apex. Type II - two canals
leaving the chamber and merging to form a single canal
I II
V VI
Fig. 13.2 Vertucci classification. Type I – a single canal
with one foramen. Type II – two canals that join in the
apical third. Type III – one canal that divides into two that
subsequently reunites and exits as one. Type IV – two
separate canals all the way to the apex. Type V – one canal
A thorough understanding of the complexities of
the root canal system is essential for understand-
ing the principles and problems of shaping and
cleaning and for performing successful microsur-
gical procedures [3].
13 Anatomy and Root Canal Morphology
III IV
short of the apex. Type III - two separate and distinct
canals from chamber to apex. Type IV - one canal leaving
the chamber and dividing into two separate and distinct
canals
III IV
VII VIII
that divides just short of the apex. Type VI – two canals
that unite in the root and divide again at the apex. Type VII
– one canal that divides, reunites and finally exits through
two apical foramina. Type VIII – three separate canals in
one root
In order to grasp the varying anatomy that can
occur with the teeth, a number of classification
systems have been proposed. Weine’s classifica-
tion of root canal morphology was based on the
number of canal orifices, the number of canals
13.1 Overview of Root Canal Anatomy
and the number of foramina in each tooth [4] (see
Fig. 13.1). A more comprehensive classification
was provided by Vertucci, resulting in eight cat-
egories based on 2,400 extracted teeth that were
rendered transparent and treated with a dye injec-
tion technique [5] (see Fig. 13.2). These classifi-
cation systems provide us with a further insight
into the complexities associated within the root
canal system and help visualise the internal anat-
omy that we may become accustomed to encoun-
tering when carrying out preparation procedures.
Maxillary central and lateral incisors generally
have one canal [3, 5]. When more than one canal is
present, the possible configurations include two
canals joining into one apical foramen (Vertucci
type II) [6], two separate canals in one root (Vertucci
type IV) [5], two canals in two separated roots or
two or more canals associated with developmental
abnormalities such as germination, fusion and dens
invaginatus [7, 8]. Maxillary incisors with more
than one root canal are rare and adequate access
opening and observations of intra-operative radio-
graphs should help in these difficult cases.
The majority of maxillary canine teeth have
one canal in one root [5]. Morphological varia-
tions do exist but are rare where more than one
canal is present [9].
The most common canal configuration for the
maxillary first premolar is two separate canals in
one root (Vertucci type IV) with a frequency of
about 60–65 %. One canal that extends from the
pulp chamber and dividing in the mid-root into two
canals (Vertucci type V) can occur in 6–7 % of
cases. In about 8–9 % of cases, the maxillary first
premolar can have one canal and in 16–18 % two
canals joining into one. On rare occasions three
canals (mesio-buccal, disto-buccal and palatal) can
occur in 2–6 % with a root disposition similar to the
first permanent maxillary molar tooth [5, 10–12].
Maxillary second premolars usually have one
canal in one root (Vertucci type I) in 38–48 % of
cases, two canals joining in one root (Vertucci
type II) in 20–22 % of cases and one canal sepa-
rating into two canals that rejoin in the apical third
in 5–10 % of cases (Vertucci type III). Two canals
in two roots can occur in the region of 10–20 % of
cases and one canal that splits and exits as two
(Vertucci type V) in 6–9 % of cases. Rarely two
181
canals that rejoin and split again (Vertucci type
VI) occur in 2–5 % of cases. Three separate canals
occur in the frequency of 1–2 %. Due to the aber-
rant canal morphology in these teeth, clinicians
should pay close attention to both pre- and intra-
operative radiographic examinations and clinical
pulpal floor anatomy [5, 10–12].
A wide range of variation exists for the maxil-
lary first permanent molar in the literature. It is
generally accepted that this tooth has three roots
(95 %) and four canals. Four percent of teeth have
only two roots. The broad bucco-lingual dimen-
sion of the mesio-buccal root and associated con-
cavities on the mesial and distal surface is
consistent with the majority of mesio-buccal roots
having two canals. The incidence of root fusion of
two or three roots is approximately 5.2 %. Conical
and C-shaped root morphology is very rare
(<1 %). The incidence of two canals in the mesio-
buccal root is 60 % and one canal to be about
40 %. The incidence of more than one disto-buc-
cal or palatal root is rare (<1 %) [13–21].
The majority of maxillary second permanent
molars have three roots with four root canals
(90 %). Six percent may present with two roots
and 3 % with a single root. Vertucci described the
mesio-buccal root of having one canal in 71 % of
cases (type I), two canals joining in 17 % (type II)
of cases and two separate canals in 12 % of cases
(type IV). The incidence of C-shaped canals is
very rare in this subgroup of teeth [5, 15, 22].
The morphology of mandibular central and lat-
eral incisors is not very dissimilar with the majority
of teeth having two canals (25–40 %) [5, 23, 24].
The mandibular permanent canine tooth often
has a single root (98 %) with a single canal and one
apical foramen (92 %). Five percent of cases have
two canals, which are confluent in the apical third
forming one canal. The incidence of two canals
and two separate roots is rare (<3 %) [5, 25].
A literature review of the root canal morphol-
ogy of the mandibular first permanent premolar
revealed that these teeth were one (98 %), two
(1.8 %) and rarely three or four rooted (<0.1 %).
Internal canal morphology revealed the majority
of canals were single (76 % type I). Studies and
case reports have also confirmed variation of
canal morphology where division of the canal
182
occurs in the middle or apical third into buccal
and lingual branches (type II and IV). Rarely
three canals can be present and occasionally the
presence of C-shaped canals [5, 26–30].
The majority of mandibular second permanent
premolars have a single root canal system (97.5 %
type I) and two canals in the remainder (2.5 %
type IV). The frequency of three of more canals
is very rare (<0.4 % type VIII) [5, 29–31].
The majority of mandibular first permanent
molars are often found to be two rooted with various
canal configurations existing. Often two separate
canals occur in 59 % of teeth (type IV), two canals
conjoining apically in 28 % of teeth (type II) and a
single canal system in 12 % of teeth. Occasionally
three canals may be present in 1 % of teeth (type
VIII). The frequency of the middle mesial canal var-
ies between 1 and 7 % with variations of either con-
joining in the middle or apical third or rarely with
three separate exits apically. Distal roots often have
one single canal in 70 % of teeth (type I), two canals
that join into one in 15 % of teeth (type II), two sepa-
rate canals in 5 % of teeth (type IV), one canal that
divides into two in 8 % of teeth and one canal that
divides into two then joins again in the apical third,
forming a single canal in 2 % of teeth (type III).
Overall the distal canal often presents with two or
more canals in 30 % of cases. A major variant of root
morphology known as radix entomolaris can occur
rarely in 5 % of Caucasians but more often in popu-
lations with mongoloid traits (5–30 %) [5, 32–37].
Mandibular second permanent molars usually
have two roots (mesial and distal). In the mesial root
a type I canal configuration may be present (27 %),
two canals which co-join apically (38 % type II) and
two separate canals (38 % type IV). In the distal root,
variations of type I (92 %), type II (3 %) and type IV
(5 %) can be found. The incidence of a C-shaped
canal system in this particular tooth group varies
between 2 and 30 % and found often with a higher
prevalence in the Chinese population [5, 38–42].
The root morphology and canal anatomy of
maxillary and mandibular third molars is highly
variable with often fusion involving one or more
of the roots [43].
To ensure that all internal anatomy is cor-
rectly identified and treated, good preoperative
radiographs, correct access cavity preparation,
enhanced lighting, use of the dental operating
13 Anatomy and Root Canal Morphology
microscope and controlled use of ultrasonic instru-
ments are necessary tools that must be adopted.
The clinical impact of missed anatomy is likely a
failure in the future, resulting in either costly re-
treatment or worse still extraction of the tooth. On
the other hand, localisation and treatment of all
canal anatomy will typically lead to a favourable
outcome with complete clinical and radiographic
healing. Cone-beam technology has been present
for the last 30 years, but recent convergence and
innovations have lead to the viable application of
cone-beam volumetric tomography (CBVT) or
cone-beam computed tomography (CBCT) in the
dental office. Together these advantages have
allowed CBVT to become a valuable tool in the
modern endodontic practice, allowing us to truly
appreciate the difficulties of treating these three-
dimensional spaces that are more complex than
we could have imagined [44–46] (see Chap. 12).
13.2 Maxillary Central
Incisor Teeth
The root of the maxillary central incisor is often
bulkier than the lateral with cross-sectional anat-
omy varying from triangular, circular or oval in
shape. The canal is often tapering towards the
apex in mature teeth with minimal curvatures in
the apical portion (Fig. 13.3).
The access cavity is initiated by penetrating
the bur occlusal to the cingulum, avoiding the
incisal edge. Once penetration to the root canal is
achieved, the access cavity must be refined in a
mesio-distal direction to remove the entire roof
associated with the pulp horns. The access cavity
achieves a roughly triangular shape with this
preparation, which mirrors the anatomy of the
pulp chamber (see Fig. 13.4).
Lateral canals may be present in the middle or
apical third and the occurrence of a second canal
is very rare. Due attention must be given to canals
with very wide-open apices (blunderbuss teeth)
and also narrow calcified canals (calcific meta-
morphosis) typically encountered following a
traumatic incident. A sharp bend or curvature in
the root would indicate previous trauma or bony
interference during root formation (dilacerations),
which may also affect management.
13.2 Maxillary Central Incisor Teeth 183

22.5 mm

Number of Canal configuration Comments Author(s)

canals and average length

Vertucci type I Vertucci

1 22.5 mm
Triangula/ovoid lingual access just above the
cingulum (shape must include pulp horns and
lateral canals). Lingual shoulder may prevent
direct access. Apical terminus may not exit at
the radiographic apex.

Be aware of calcific metamorphosis which

can make access difficult.

Fig. 13.3 Overview of maxillary permanent central incisor teeth

a b c

d e f

Fig. 13.4 Clinical photographs showing step-by-step
access preparation in an anterior maxillary central incisor.
Note (a) preoperative view (dotted line representing
intended triangular access incorporating pulp horns),
(b) initial bur penetration, (c) root canal penetrated,
(d) widening of access in a mesial and distal direction to
ensure pulp horns are incorporated, (e) use of ultrasonics
to remove overhanging dentine and to ensure pulp horns
are free of any tissue remnants and (f) final access prepa-
ration completed
184 13 Anatomy and Root Canal Morphology

22.0 mm

Number of Canal Comments Author(s)

canals configuration and
average length

Vertucci type I Triangular/ovoid access should include pulp Vertucci

horns during access preparation. Portal of exit
may not be at radiographic apex. Note often
22.0 mm distal apical curvature.
1
Be aware of dilacerations,dense in dente or
palatal-radicular groove which can affect
outcome and change management.

Fig. 13.5 Overview of maxillary permanent lateral incisor teeth

13.3 Maxillary Lateral
Incisor Teeth
The lateral incisor is often smaller in comparison
to its neighbouring central counterpart. The root
is often slender with an apical curvature gener-
ally in a disto-palatal direction.
The presence of extra roots or occurrence of
developmental grooves is more likely in this
tooth group. Tooth invaginations (dens in dente)
are also a common finding, which complicates
endodontic management. Early recognition is
essential and referral is probably best considered
(Fig. 13.5).
In this tooth, the access cavity is created in the
same way as in the central incisor. The pulp horns
are often closely situated or singular in this tooth,
resulting in a final shape that is more likely to be
ovoid as opposed to triangular. Care must be
taken when negotiating the apical curvature in
this tooth, particularly with larger file sizes,
which can result in canal transportation or ledg-
ing if not correctly identified (see Fig. 13.6).
13.4 Maxillary Canine Teeth
These teeth can be one of the longest encountered
with roots that are irregularly tapered and wide in
a labio-palatal direction. The canal is typically a
type I configuration with a root curvature apically
often in a distal direction although can occur in
any direction (Fig. 13.7).
The access cavity begins about halfway up the
crown on the palatal side (see Fig. 13.8). With an
ovoid pulp chamber and a single horn, the access
cavity is oval in outline and shape. The root canal
is quite straight in the coronal and middle third
and long enough to require the use of long 30-mm
instruments.
13.4 Maxillary Canine Teeth 185

a b c d

Fig. 13.6 Clinical radiographs demonstrating manage-
ment of maxillary lateral incisor. Note the apical curvature
that cannot be appreciated due to the distal and palatal
curvature. (a) Preoperative view with large peri-radicular
radiolucent lesion and (b) completed endodontic treat-
ment of tooth 22. Note distal curvature of apical third
maintained. Significant reduction of peri-radicular lesion
achieved following chemo-mechanical debridement and
interim intra-canal dressing of calcium hydroxide over a
3-month period, (c) 6-month follow-up and (d) 18-month
follow-up showing continued healing

27.0 mm

Number of Canal Comments Author(s)

canals configuration
and average
length

Vertucci type I Lingual access cavity is ovoid in shape above Vertucci

cingulum. Note the root can curve in any
direction in the apical third (but usually
1 27.0 mm buccal). Apical foramen frequently not found
at anatomic apex.

Note possibility of buccal apical dilaceration

Fig. 13.7 Overview of maxillary permanent canine teeth

186
a b
Fig. 13.8 Clinical photographs demonstrating access cavity preparation in a maxillary canine tooth. Note (a) preopera-
tive view and (b) completed access preparation showing ovoid outline
Canines with a normal crown and root but
with two canals are rare and difficult to identify
because the canals may be superimposed. An
adequate pulp chamber opening and careful
observation of intra-operative radiographs may
help in these difficult cases.
13.5 Maxillary Premolar Teeth
The maxillary first premolar has variable mor-
phology but is generally considered to have two
roots and two canals (see Fig. 13.9). The second
premolar although variable at times generally
presents with a single-rooted single canal system
(see Fig. 13.10).
Careful radiographic assessment is essential
in order to ascertain the likely number of roots
and canal morphology before any operative inter-
vention. Peri-apical radiographs give a two-
dimensional image of a three-dimensional root
canal system, so a minimum of two radiographs
should be taken to reveal external and internal
features of the tooth. A parallel radiograph should
be taken with either a mesial or distal horizontal
tube shift. The second angled radiograph may
help visualise superimposed roots, displace the
13 Anatomy and Root Canal Morphology
zygomatic process of the maxillary bone and
increase the chances of observing additional root
canals present.
The intra-oral radiograph should be carefully
inspected for any sudden changes in the radio-
graphic density of the root canal space, which
may indicate bifurcation or trifurcation of the
roots. Any sudden narrowing or disappearance
may indicate branching of the root canal system
often encountered in these teeth. The same
principles can be applied during peri-operative
treatment whereby any asymmetry of the file
placed in the canal can also indicate the presence
of a second root system.
The pulp chamber of the upper first and sec-
ond premolar is oriented more towards the bucco-
lingual direction since in the great majority of
cases, it has two canals beneath the respective
cusps (see Figs. 13.11 and 13.12). The point of
entry of the bur is the middle of the central sulcus
drilling parallel to the long axis of the tooth.
The floor of the pulp chamber should be
carefully examined looking at the position and
symmetry of the canals. Asymmetry is often a
good indication of additional anatomy that
may be present. Upper premolars with three
canals require a modified access cavity with a
13.5 Maxillary Premolar Teeth 187

21.0 mm

Number of Canal configuration and Comments Author(s)

canals/roots average length

Canals
1 26 % Access preparation oval in shape with greater extension
Vertucci type I,II or IV
2 65 % towards buccal and lingual.
3 3−6 % Note that if three roots are present then buccal roots can
Vertucci
be very thin. Anatomy of three rooted premolar similar to
Root s 1st molar in terms of canal positioning.
1 37 %
2 57 % Premolar teeth may have mesial concavity liable to strip
21.0 mm
36% perforation and post treatment fracture risk is high.

Fig. 13.9 Overview of maxillary permanent first premolar teeth

21.0 mm

Number of Canal configuration and Comments Author(s)

canals/roots average length

Canals/
Foramina Access preparation oval in shape with greater extension
1 1 48 %
Vertucci type I,II or IV towards buccal and lingual.
2 1 27 %
Note that if three roots are present then buccal roots can
2 2 24 % Vertucci
be very thin. Anatomy of three rooted premolar similar to
3 1 1%
1st molar in terms of canal positioning.
Seelig & Gillis
Roots
1 48 % 21.0 mm Premolar teeth may have mesial concavity liable to strip
2 51 % perforation and post treatment fracture risk is high.
31%

Fig. 13.10 Overview of maxillary permanent second premolar teeth

188 13 Anatomy and Root Canal Morphology

a b

Fig. 13.11 Preoperative clinical photograph showing (a) occlusal anatomy of an upper maxillary premolar tooth and
(b) completed ovoid access preparation extended in a bucco-palatal direction

a b c d

Fig. 13.12 Clinical radiographs and photographs dem- radiograph demonstrating a two-rooted tooth, (b) MAF,
onstrating endodontic treatment of a maxillary first pre- (c) cone fit and (d) final obturation showing Vertucci IV
molar tooth with two canals. Note (a) preoperative canal configuration

mesio-distal extension in the buccal portion of 13.6 Maxillary Molar Teeth

the traditional cavity. This modification, result-
ing in a T-shaped access, permits good access
to both buccal canals. The presence of three
canals is higher in the first premolar compared
to the second but nevertheless rare. The ana-
tomical roots are similar to the first molar
whereby an MB, a DB and a P root may be
present.
Treatment of maxillary premolars requires
extra attention due to their extreme variability
that can be encountered. Caution is advised due
to the higher risk of failing to treat all internal
anatomy, and a dental operating microscope or
other forms of magnification are a necessary tool
when dealing with these teeth.
The literature shows a wide variation in anatomy
of the maxillary molars although the average
tooth often has three roots and four canals
(see Figs. 13.13 and 13.14). The palatal root is
often the longest with a curvature in the apical
third towards the buccal. The disto-buccal root,
which is shorter in comparison, may curve
towards the mesial or distal in the apical third.
The mesio-buccal root shows the greatest varia-
tion with a root that is broad in the bucco-palatal
plane and narrowing in the mesio-distal place.
This ribbon-shaped root will generally exit the
crown mesially but can commonly abruptly
curve towards the distal. Curvatures are often
13.6 Maxillary Molar Teeth 189

MB1
DB

21.0 mm

MB2

Number of Canal Comments Author

canals/roots configuration and
average length

MB Canals/ Type I, II or III MB root Access for the maxillary molar as for all molars is initially Kulild and
Foramina Buccal 19 mm triangular. The preparation is positioned mesial to the transverse Peters
1 1 45 % Palatal 21 mm ridge. Variations from the three-sided form may be made when Vertucci
searching for the MB2 by adding a fourth short side, if necessary, Wiene
2 1 37 %
forming a trapezoid.
2 2 18 %
Palatal canal often curves in apical third (usually buccal).
3 1 <1 %

Roots
Always assume 4 canals until proven otherwise.
1 rare
24% Be aware of danger zone on MB root (particularly when preparing
3 95 % MB2 and risk of root perforation.

Fig. 13.13 Overview of maxillary permanent first molar teeth

a b c

d e f M B2 M B1

P
DB

Fig. 13.14 Clinical radiographs demonstrating root canal view, (b) IAF, (c) mid-fill and (d and e) final obturation
treatment carried out in a permanent maxillary first molar using warm vertical compaction. (f) MB2 canal was located
with three roots and four canals. Note (a) preoperative following ultrasonic troughing in this area (arrowhead)
190
a b
Fig. 13.15 Clinical photographs demonstrating cleared
maxillary first permanent molar teeth showing complex
canal anatomy. (a) Maxillary first permanent molar show-
ing the MB root. Note Vertucci classification VI (2–1–2)
encountered in the apical third with possibilities
of convergence and joining of additional mesio-
palatal canals if present (see Fig. 13.15).
Access preparation will be mesial to the exter-
nal oblique ridge, allowing it to be maintained
during preparation whereby enhancing the
structural strength of the tooth. The orifice of the
palatal canal is often the most prominent beneath
the mesio-palatal cusp. The mesio-buccal canal
often lies directly beneath the mesio-buccal cusp
tip and the disto-buccal canal can often be found
2–3 mm distal to this canal and slightly towards
the palatal. Careful inspection of the floor of the
pulp chamber may reveal additional anatomy.
Recommended clinical approaches when
treating maxillary molars include:
1. Take two diagnostic radiographs, one parallel
and one either with a mesial or distal tube
horizontal tube shift, to correctly assess and
identify external and internal anatomy.
2. Careful removal of the pulp chamber roof is
carried out using a non-end cutting to avoid
damage to the pulpal floor. Dark developmental
13 Anatomy and Root Canal Morphology
with a lateral canal from the MB1 canal. (b) Maxillary
first permanent molar with two palatal canals. Note
Vertucci classification II (2–1) with interconnecting fins
and communication between both canals
lines on the floor of the pulp chamber should
be observed like a ‘road map’ to identify pos-
sible root canals present.
3. Careful observation of the pulp chamber floor
may also indicate additional root canal anat-
omy using sodium hypochlorite which may
effervesce.
4. Use of the dental operating microscope or
dental loupes with adequate illumination is
essential to correctly identify internal anatomy
and avoid iatrogenic damage to the floor of the
pulp chamber.
5. Access cavity preparation does not need to be
extended beyond the marginal ridge (see
Fig. 13.16). Loss of marginal ridge greatly
reduces the strength of the tooth.
6. Refinement of the access cavity will be
required in the mesio-palatal direction using a
rhomboid access. The MB2 canal is often pal-
atal and often mesial in a line drawn between
the MB1 and the palatal canal (see Fig. 13.16).
7. Use of methylene blue dye stains can be use-
ful to highlight the pulp chamber anatomy.
13.7 Mandibular Incisor Teeth
a b
DB
d e
M B1
DB
P P
Fig. 13.16 Clinical photographs demonstrating access
cavity preparation and refinement during the treatment of a
maxillary permanent first molar. Note (a) calcified floor of
pulp chamber with only DB canal located, (b) ultrasonic
8. Trough and search with a low-speed bur or
ultrasonic tip beginning from the MB1 orifice.
Be careful not to exceed a depth of 2–3 mm.
The maxillary second permanent molar will
often have similar root canal morphology to the
first (see Fig. 13.14). The roots may be fused with
less divergence in some cases. The access cavity
is similar to the upper first molar although the
pulp chamber floor of the upper second molar
may be flatter mesio-distally. The disto-buccal
canal may often be found to be more palatally
displaced and in some cases halfway between the
palatal and the mesio-buccal canals. The buccal
canal orifices may be closer together, and in some
cases, all three canals may be found in almost a
straight line, resulting in an access shape more
triangular rather than trapezoid.
13.7 Mandibular Incisor Teeth
The majority of these teeth are single rooted and
narrower mesio-distally compared to the bucco-
lingual width. Over 40 % of these teeth will have
191
c
DB
P
f M B1
M B2
M B2
DB
troughing carried out, (c) DB and P canal orifices located,
(d) MB1 canal orifice located, (e) MB2 canal orifice located
and (f) final four canals cleaned and shaped. Access cavity
is not extended beyond marginal ridge (red dash line)
two canals, which can join in the apical third of
the root. An approximal concavity on the mesial
and distal surface may be present which makes
these teeth susceptible to iatrogenic perforation if
care is not taken during the preparation phase.
The root may be curved in the apical
region, more often than not, towards the distal but
occasionally towards the labial. The access cavity
needs to be prepared with a small diamond bur
due to the narrow mesio-distal width creating
either an ovoid or elliptical cavity. To ensure that
the lingual canal is not missed, a straight line
access is important, requiring the appropriate use
of ultrasonic instrumentation to remove any
interfering dentine triangles that may be present.
The access cavity may need to be extended from
the incisal edge towards the cingulum bulge
(Fig. 13.17).
Careful radiographic assessment with a mesial
or distal horizontal tube shift should demonstrate
the presence of one or two canals. Assessment of
adjacent teeth may also give an indication of the
likelihood of two canals, depending on root
morphology seen.
192 13 Anatomy and Root Canal Morphology

70 % 5% 22 %

22.5 mm

Number of Canal Comment s Author(s)

canals/roots configuration and
average length

Canals/Foramina
1 70 % Vertucci Type I, II, III
2 1 5% Access cavity must include pulp horns and lateral canals or fins. Final
and IV
1 2 1 22 % access shape may be ovoid or elliptical. Note portal of exit may not Vertucci
2 2 3% be at the radiographic apex. Benjamin & Dawson

Roots
1 60−80 % 22.5 mm
2 20−40 %

Fig. 13.17 Overview of mandibular permanent central incisor teeth

The mandibular permanent lateral incisor
tends to be very similar to the central incisor in
terms of root canal morphology with a slight
difference in the length (this tooth may be longer
in comparison) (Figs. 13.18 and 13.19).
13.8 Mandibular Canine Teeth
The mandibular canine tooth resembles the
maxillary counterpart although its dimensions
may be smaller. Morphologically the tooth is
narrow mesio-distally and wider in the
bucco-lingual direction. It rarely has two root
canals, which may be confluent or two sepa-
rate roots independent of each other (Figs. 13.20
and 13.21).
13.9 Mandibular Premolar Teeth
Similar to its maxillary counterpart, these teeth
can exhibit a wide range of variation, often
with difficult challenges when more than one
root canal is present. Often the two cusps of
the mandibular first premolar are asymmetric
with a more pronounced cusp buccally. The
mandibular second premolar will have cusps of
equal size more often than not. The pulp cham-
ber, which is ovoid, is usually found below the
buccal cusp, requiring any penetration to be
directed towards this side. Care must be taken
lingually since any parallel bur penetration
along the long axis of the tooth may result in
a lingual perforation. If an additional lingual
canal is present, its division from the main canal
may be quite sharp, almost at a right angle,
posing difficulties in negotiation initially. This
may necessitate widening of the initial access
towards the lingual using ultrasonics under
constant visualisation using appropriate magni-
fication (Fig. 13.22).
Careful radiographic interpretation may give
clues as to the number of likely root canals
present in these teeth. If there is one canal, it will
lie in the centre of the root and any subsequent
file placement should be centred on the
radiograph. If the file appears off-centre, then
13.10 Mandibular Molar Teeth 193

75 % 2% 18 %

22.5 mm

Number of Canal Comment s Author(s)

canals configuration and
average length

Canals/Foramina
1 75 % Vertucci type I, II, III
21 5% and IV
1 2 1 18 % Access cavity must include pulp horns and lateral canals or fins. Note
portal of exit may not be at the radiographic apex. Vertucci
22 2%
Benjamin & Dawson
Roots
1 60−80 % 22.5 mm
2 20−40 %

Fig. 13.18 Overview of mandibular permanent lateral incisor teeth

a b c d e f

Fig. 13.19 Clinical radiographs and photograph demon- cavity preparation, (c, d) MAF showing confluence of
strating endodontic treatment of mandibular incisor teeth buccal and lingual canals and (e, f) obturation following
with two canals. Note (a) preoperative view, (b) access warm lateral compaction technique

there is likely to be an additional canal present. 13.10 Mandibular Molar Teeth

A sudden disappearance of the root canal in the
middle or apical third may also indicate the pos-
sibility of bifurcation or trifurcation of the canal
system. Occasionally the teeth may have obvious
additional roots with separation occurring in the
middle or apical third (Figs. 13.23, 13.24, 13.25
and 13.26).
Mandibular first permanent molars usually have
two roots, one mesial and one distal, with three
canals (MB, ML and distal) (see Fig. 13.27).
The distal root is often narrower in a bucco-
lingual direction but equal in mesio-distal width
when compared to the mesial roots. The distal
194 13 Anatomy and Root Canal Morphology

78 % 14 % 6%

22.5 mm

Canal
Number of Comments Author
configuration
canals
andaverage
length

Canals/Foramina
1 78 %
2 1 14 % Type I, II, III or IV
1 21 2% Access cavity must include pulp horns and lateral canals or fins.
2 2 6% Note portal of exit may not be at the radiographic apex. Vertucci

Roots 22.5 mm
1 94 %
2 6%

Fig. 13.20 Overview of mandibular permanent canine teeth

a b c

Fig. 13.21 Clinical radiographs demonstrating a two-rooted mandibular canine tooth. Note (a) preoperative view,
(b) MAF and (c) final obturation
13.10 Mandibular Molar Teeth
70 %
Number of Canal configuration and
canals/roots average length
Canals
1 70 %
121 4 % Vertucci type I, III, IV, V or VIII
2 2 1.5 %
1− 2 24 %
3 >0.5 %
Roots
1 74 %
21.0 mm
2 25 %
3 1%
Fig. 13.22 Overview of mandibular permanent first premolar teeth
root may be single with a large oval cross section
curving towards the distal at the apex. It is often
helpful to carefully examine the single root,
which may bifurcate further down the canal into
two separate foramina. Occasionally a second
disto-lingual canal may be present which curves
towards the mesial (see Fig. 13.28). Rarely three
separate distal canals may be present with the
presence of a disto-buccal, disto-lingual and
middle distal canal.
The mesial root exits the crown in a mesial
direction and then gradually curves distally in the
apical third. The mesial root will often contain
two canals (mesio-buccal and mesio-lingual).
Occasionally an additional middle mesial canal
may be present in the developmental groove
between the mesial canals. It should always be
searched for during access preparation (see
Sect. 13.14). The mesio-buccal canal, like its
maxillary counterpart, can be difficult to treat
due to its tortuous path, which can alter its
195
4% 25 %
Comments Author(s)
Access preparation oval in shape with greater extension
towards buccal and lingual.
Note that if three roots are present then buccal roots can
be very thin. Anatomy of three rooted premolar similar to
Carns & Skidmore
1st molar in terms of canal positioning.
Premolar teeth may have mesial concavity liable to strip
perforation and post treatment fracture risk is high.
direction in both the mesio-distal and bucco-
lingual dimensions. The lingual canal on the
other hand tends to be straighter in comparison.
An additional third root known as radix
entomolaris (RE) (see Figs. 13.29 and 13.30)
located disto-lingually can be seen in mandibular
molars (often mandibular first molar). An addi-
tional root on the mesio-buccal aspect is called
radix paramolaris (RP). Patients who are mon-
goloid will have a higher predisposition to this
type of additional anatomy.
An accurate diagnosis of these supernumerary
roots (RP and RE) can avoid the complication
of ‘missed canals’ during root canal treatment.
A thorough inspection of the preoperative radio-
graph with an additional second radiograph taken
from a more mesial or distal angulation (30°)
should reveal the outline of any additional root
without superimposition.
The mandibular second molar’s anatomy is
very much alike its first molar counterpart,
196 13 Anatomy and Root Canal Morphology

91 % 6% 2.5 %

Number of Canal configuration and Comments Author(s)

canals/roots average length

Canals/
Foramina
1 1 91 % Access preparation oval in shape with greater extension
2 1 6% Vertucci type I, II or IV towards buccal and lingual.
12 2.5 % Note that if three roots are present then buccal roots can
3 <0.5 % be very thin. Anatomy of three rooted premolar similar to Vertucci
1st molar in terms of canal positioning. Cleghorn et al
Roots
1 99 % 21.0 mm Premolar teeth may have mesial concavity liable to strip
2 0.3 % perforation and post treatment fracture risk is high.
3 0.1 %

Fig. 13.23 Overview of mandibular permanent second premolar teeth

although the incidence of two canals in the distal
root is much smaller. The second molar tooth
usually has two roots and three root canals, but
variations in the number of roots as well as canal
morphology are not uncommon (see Fig. 13.31).
These variations include a single canal, two
canals and five canals. Often the second molar
has roots that may be shorter and the canals can
be more curved.
The shape of the pulp chamber is usually more
oval and less triangular in the mandibular second
molar tooth. Preparation of the access should be
directed more distal to the mesial marginal ridge,
within the middle third bucco-lingually and
mesial to the transverse ridge. When four canals
are present, the access preparation will need to be
refined to a more rhomboid shape to facilitate
instrumentation.
C-shaped root canal anatomy mainly occurs
in mandibular second molars requiring early
recognition and modification of all procedures
throughout the treatment stages to ensure opti-
mal treatment can be provided. Anatomical vari-
ation resulting in canal anastomoses hinders
chemo-mechanical procedures and increases
obturation difficulties seen with such teeth (see
Sect. 13.5).
13.11 Incomplete Root
Development
Teeth with immature wide-open apices present
a unique endodontic challenge both from a
cleaning and shaping perspective and also the
final obturation phase of treatment. These large
open apices will have divergent root canal
walls that may be thin, increasing susceptibil-
ity to root fracture with overlying peri-apical
pathology that may pose problems during the
13.11 Incomplete Root Development
a b
d e
Fig. 13.24 Clinical radiographs and photograph show-
ing endodontic treatment of a mandibular first premolar
with three root canals. Note (a) preoperative view
demonstrating additional canals and (b–d) IAF and MAF
views demonstrating files placed in MB, DB and L canals.
a b
Fig. 13.25 Clinical photographs demonstrating access
preparation and refinement in lower mandibular perma-
nent first premolar with three canals. (a) Initial access
with obvious buccal canal. Ultrasonic troughing was
carried out to locate the lingual orifice (red dotted area).
cleaning stages. The apices of these types of
teeth have been described as ‘blunderbuss’
where the walls may be convergent, divergent
or parallel. The root canal may be funnel
shaped towards the apex with a much wider
197
c
f
Note MB and L canals join in apical third, (e) final
obturation showing complex anatomy and (f) access
cavity preparation showing B and L canals. Note MB and
DB canals split in middle third of canal
c
(b) Lingual canal located and (c) B and L canals following
cleaning and shaping. Note the buccal canal had a single
opening which splits into MB and DB canals in the middle
third of the canal
mesio-distal width compared to the coronal
aspect. If a root canal undergoes necrosis prior
to complete root development either due to
caries or trauma, then an open apex may
persist.
198 13 Anatomy and Root Canal Morphology

a b c

Fig. 13.26 Clinical radiographs demonstrating manage- (a) preoperative radiograph, (b) MAF and (c) final
ment of a mandibular second permanent premolar obturation (Courtesy of Dr Mark Stenhouse)
tooth with two separate roots and root canals. Note

a b c

d e

Fig. 13.27 Clinical photographs showing treatment of ML canals, (c) mid-fill, (d) warm vertical compaction
lower first molar with three roots and three canals. Note using Schilders technique and (e) final radiograph show-
(a) preoperative radiograph demonstrating very long roots ing straight line access form
(>23.00 mm), (b) IAF confirming confluence of MB and

The challenges faced when cleaning these particularly when using sodium hypochlorite
canals are the risk of apical extrusion of common solutions. Chemo-mechanical preparation tech-
irrigants with a higher propensity for accidents niques are also modified since overzealous
13.12 Dens Invaginatus
a b
d e
Fig. 13.28 Clinical radiographs and photographs
showing endodontic management of a mandibular
permanent first molar with three roots and four canals.
Note (a) preoperative view showing extensive peri-
radicular radiolucent lesion, (b) parallel bitewing
radiograph confirming supra-crestal restorative margins
preparation using large stiff files may predispose
to possible fracture in the future.
A number of techniques have been described
in the literature in regard to obturating the canal
space effectively. These can be divided broadly
into techniques without creating an apical barrier
and techniques that do so. The former include
using a customised cone technique using rolled
gutta-percha and chloroform wicking, which
allows for an impression of the unusual apical
anatomy. The risk of extrusion of material beyond
the confines of the canal is high and so a barrier
technique may be preferred.
A common method of inducing root end cal-
cification or apexification was to use long-term
calcium hydroxide dressings. The treatment has
gone out of favour due to the inherent time taken
for closure to occur, the technique sensitivity
with barrier formation not guaranteed, the fur-
ther risk of root fracture due to the material
itself and the development of newer materials
and techniques that are more predictable. A
one-step apexification procedure can be carried
199
c
f
and allowing for accurate measurement of pulp chamber
dimensions, (c) intra-oral draining sinus adjacent to the
tooth, (d) IAF, (e) mid-fill and (f) final obturation using
warm vertical compaction. Note MB and ML and DB and
DL canals join in the apical third
out with mineral trioxide aggregate using an
artificial barrier if required (see Figs. 13.32,
13.33 and 13.34).
The advantages of using MTA include non-
cytotoxicity, reduced treatment times, minimal
delay in restoring the tooth thereby reducing the
risk of fracture and secondary infections, and the
avoidance of changes in the mechanical proper-
ties of dentine due to prolonged use of calcium
hydroxide. Apexification in one visit by placing
an apical plug of MTA is a predictable and repro-
ducible clinical procedure. Use of intra-canal cal-
cium hydroxide medicament is still required in
cases where there is evidence of peri-radicular
pathology (see Fig. 13.33).
13.12 Dens Invaginatus
Tooth invaginations (dens in dente) are due to a
disturbance of epithelial and mesenchymal
interactions, which can affect the shape of the
tooth. The malformation of the teeth results
200 13 Anatomy and Root Canal Morphology

43 % 28 % 70 % 15 % 5%

22.5 mm M M D D D

Number of Canal configuration Comments Author

canals and average length

Mesial root
I 12 %
21 28 %
The pulp chamber floor will often be trapezioidal
22 43 %
rather than triangular especially if two seperate
12 8 %
distal canal orifices are located. The orifices of the
212 10 %
Type I mesial and distal canals will often lie in the mesial
3 <1 % Vertucci,
22.5 mm 2/3rd of the crown.
Distal root
1 70 % The two rooted molar often has a canal
21 15 % configuration of three canals or more.
22 5 %
12 8 %
212 2 %

Fig. 13.29 Overview of mandibular first permanent molar teeth

a b c

d e f

Fig. 13.30 Clinical radiographs demonstrating MAF, (c) mid-fill, (d) completed obturation using warm
endodontic management of a mandibular first perma- vertical compaction, (e) final post obturation view and
nent molar tooth exhibiting radix entomolaris. Note (a) (f) 12 month review
preoperative view showing additional distal root, (b)
13.12 Dens Invaginatus 201

26 % 38 % 27 % 92 % 3% 4%
22.5 mm

M M M D D D

Number of Canal configuration Comments Author

canals and average length

Mesial root
1 27 %
21 38 % If two rooted with a canal configuration of
22 26 % three canals then a trapezoidal access similar to
12 9% first mandibular molar required.
Type I
Vertucci
22.5 mm
Distal root Fusion of roots common and radiographic
1 92 % appearance of a single root may indicate the
21 3% presence of a C-shaped canal system.
22 4%
12 1%

Fig. 13.31 Overview of mandibular second permanent molar teeth

a b c d

e f g h

Fig. 13.32 Clinical radiographs showing a case demon- inter-appointment calcium hydroxide dressing (placed for
strating incomplete root development. (a) Preoperative 4 weeks), (f, g) apical 4-mm plug of MTA and (h) com-
view of tooth 21 with immature apex, (b) gutta-percha pleted root filling (note gutta-percha was used in coronal
sinus traced to peri-apex of tooth 21, (c) IAF, (d) MAF, (e) 2/3rd)
202
a b
e f
i j
Fig. 13.33 Clinical radiographs demonstrating blunder-
buss root of tooth 12 with a peri-radicular radiolucent
lesion. Note (a) preoperative view, (b) MAF confirming
working length, (c) initial calcium hydroxide dressing, (d)
4-week review, (e) second intra-canal calcium hydroxide
dressing, (f) 4-week review, (g) further 4-week review, (h)
from an infolding of the dental papilla during
tooth development. Teeth most affected are
maxillary lateral incisors. The malformation
shows a broad spectrum of morphologic
variations and frequently results in early pulp
necrosis. Root canal therapy may present severe
problems because of the complex anatomy of
the teeth.
The process takes place during tooth
development as a result of either apical prolifera-
tion of a portion of the internal enamel epithelium
13 Anatomy and Root Canal Morphology
c d
g h
k l
further 4-week review showing significant reduction in
lesion size, (i) further intra-canal medication placement
prior to obturation, (j) MTA placement in apical third, (k)
gutta-percha backfill and (l) post-operative view of com-
pleted case. Coronal third note placement of composite
resin restoration to strengthen tooth
of the enamel organ into the dental papilla or due
to retarded growth of part of the tooth germ. The
invagination may or may not communicate with
the dental pulp. The invaginations can be classi-
fied as:
1. Type 1. The enamel-lined invagination is of
the minor form and confined to the crown
only. It does not extend beyond the amelo-
cemental junction.
2. Type 2. The enamel-lined invagination invades
the root but remains confined within it as a
13.13 MB2 Canals
a b
d e
g h
Fig. 13.34 Clinical photographs showing tooth 12 MTA
apexification procedure. Note (a) intra-canal dressing of
calcium hydroxide, (b) following removal of dressing, (c)
high-power magnification showing bleeding at peri-apex
blind sac. It may communicate with the pulp.
The invagination does not breach the peri-
odontal ligament and may or may not be
dilated. If the periodontal ligament is
breached, there may be corresponding dilation
of the root or crown.
3. Type 3a. The lined invagination penetrates
through the root and opens apically or later-
ally at a foramen. There is usually no commu-
nication with the pulp, which lies compressed
within a wall around the invagination. More
often than not, the invagination is lined by
cementum and enamel.
203
c
f
of tooth, (d) placement of barrier, (e) placement of MTA,
(f) use of premeasured paper points to pack MTA in apical
third, (g) completed MTA placement and (h) gutta-percha
backfill
4. Type 3b. This is the same as type 3a with the
difference of communication with the peri-
odontal ligament. There is no communication
with the pulp (Fig. 13.35).
13.13 MB2 Canals
Maxillary molars generally have three roots and
can have three mesial canals, two distal canals
and two palatal canals. The mesio-buccal root
generally has two canals and sometimes more.
The location of the canals can vary greatly
204
a b
e f
Fig. 13.35 Clinical radiographs and photographs dem-
onstrating (a) preoperative view of tooth 22 showing dens
invaginatus, (b) gutta-percha sinus traced to peri-apex of
tooth 22, (c) MAF and (d) surgical exploration using a
papillary preservation flap. Note the buccal cortical plate
between individuals but is consistently located
mesial to or directly on a line perpendicular to the
MB1 and palatal orifices. Not all MB2 orifices
located can be negotiated to full length in all
cases (Fig. 13.36).
Negotiation of the MB2 canal is often difficult
due to a ledge of dentine that covers its orifice
(Fig. 13.37), the mesio-palatal orientation of its
orifices on the pulpal floor and its torturous
pathway that it can take with abrupt curvatures
anywhere along its length.
Initial troughing using ultrasonics from the
MB1 canal towards the mesio-palatal aspect
along the developmental groove (if present) may
allow localisation of any additional canal
entrances (Figs. 13.37 and 13.38). This proce-
dure requires a shifting of the access cavity
mesially in some cases. Troughing may be
necessary to a depth of 0.5–3 mm.
Often when inspecting the MB isthmus line
in a mesio-palatal direction, the use of a DG16
13 Anatomy and Root Canal Morphology
c d
g
has been breached revealing the unusual anatomy of the
root surface of tooth 22. (e) Coronal gutta-percha root
filling (f) and (g) MTA root end filling used to obturate the
apical defect
Endodontic Explorer probe may be useful in
determining whether any ‘catch’ in the dentine
is present. This will usually indicate the location
of the MB2 orifice (Fig. 13.38c). Once the
orifice is located, canal preparation can proceed
with selected instrumentation technique. Care
must be taken when preparing the MB2 canal
due to the risk of strip perforation and so
instrument sizes may need to be adjusted
accordingly.
When assessing for the presence of second
canals in the mesio-buccal root, placement of
endodontic files in the canal and taking a disto-
angular radiograph may offer some insight. If
the file appears to be off-centre within the root,
there is usually another canal to be found. If the
file appears off-centre apically, then the canals
are likely to be separate in the apical portion. If
the file appears centred apically but off-centre
coronally, then it is likely that the two canals
merge in the apical portion of the tooth.
13.13 MB2 Canals 205

MB1
MB2 MB1 MB2

P
DB
P DB
P

DB MB1
MB2

Number of canals Canal configuration Comments Author(s)

and average length

45 % one single canal Weine Type I Kulild and Peters

The mesio-buccal root almost always has some apical
system
curvature, sometimes as great as 90° or more.
Weine Type II Cleghorn, Christie & Dong
55 % two or more } An overhang of dentine frequently obscures the MB2
canals Weine Type III orifice necessitating removal of the overhang before Vertucci
the orifice can be identified.
Weine Type IV
Variations from the three-sided triangular form may
Average buccal root be made when searching for the MB2 by adding a
length 19mm fourth short side, if necessary, forming a trapezoid.

Fig. 13.36 Overview of maxillary permanent molars and the MB2 canal system

a b c d
P
P P P

M B2
DB DB DB
DB
M B1 M B1 M B1
M B1

Fig. 13.37 Diagrams showing access cavity of an upper
first permanent molar tooth and refinement to locate the
MB2 canal. Note (a) the mesial wall of the access cavity
is refined to create a trapezoid shape, enabling location of
additional MB canals if present; (b) ultrasonic troughing
is carried out from the MB1 canal towards the mesial; (c)
care must be taken when troughing this area for risk of
perforation and (d) completed refinement with MB2 ori-
fice located

The mesio-buccal root is often described as a Common canal configurations encountered in

ribbon of tissue that may end in 1, 2 or 3 separate
foramina. The presence of three MB canals is
often rare, but careful inspection mesial to a line
joining the MB and P canals is essential to ensure
successful root canal therapy of this tooth
(Fig. 13.39).
mesio-buccal roots of maxillary first molars
include Vertucci types I, II, IV and V, although
any configuration may be possible (Figs. 13.40
and 13.41).
Frequent failure associated with upper maxillary
molars may often be attributed to the inability to
206
a MB1
DB
c d
Fig. 13.38 Clinical photographs showing identification,
preparation and location of the MB2 canal. Note (a) pre-
operative view following initial access cavity preparation,
(b) ledge of dentine that often obscures the MB2 canal
locate the MB2 canal. The use of the dental operat-
ing microscope is an indispensable tool when try-
ing to locate additional anatomy in these teeth.
Additional scheduling of adequate chair time to
facilitate canal localisation has also been shown to
dramatically increase the chances of MB2 canal
location. When treating the MB2 canal system, the
clinician must also be aware of the greater risk of
either iatrogenic perforations when searching for
such canals, the risk of strip perforations during
preparation and file separation particularly if the
canal merges with the MB1.
13.14 Middle Mesial Canals
A middle mesial canal is sometimes present
between the developmental groove that occurs
between the mesio-buccal and mesio-lingual
13 Anatomy and Root Canal Morphology
b
MB2
entrance, (c) initial sticky point of entry to MB2 canal ori-
fice and (d) following careful negotiation and canal prepa-
ration of the MB2 canal
canal in lower mandibular permanent molars.
A bur is used to remove any dentinal overhangs
from the mesial axial wall, which would prevent
direct visualisation and access to this groove.
Under appropriate magnification and illumina-
tion, the groove between the MB and ML ori-
fices should be carefully explored. If an orifice,
depression of point of sticking on entry with a
sharp endodontic explorer, is noted, then the
groove should be carefully troughed using ultra-
sonics. The point of entry is then carefully
negotiated using small stainless steel files (08,
10K files) to see whether the canal is a separate
entity or if it merges with one of the other
canals. Care must be taken when using ultrason-
ics due to the risk of iatrogenic perforation in
this area, and preparations should be directed
against the danger zones such as the furcation
area (Fig. 13.42).
13.15 C-Shaped Canal Systems
a b
c d
Fig. 13.39 Clinical photographs and radiograph show-
ing a permanent maxillary first molar tooth with three MB
root canals. (a) IAF in MB3, (b) IAF in MB2 and MB3,
(c) completed preparation of MB root showing MB1,
13.15 C-Shaped Canal Systems
The C-shaped canal configuration has been
mostly reported in mandibular second molars
although its occurrence is not limited to. They
have been named accordingly due to the cross-
sectional morphology of the root and root
canal. Instead of having discrete separate root
canal orifices and canals, the pulp chamber
may be of a C shape with a single ribbon-
shaped orifice with a 180° arc or more. Below
the orifice level, the roots of C-shaped canal
system may harbour a multitude of anatomical
variations. They can be broadly classified as
either having a single ribbon-like C-shaped
canal system from orifice to apex or three or
more distinct canals that communicate with
each other through fins or webs throughout the
entire root.
207
MB2 and MB3 and (d) final post-operative radiograph
demonstrating five root canals obturated. Note MB2 and
MB3 confluent in apical third
Once recognised, the C-shaped canal pro-
vides unique endodontic challenges to the
clinician with respect to both chemo-mechanical
debridement and obturation (Fig. 13.43).
The preoperative awareness of the presence
of a C-shaped canal configuration can be use-
ful from a treatment perspective. Common
characteristics include the presence of a single-
rooted tooth or as two distinct roots with a
communication. The access cavity may reveal
the unusual pulp chamber anatomy and on
occasion following initial preparation stages
(Fig. 13.44).
During the preparation stages, it may be
obvious that a C-shaped canal system exists and
the passing of an endodontic instrument should
occur throughout the ‘C’, indicating that this is
throughout the entirety of the root canal sys-
tem. Care should be taken when instrumenting
208
a b
c d
Fig. 13.40 Clinical photographs and radiographs show-
ing upper permanent maxillary molar teeth with MB2
canals. Note (a) MB2 only partially negotiated, (b)
the isthmuses since iatrogenic damage with
larger instruments may be possible due to the
inherent thinness of walls in this area.
Alternative cleaning techniques will also need
to be employed due to the unusual anatomy
with fins and webs communicating throughout.
Ultrasonic irrigation or sonic devices must be
utilised in order to ensure that non-instrumented
walls (for which there will be a higher predis-
position) are effectively cleaned. On occasion
the mesio-lingual canal may be separate to the
distal and mesio-buccal which merge some-
where along the root length. Care must be taken
since the risk of over-instrumentation is high
with canals sometimes exiting at one anatomi-
cal apex.
Obturation techniques also require modi-
fication when dealing with this type of anat-
omy. Due to the isthmuses, communications
13 Anatomy and Root Canal Morphology
Vertucci type V MB canal configuration, (c) Vertucci type
IV MB canal configuration and (d) Vertucci type II MB
canal configuration
and presence of fins and webs, cold lateral
compaction is probably not ideal when
attempting to three-dimensionally create a
seal. The applications of thermoplasticised
gutta-percha techniques using a suitable sealer
are recommended.
From a restorative point of view, the clinician
must bear in mind that post placement if desired
may be fraught with danger. Placement of posts
in the mesio-buccal and lingual canals may result
in perforation. Risk of root perforation is also
higher due to thinner walls of the C-shaped
canals.
The patient should be warned about the long-
term prognosis of C-shaped canals and that
despite adherence to sound principles of
chemo-mechanical preparation, obturation and
restoration techniques, these teeth may be subject
to failure (Fig. 13.45).
13.15 C-Shaped Canal Systems 209

a b

c d

Fig. 13.41 Clinical radiographs showing upper perma- MB canal configuration in the first maxillary molar and
nent maxillary molar teeth with MB2 canals. Note (a) Vertucci type II in the second maxillary molar tooth in the
Vertucci type VIII MB canal configuration, (b, c) Vertucci same patient
type IV MB canal configuration and (d) Vertucci type II

a b c

MB ML MB ML MB ML
MM

d e f

MM

MB ML

Fig. 13.42 Diagrams and clinical radiographs showing uncover orifice of (c) middle mesial canal (MM) location;
(a) isthmus between mesio-buccal (MB) and mesio- (d) preoperative view of tooth 46; (e) MB, ML and MM;
lingual (ML) canals; (b) troughing of this area using and (f) final obturation showing confluence of three mesial
ultrasonics to remove pulpal tissue remnants and also canals
210
a b
d e
Fig. 13.43 Modified classification of C-shaped canals
described by Fan et al. 2004. (a) Category I, the shape was
an interrupted ‘C’ with no separation or division. (b)
Category II, the canal shape resembles a semicolon result-
ing from a discontinuation of the ‘C’ outline. (c and d)
a b
Fig. 13.44 Clinical photographs showing (a) C-shaped
canal configuration in a lower permanent mandibular sec-
ond molar. Note (b) irregular C-shaped canal system
13 Anatomy and Root Canal Morphology
c
f
Category III, 2 or 3 separate canals. (e) Category IV, only
one round or oval canal in the cross section and (f) no
canal lumen could be observed (which is usually seen near
the apex)
(black) and furcal danger area (red) where strip perfora-
tion can occur if care is not taken during the preparation
technique
References
a b
d e
Fig. 13.45 Diagram (a) internal coronal pulp anatomy
and radiographs series showing (b) preoperative view of
tooth 47 distal bridge abutment with single conical root
form, (c) IAF confirming C-shaped anatomy, (d) mid-fill
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 Rubber Dam
14

Summary
Rubber dam is recommended for all nonsurgical endodontic procedures.
The literature suggests that rubber dam is not routine practice for many
dentists, and many unfounded reasons have been cited.

Clinical Relevance tion, prevent inhalation and ingestion of instru-

Rubber dam is essential not only for providing
an aseptic technique, which is the premise of
root canal treatment, but also from a safety and
medicolegal perspective. Failure to use rubber
dam has been shown to indirectly affect out-
come by choice of irrigant used. Numerous case
reports have been described in the literature
demonstrating ingestion or inhalation of instru-
ments when dam has not been used. From a
medicolegal standpoint when root canal treat-
ment is undertaken and mishap occurs, the case
is indefensible when rubber dam has not been
used as a preventive measure. If rubber dam
cannot be placed or tolerated by the patient, then
perhaps other alternative treatments should be
provided.
14.1 Overview of Rubber Dam
Usage in Endodontics
Root canal treatment procedures should be car-
ried out only when the tooth is isolated by rubber
dam to prevent salivary and bacterial contamina-
ments and prevent irrigating solutions escaping
into the oral cavity [1]. Tooth isolation using the
dental dam is the standard of care; it is integral
and essential for any nonsurgical endodontic
treatment [2]. However, not all dentists are accus-
tomed to or routinely use a dental dam when
embarking on nonsurgical root canal treatment.
Surveys taken in several countries have con-
firmed, time after time, that rubber dam usage
when performing root canal treatment is not the
standard of care [3–6].
Many reasons have been cited in the literature
as to why this simple technique has not been rou-
tinely advocated including cost of equipment and
material, difficulty in use, time required for appli-
cation and lack of patient acceptance [7, 8].
These reasons tend to be unfounded and in fact
patients themselves tend to be more appreciative
as to treatment under rubber dam providing satis-
faction for most [9].
Most dentists are educated in rubber dam
use in dental school, but there is often disparity
between what is taught for endodontic proce-
dures as an undergraduate and what is practised

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 213
DOI 10.1007/978-3-319-15591-3_14, © Springer International Publishing Switzerland 2015
214 14 Rubber Dam

having graduated. One study even demon-
strated that despite the majority of question-
naire respondents having postgraduate training
in the last 2 years, only a minority used rubber
dam routinely for endodontic treatment [10]. It
has been suggested that predoctoral dental edu-
cators need to look for opportunities for
improvement to reduce the discrepancy
between what is taught and the general practice
of dentistry [11].
It has been shown without doubt that one of
the major benefits of using rubber dam is to pro-
vide protection to the patients’ oropharynx by
preventing inhalation or ingestion of endodontic
instruments or materials during treatment proce-
dures [12–14] (Fig. 14.1). From a medicolegal
standpoint, dental defence organisations have
reported that any injury inflicted whilst not using
a rubber dam during root treatment is deemed
‘indefensible’ [14].
Rubber dam usage during nonsurgical root
canal treatment confers several advantages to
both clinician and patient (see Table 14.1).
A modified disinfection protocol can be used
following assembly of rubber dam using a
combination of 30 % hydrogen peroxide, 5 or
10 % iodine tincture, 1–5 % sodium hypochlorite
solution and 0.2 % chlorhexidine solution to
ensure the field is decontaminated prior to access
preparation [15].
It has been recommended that seepage of fluid
may be prevented by using a paste such as a mix-
ture of zinc oxide powder and denture adhesive
Table 14.1 Advantages of using rubber dam
Medicolegal considerations – the prevention of
ingestion or inhalation of endodontic instruments or
materials
Enhanced patient safety – prevention of ingestion of
harmful endodontic materials such as irrigation
solutions. Protection of soft tissues such as lips, cheeks
and tongue from trauma
Aseptic working environment – prevention of salivary
contamination of the tooth resulting in microbial
contamination of root canal in vital cases and further
infections in non-vital cases
Improved access – rubber dam provides visual contrast
which is helpful when working under a dental operating
microscope or magnification such as dental loupes
Improved patient comfort – most patients find the use
of rubber dam a comfort since they know that fluids are
prevented from accumulating in the mouth and the
tongue can move freely without risk of injury
Reduction of aerosol contamination – results in less
cross contamination for both patient and clinician/
dental assistant

Fig. 14.1 Abdominal

radiograph taken in an
accident and emergency
department after a patient
had swallowed an
endodontic instrument.
The patient had been
undergoing root canal
treatment without the use
of rubber dam resulting in
this unacceptable outcome.
The patient was referred to
the Oral Maxillofacial
department and following
appropriate investigations
the instrument was
retrieved using endoscopy
by the Gastro-enterology
team (Courtesy of Dr Mark
Singh Oral & Maxillofacial
consultant)
14.2 Rubber Dam Armamentarium 215

between the tooth and the dam [16]. A commer-
cially available cellulose/zinc oxide material
(OraSeal, Ultradent Products, Inc., South Jordan,
UT, USA), which forms a firm gel on contact
with saliva, is able to patch small leaks
conveniently.
There are numerous case reports of patients
who develop immediate- or delayed-type allergic
reactions following the use of latex rubber dam
[17]. The patient must be questioned as to any
possible latex allergy in their medical history
questionnaire prior to commencement of treat-
ment. In cases where there is suspicion of latex
allergy, non-latex rubber dam and gloves are
recommended.
14.2 Rubber Dam
Armamentarium
Rubber dam
Various rubber dams are available in pre-cut
squares of various colours (green, black and pur-
ple) and thickness (such as light, medium, heavy
and extra heavy). Thin rubber dam (light) is
much easier to apply but is more subject to tear-
ing. Conversely thicker dam (heavier) is more
difficult to pass through interproximal contacts
but more resistant to tearing. The rubber dam
should be stored in a cool dry environment to
retain its elasticity, preventing the possibility of
tearing when stretched.
Rubber dam clamps
The rubber dam clamp helps anchor the rub-
ber dam to the tooth. Numerous rubber dam
clamps are available depending on the manu-
facturer. Essentially clamps can be classified as
either winged or wingless, consisting of a set
of jaws (serrated or non-serrated) connected to
a bow. Clamps come in various sizes and are
selected according to tooth selection (anterior,
canine/premolar and molar), operator prefer-
ence and application technique to be employed
(clamp first, bow first or anterior tooth). The
selected clamp should have a four-point con-
tact on the tooth, avoiding the gingivae if pos-
sible, thereby minimising trauma (Figs. 14.2
and 14.3).
Rubber dam napkin
This is used primarily for patient comfort. It
reduces the potential for skin irritation that may
be caused by contact of rubber dam directly to
skin and also helps absorb saliva that may have
leaked from the oral cavity.

a Winged clamp b Wingless clamp

2 2

4
4
1 3 5 3
5

4
1 4

Fig. 14.2 Diagrams representing anatomy of a (a) winged and (b) wingless rubber dam clamp. Note (1) clasp arm
consisting of lingual and buccal wings, (2) distal bow, (3) jaws, (4) contact points and (5) perforation
216 14 Rubber Dam

a b

c d

Fig. 14.3 Clinical photographs showing various clamps used for (a, b) the posterior teeth, (c) anterior teeth and (d)
premolars and canines

Clamp forceps acceptance and comfort and also operator visi-

The purpose of the clamp forceps is to provide
anchorage for the selected clamp when placing,
adjusting and removing the clamp to and from
the tooth.
Rubber dam punch
The function of the punch is to make the nec-
essary holes in the rubber dam corresponding to
the number of teeth to be isolated. The author
prefers to use a single-tooth isolation method
where one hole is made in the centre of the rubber
dam for the clamp. Where a split dam technique
is used or isolation of the anterior teeth, two or
more holes can be made to help retention of the
dam. The punch is designed to create holes of
various diameters according to the size of the
tooth and clamp that is selected. The author also
punches a hole in one corner of the dam, which
aids the operator when reassembling the rubber
dam and frame from time to time.
Rubber dam frames
A rubber dam frame is used to retract the
edges of the rubber dam, improving patient
bility. Frames are either plastic or metal and
secured in place by retaining spikes (Figs. 14.4
and 14.5).
Floss
A 10-in. piece of floss can be used to attach to
the retainer and threaded through both holes and
wrapped around the bow to prevent inhalation or
ingestion of the clamp should it break. Waxed
floss is also useful for interproximal contacts to
ensure that the rubber dam is carried through the
contact, ensuring maximum coverage and pre-
vention of salivary contamination (Fig. 14.6).
Wedgets/OraSeal
Special elastic wires of various thicknesses
are available to be placed through the interproxi-
mal contact to enhance rubber dam isolation such
as the anterior teeth. OraSeal caulking can be
used to seal around the isolated tooth optimising
isolation, preventing ingress of saliva into the
operating field and also preventing egress of end-
odontic medicaments and irrigants, which can be
irritating to the patient.
14.3 Clamp First Technique 217

a b c

d e f

Fig. 14.4 Clinical photographs showing (a) rubber dam frames (metal and plastic), (b) rubber dam forceps and hole
punch, (c) rubber dam (latex-free and latex), (d) wedgets, (e) OraSeal caulking and (f) patient napkin

a b c

d e f

Fig. 14.5 Clinical photographs demonstrating (a) rubber reassembly, (c) typical punched dam, (d) rubber dam
dam punch, (b) punch used to make a hole in the corner of clamps, (e) clamp forceps and (f) clamp forceps attached
the dam for easy reorientation during dismantling and to selected anterior clamp. Note ligated floss

14.3 Clamp First Technique This technique involves placing the clamp on
the tooth first. The clamp is ligated as described
Note that the rubber dam has been pre-prepared earlier. Winged or wingless clamps can be
with corresponding holes according to isolation selected, but the latter will make it much easier to
of the tooth or teeth. stretch the dam over the clamp without risk of
218
a b
Fig. 14.6 Clinical photographs showing (a) incorrect and (b) correct ligation of the clamp to ensure if breakage occurs,
then the clamp is easily retrievable
tearing. Once the rubber dam and frame is in
place, the area should be disinfected using a com-
bination of sodium hypochlorite and chlorhexi-
dine solution.
A clamp is selected with a piece of floss
attached, to prevent aspiration, and placed
directly on the tooth using the clamp forceps
(Fig. 14.7a). The clamp is passed over the
bulbosity of the tooth to the level of the gingivae.
Care is taken to ensure that the clamp rests on the
tooth, not the gum, if possible to prevent trauma
to the soft tissues. The clamp is checked to ensure
that it is stable (Fig. 14.7b).
The next step is to carefully pass the rubber
dam over the clamp. The rubber dam is first
pulled over the bow of the clamp and then over
the winged/wingless buccal and lingual aspects
(Fig. 14.7c). Finally the dam is pushed into the
proximal spaces using floss. The periphery of the
tooth can be sealed using OraSeal caulking to
prevent salivary seepage into the tooth during the
procedure (Fig. 14.8e).
14.4 Bow First Technique
Note that the rubber dam has been pre-prepared
with corresponding holes according to isolation
of the tooth or teeth.
14 Rubber Dam
The bow technique can be applied without the
aid of a dental assistant. The clamp forceps are
first attached to the corresponding clamp. The
rubber dam sheet is then pulled over the bow of
the clamp and the rubber gathered prior to clamp
attachment in the mouth. The clamp is then
attached to the tooth. Once the clamp is seated in
the correct position, the rubber dam is pulled over
the buccal and lingual wings, bringing the dam
into its correct position, sealing the selected tooth
(Fig. 14.8).
14.5 Anterior Teeth Technique
Note that the rubber dam has been pre-prepared
with corresponding holes according to isolation
of the tooth or teeth.
In this situation the clamp to be used is
selected and tried in the mouth first to check posi-
tioning, fit and stability. Once satisfied, the rub-
ber dam is carried to the mouth and the punched
hole is spread wide with the index fingers. The
rubber is then pulled down around the tooth or
teeth. The clamp preassembled with clamp for-
ceps is placed over the isolated tooth. This tech-
nique is suited to the anterior teeth when an
anterior cervical clamp with two bows (Fig. 14.9)
is selected for isolation.
14.5 Anterior Teeth Technique 219

a b

c d

Fig. 14.7 Clinical photographs showing (a) clamp trans- passed over bow first and then the lingual/buccal aspects
ferred to the tooth to be treated using clamp forceps, (b) of clamp and (d) frame attached to dam ready for access
clamp in position and checked for stability, (c) rubber dam preparation

a b c

d e f

Fig. 14.8 Clinical photographs demonstrating the bow first (c) seating the dam over the corresponding clamp. (d) A flat
technique. (a) The clamp and rubber dam attached to the plastic instrument can be useful when trying to seat the rub-
bow is transferred to the tooth, and (b) once the clamp is ber dam over the wings of the clamp, and (e, f) caulking
attached and in position, the dam can be gathered up before being placed around the tooth to complete the seal
220
a b
c d
Fig. 14.9 Clinical photographs demonstrating the ante-
rior teeth technique. (a, b) Rubber dam is stretched over
the anterior front teeth, (c) the double-bow anterior clamp
14.6 Split/Slit Dam Technique
This technique is particularly useful in cases
which are difficult to isolate due to situations
such as a broken down teeth, patients with fixed
orthodontic appliances, cases where the fixed
prosthesis is dismantled making clamp attach-
ment difficult or prosthodontic bridges with lack
of interproximal space. One or both of the neigh-
bouring teeth can be used to attach the rubber
dam using clamps or a combination of clamps
and wedgets. Three holes can be placed in the
rubber dam, anchoring the dam to the posterior
tooth via a clamp and anteriorly by a wedget.
Alternatively the holes created in the dam are
linked together by either making a third hole
between the two or using scissors to remove the
rubber between the holes. This technique can be
prone to more leakage around the tooth being
treated, requiring additional measures to seal any
perforations evident (Fig. 14.10).
14 Rubber Dam
is positioned using the clamp forceps, and (d) the tissue
napkin and frame are attached. Note the patient can
breathe easily from the nose
14.7 Latex Allergy
Non-latex rubber dam is available for use with
patients who have known or suspected allergy to
latex. The non-latex silicone rubber dam tends to
be much more tear resistant due to its increased
flexibility. The author finds that selection of the
smallest hole possible on the hole punch is suit-
able for ensuring that the tightest contact between
the dam and the tooth is achieved when placed.
Clinical Hints and Tips
• Holes punched in the rubber dam too close
together results in leakage. Holes placed
too far apart results in the dam bunching
up. Placement of holes should be in the
centre. If placed too low on the dam, the
patient’s nose or eyes may be covered. If
the hole is placed too high on the dam, then
this will result in the dam not extending
over the upper lip.
References
a b
c d
Fig. 14.10 Clinical photographs demonstrating (a, b)
tooth 14 which had a post and core restoration dismantled
prior to nonsurgical endodontic re-treatment (c), and (d)
• Holes should be punched clearly without
any ragged edges; otherwise there is risk of
the dam tearing when stretched.
• Clamp should be selected according to
tooth position in the mouth. For example,
the anterior teeth are easily isolated with a
double-bow clamp. A second or third pos-
terior molar, where access is limited, would
be suitable to a wingless clamp using the
bow technique.
• Four-point contact should be present when
clamp is placed on the tooth and the clamp
should be stable when pushed with the
fingers.
• All clamps should be ligated with dental
floss to prevent accidental aspiration/
ingestion.
• Use of the rubber dam napkin is not only
important for patient comfort but also to
reduce skin irritation.
221
shows the use of a split dam technique whereby the poste-
rior tooth is used for rubber dam anchorage using a clamp
and the anterior tooth stabilised with a wedget
References
1. Quality Guidelines for endodontic treatment: consen-
sus report of the European Society of Endodontology.
Int Endod J. 2006;39:925.
2. American Association of Endodontists. Guidelines
and position statements. Dental Dams. 2010.
3. British Endodontic Society. The practice of endodon-
tics by different groups of dentists in England. Int
Endod J. 1983;16:185–91.
4. Whitworth JM, Seccombe GV, Shoker K, Steele
JG. Use of rubber dam and irrigant selection in UK
general dental practice. Int Endod J. 2000;33:435–41.
5. Hommez GM, Braem M, De Moor RI. Root canal treat-
ment performed by Flemish dentists. Part I. Cleaning
and shaping. Int Endod J. 2003;36:166–73.
6. Vadhera N, Makkar S, Kumar R, Aggarwal A, Pasricha
S. Practice profile among endodontists in India: a
nationwide questionnaire survey. Indian J Oral Sci.
2012;3:90–3.
7. Saunders WP, Chestnutt IG, Saunders EM. Factors
influencing the diagnosis and management of teeth
with pulpal and periradicular disease by general dental
practitioners. Br Dent J. 1999;187:548–54.
222
8. Koshy S, Chandler NP. Use of rubber dam and its
association with other endodontic procedures in New
Zealand. N Z Dent J. 2002;98:12–6.
9. Kapitan M, Hodacova L, Jagelska J, Kaplan J,
Ivancakova R, Sustova Z. The attitude of Czech dental
patients to the use of rubber dam. Health Expect.
2013. doi:10.1111/hex.12102.
10. Palmer NAO, Ahmed M, Grieveson B. An investiga-
tion of current endodontic practice and training needs
in primary care in the north west of England. Br Dent
J. 2009;206:E22.
11. Hill EE, Rubel BS. Do dental educators need to
improve their approach to teaching rubber dam use?
J Dent Educ. 2008;72:1177–81.
12. Susini G, Pommel L, Camps J. Accidental ingestion
and aspiration of root canal instruments and other
14 Rubber Dam
dental foreign bodies in a French population. Int
Endod J. 2007;40(8):585–9.
13. Israel HA, Leban SG. Aspiration of an endodontic
instrument. J Endod. 1984;10(9):452–4.
14. Singh M, Pepper T, Kiani H, Paul R. Letters to the
editor. Lost file? Br Dent J. 2008;12:638–9.
15. Moller ÅJR, editor. Microbiological examination of
root canals, and peri-apical tissues of human teeth
methodological studies [master’s thesis]. Lund:
University of Lund; 1966.
16. Weisman MI. Remedy for rubber dam leakage prob-
lems. J Endod. 1991;17:88–9.
17. Chin SM, Ferguson JW, Bajurnows T. Latex allergy in
dentistry. Review and report of case presenting as a
serious reaction to latex dental dam. Aust Dent J.
2004;49(3):146–8.
 Analgesics, Anaesthetics,
Anxiolytics 15
and Glucocorticosteroids Used
in Endodontics

Summary
Patients are often apprehensive when undergoing root canal treatment and
pain is often taken as synonymous with these procedures. Pain manage-
ment involves correct diagnosis, appropriate dental treatment and adjunc-
tive drug therapy where indicated. Endodontic pain will be of inflammatory
origin and nonsteroidal anti-inflammatory drugs are the preferred choice
for relief. Paracetamol provides effective analgesia with limited anti-
inflammatory action. Effective pain management strategies are discussed
for pre-, peri- and post-operative endodontic procedures.

Clinical Relevance treatment itself is painful [1]. These factors make

Effective pain management is a critical skill in
order to attain patient satisfaction and trust when
undergoing invasive root canal treatments. From a
patients’ point of view, this aspect of treatment is
often judged as more important than the challeng-
ing clinical practice of root canal itself. Several
methods of pain relief are discussed, based on sci-
entific evidence that will aim to provide adequate
relief for patients experiencing pain and avoiding
preconceived misconceptions that can be avoided
by the use of modern pharmacology.
15.1 Overview of Analgesics,
Anaesthetics, Anxiolytics
and Glucocorticosteroids
Used in Endodontics
Many patients frequently surmise root canal treat-
ment as a painful procedure as a result of previous
painful experiences and the perception that the
pain management more challenging with the clini-
cian not only trying to provide effective pharmaco-
logical relief but also removing preconceived ideas
that provide barriers in the way of effective pain
management strategies. The first signs of irrevers-
ible pulpal damage may be a patient presenting
with a ‘hot’ tooth with spontaneous moderate to
severe pain. The association of a painful experi-
ence is reinforced in the patients’ mind and proves
to be a further challenge to the clinician due to dif-
ficulties in achieving adequate pulpal anaesthesia.
Effective strategies for the management of pain
in the dental practice should follow the ‘3D prin-
ciple’ of diagnosis, dental treatment and drugs.
The first and most important step is to diagnose
the condition correctly identifying the cause of
the pain. Secondly appropriate dental treatment
should then be undertaken to remove the cause
providing rapid resolution of the symptoms.
Finally drugs can be used as an adjunctive therapy
to provide additional relief [2, 3].

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 223
DOI 10.1007/978-3-319-15591-3_15, © Springer International Publishing Switzerland 2015
224 15 Analgesics, Anaesthetics, Anxiolytics and Glucocorticosteroids Used in Endodontics
Drugs available for the acute pain manage-
ment can be classified into two major groups:
the non-narcotic analgesics (e.g. nonsteroi-
dal anti-inflammatory drugs (NSAIDs) and
paracetamol) and opioids (narcotics). Aspirin,
ibuprofen and paracetamol and the most com-
mon ‘over-the-counter’ non-narcotic analgesics
are commonly used for managing dental pain.
Three principle pharmacological approaches for
the management of posttreatment endodontic
pain include:
(a) Drugs that block inflammatory mediators
that sensitise or activate pulpal nociceptors
(sensory neurones that respond to pain)
(b) Drugs that block the propagation of impulses
along the peripheral nerves
(c) Drugs that block central mechanisms of pain
perception and hyperalgesia
Pain management strategies during root canal
treatment can be based on one or a combination
of these mechanisms [4, 5].
Pre-emptive analgesia is the term used to
describe the administration of an NSAID before
the onset of pain (preventive measure) to sup-
press the release of inflammatory mediators (par-
ticularly prostaglandins), which contribute to the
sensitisation of peripheral nociceptors [6, 7].
NSAIDs have been the traditional treatment
for moderate endodontic pain management.
Their mode of action is primarily through the
inhibition of cyclooxygenase (COX) enzymes 1
and 2. COX-1 is expressed throughout the body
and has a protective role in the stomach mucosa,
kidney function and platelet action. COX-2 is
induced by various endogenous compounds such
as cytokines and endotoxins in inflammatory
cells and is responsible for elevated prostaglan-
din production during inflammation [8–10].
Patients unable to tolerate NSAIDs include those
suffering from gastrointestinal disorders (ulcers,
ulcerative colitis), asthmatics or hypertensive
patients (due to direct interactions with antihy-
pertensive drugs or indirect effects due to the
renal impairment) [11].
An alternative approach to treating a small
proportion of patients who still report pain after
administration of either an NSAID or paracetamol
alone includes co-prescribing both drugs concur-
rently or combining either the NSAID or
paracetamol with an opioid [12–14].
Corticosteroids (glucocorticosteroids) inhibit
immune and inflammatory responses decreasing
cytokine production, vasoactive and chemoat-
tractive factors, secretion of lipolytic and proteo-
lytic enzymes, extravasation of leucocytes to
areas of tissue injury and fibrosis [15]. Several
double-blind, random, prospective, placebo-
controlled studies in endodontics have demon-
strated the administration of adjunctive steroids
being beneficial in reducing endodontic post-
treatment pain [16–22]. Caution is urged when
considering the use of steroids particularly in
view of any medical history that may warrant
contraindication [21].
Local anaesthesia is the mainstay of pain con-
trol techniques used in dentistry since its incep-
tion in 1859 by Albert Niemann who refined the
coca extract to the pure alkaloid form and naming
this drug ‘cocaine’. Today there is a spectrum of
local anaesthetics that permit pain control to be
tailored to the specific needs of the patient includ-
ing short-, intermediate- and long-acting drugs
[22]. Two proposed theories for the action of
local anaesthetics include the non-specific mem-
brane expansion theory and specific binding the-
ory. In the former, swelling of the nerve membrane
occurs from absorption of the lipophilic local
anaesthetic resulting in inhibition of sodium into
the cells, preventing nerve depolarisation and
thus firing. The latter, now widely accepted,
infers that specific binding receptors on the
sodium channels are present for local anaesthetic
agents to interact regulating influx of ions affect-
ing depolarisation.
The primary local anaesthetics used in end-
odontics today are the amide-type local anaes-
thetics which have varying degrees of duration
that can be selected according to specific
patient and procedure needs (Tables 15.1 and
15.2) [23].
The availability of a variety of local anaes-
thetic agents enables the clinician to select an
15.1 Overview of Analgesics, Anaesthetics, Anxiolytics and Glucocorticosteroids Used in Endodontics 225

anaesthetic that possesses properties such as 3 to 5 h) and are commonly used for endodontic
time of onset and duration, haemostatic con- procedures [24–30].
trol and degree of cardiac side effects that are Articaine has become a very popular local
appropriate for each individual patient and for anaesthetic in recent times with claims of superi-
specific dental procedures. Lidocaine, mepiva- ority over existing anaesthetic agents in cases
caine and prilocaine, combined with a vasocon- such as a difficult ‘hot pulps’ where extirpation
strictor, provide reliable and profound pulpal requiring profound anaesthesia has not been
anaesthesia for approximately 60 min (with a achieved despite any clear evidence in the litera-
duration of soft-tissue anaesthesia lasting from ture. Anecdotal evidence regarding a greater risk
of long-lasting paraesthesia, especially the lin-
Table 15.1 Currently available amide-type dental local gual nerve, when this drug is administered as a
anaesthetic formulations regional block, has also been reported [31–35].
Local Amount (mg) in Long-acting drugs such as bupivacaine have
anaesthetic % Vasoconstrictor 1.8 ml capsule been shown to be useful in reducing or prevent-
Articaine 4 1:100,000 72 ing post-operative discomfort in conjunction
adrenaline with orally administered nonsteroidal anti-
Bupivacaine 0.5 1:200,000 9 inflammatory drugs [36, 37].
adrenaline
Anaesthetic failure after an inferior alveolar
Lidocaine 2 1:100,000 36
adrenaline nerve block may be caused by several factors
2 1:50,000 36 including collateral innervation [38–40], acces-
adrenaline sory innervation such as the mylohyoid nerve in
2 No 36 mandibular posterior molar teeth [41, 42],
vasoconstrictor inflammation-induced acidosis causing ‘ion trap-
Mepivacaine 2 1:20,000 36 ping’ of local anaesthesia [43], pulpal sensitised
levonordefrin
nociceptors increasing anaesthetic resistance,
3 No 54
vasoconstrictor central sensitisation [44] and psychological fac-
Prilocaine 4 1:200,000 72 tors [45–47].
adrenaline The use of topical anaesthesia has been investi-
4 No 72 gated in numerous studies and despite no reports of
vasoconstrictor significance influence on pain during either needle

Table 15.2 Currently available amide-type dental local anaesthetic formulations

Local anaesthetic % Vasoconstrictor Expected duration

Brand name Pulpal (min) Soft tissue (h)
Articaine 4 1:100,000 adrenaline 60 3–5
Ubistesin™
Septocaine®
Bupivacaine 0.5 1:200,000 adrenaline 90–180 3–12
Marcaine®
Lidocaine 2 1:100,000 adrenaline 60 3–5
Xylocaine® 2 1:50,000 adrenaline 60 3–5
2 Plain no vasoconstrictor 10 1–2
Mepivacaine 2 1:20,000 levonordefrin 60 3–5
Mepivastesin™ 3 Plain no vasoconstrictor 20–40 2–3
Prilocaine 4 1:200,000 adrenaline 60–90 3–8
Citanest® 4 Plain no vasoconstrictor 5–60 2–3
226 15 Analgesics, Anaesthetics, Anxiolytics and Glucocorticosteroids Used in Endodontics
penetration or injection its use is still recom-
mended. At the very least, the patient’s perception
is one of the dentist trying to do everything possible
to minimise pain during treatment [48, 49].
Primary anaesthetic techniques commonly
used intra-orally in the maxilla include maxillary
infiltrations. Additional techniques include the
use of the posterior superior alveolar (PSA) nerve
block, infraorbital nerve block, anterior superior
alveolar (ASA) nerve block, anterior middle
alveolar (AMA) nerve block and second division
nerve blocks. In the mandible, the most common
blocks include the conventional inferior dental
nerve block, mental nerve block, long buccal
nerve block and labial and lingual infiltrations.
Alternative techniques commonly employed in
the mandible include injection of solution at or
near the condylar neck as in the Gow-Gates and
Vazirani-Akinosi techniques [43, 50–62].
Supplemental anaesthetic techniques can be
useful when conventional intra-oral anaesthesia
has failed to achieve pulpal anaesthesia for end-
odontic procedures. These include intraosseous
[63–67], intraligamentary (periodontal ligament)
[68–72] and intra-pulpal injection techniques
[73–75].
The traditional method of delivery of local
anaesthetic solutions has been achieved using
an aspirating needle and syringe. Although
this method is proven to be effective, the tech-
nique itself is not completely pain-free [76].
Alternative local anaesthetic delivery systems
and devices designed to minimise painful injec-
tions include needleless jet injector systems
(INJEX Pharma, Berlin, Germany) [77, 78],
vibrating supplementary devices (VibraJect sys-
tem, ITL Dental, Irvine, CA, USA) and [79, 80],
computer-controlled local anaesthetic devices
(the Wand, Milestone Scientific, Livingston,
NJM USA) [81–84].
Neurological complications following local
anaesthesia have been reported in the literature
including temporary facial nerve palsy and pro-
longed postinjection paraesthesia affecting the
mental nerve, inferior dental nerve and lingual
nerve. Less common nerve-related complications
include ocular and extraocular symptoms includ-
ing paralysis of extraocular muscles with associ-
ated diplopia and even amaurosis. Horner’s
syndrome-type manifestations including enoph-
thalmos, miosis and ptosis have been reported.
Bleeding, muscle trismus, systemic complica-
tions including potential toxicity, loss of con-
sciousness and generalised central nervous
system depression, anaphylaxis-related allergy or
a simple vasovagal syncope can occur after local
anaesthetic administration. The clinician should
be aware of the possible risks and methods
employed to minimise such situations [85–89].
Oral sedation is a convenient technique for
reducing anxiety experienced by some dental
phobic patients. Other choices include sedation
with nitrous oxide and oxygen, hypnosis, intrave-
nous sedation and general anaesthesia.
Benzodiazepines (diazepam, lorazepam, temaze-
pam and triazolam) have been successfully used
for oral sedation in dentistry by enhancing the
action of the neurotransmitter γ-aminobutyric
acid (GABA). This compound promotes an over-
all calming effect on the central nervous system
influencing emotional reactions, memory, think-
ing and control of consciousness, muscle tone
and co-ordination. Diazepam is the benzodiaze-
pine of choice for oral dental sedation, which
closely fulfils the criteria for an ideal sedation
agent [90–94].
Pain is a complex subject; for patients, it is an
unpleasant and emotional experience and may be
associated with actual or potential tissue damage.
In everyday clinical practice, practitioners face
challenges in not only preventing or relieving
dental pain but also ensuring that their treatment
does not inflict pain [95]. The correct use of pre-
emptive analgesics and anaesthetics armed with
the knowledge of supplemental techniques
should provide satisfactory pain relief for even
those difficult to treat endodontic cases where
patients present with a ‘hot tooth’. Occasionally
oral sedation and adjunctive use of corticoste-
roids may be indicated to further reduce anxiety
and pain in the endodontic office.
15.2 Analgesics
Pain relief as a result of endodontic intervention
alone is rarely immediate but nevertheless the
most effective strategy to reduce posttreatment
15.3 Local Anaesthetic Solutions
pain. Posttreatment pain ranging from mild to
severe may last up to 72 h in some cases requir-
ing additional posttreatment analgesics. Several
pharmacological strategies are available for
ensuring effective pain management when treat-
ing the endodontic pain patient. When prescrib-
ing analgesics, patients should be instructed to
take the medications at regular timely intervals
(e.g. 6–8 hourly) ensuring that a more consistent
blood level of the drug is achieved contributing to
better pain relief. The two most common analge-
sics that can be prescribed include NSAIDs and
paracetamol either separately or in combination.
The decision to co-prescribe is based on the addi-
tive analgesic effect when these two drugs are
taken together which is usually well tolerated by
most patients when given over a short period of
time. There may however be contraindications in
the medical history that dictates which analgesics
may best be tolerated altering the drug regime of
choice.
The mechanism of action of most NSAIDs is
believed to involve the inhibition of the cycloox-
ygenase enzyme (COX), thereby inhibiting the
synthesis of prostaglandins. Pulpal inflammation
and necrosis can lead to peri-radicular tissue
injury that can activate phospholipase, which, in
turn, releases arachidonic acid from cell mem-
branes. The arachidonic acid in turn forms the
substrate for the COX enzymes, which lead to the
synthesis of various eicosanoids. Two COX iso-
forms exist, namely, COX-1 and COX-2. COX-1
is responsible for the production of prostaglan-
dins with homeostatic functions in tissues such as
the stomach, kidney and platelets, whilst COX-2
is responsible for the production of the prosta-
glandins involved in inflammation. The therapeu-
tic effects of NSAIDs are attributable to the
inhibition of COX-2.
Some patients may not be able to tolerate
NSAIDs since inhibition of normal prostaglandin
synthesis results in a number of adverse effects.
These might include patients with gastrointesti-
nal disorders (ulcers and ulcerative colitis),
hypertension (including antihypertensive drug
interactions or the renal effects of NSAIDs) and
active asthmatics. For those patients who cannot
tolerate NSAIDs, pretreatment with paracetamol
is recommended.
227
15.3 Local Anaesthetic Solutions
Since ancient times, dentistry has unfortunately
been associated with pain and discomfort – which
has unfairly perpetuated to modern day. Prior to
anaesthesia, a surgeon or dentist’s skill was
equated with their speed of operation rather than
the quality of their work. With the advent of
anaesthesia, people have been able to undergo
more extensive procedures, free of pain, anxiety
and even memory. Despite these advances, how-
ever, people may still be apprehensive of dental
procedures.
Local anaesthetics (LAs) are drugs that lead to
a reversible block of transmission of impulses
along neural pathways, both central and periph-
eral. By doing so, they effectively block the
transmission of noxious pain stimuli along nerve
fibres, thereby rendering an area of tissue insen-
sate. Local anaesthetics exert their action by dif-
fusing across nerve membranes, down a
concentration gradient, and bind to the intracel-
lular portion of voltage-gated sodium channels
thus rendering it inactive. Local anaesthetic solu-
tions exist in a solution consisting of an ionised
and unionised fraction. It is the unionised frac-
tion that is lipophilic and able to diffuse across
the phospholipid bilayer of nerve cells and act at
the voltage-gated sodium channels. Local anaes-
thetics are weak bases with a pKa >7.4 (the pKa of
a drug is the pH at which 50 % is ionised and
50 % is unionised). As a result, at a physiological
pH (7.4), most of the drug is in the ionised form.
The clinical correlation of this is that in
infected, acidic or devitalised tissues, local
anaesthetics may take a longer time to take
affect (if at all) as majority of the drug is in the
ionised form and cannot diffuse across the cel-
lular membrane. Conversely, in order to have a
faster speed of onset, some practitioners add the
base sodium bicarbonate, thus increasing the
unionised fraction of the drug. Other clinical
characteristics include potency and duration of
action. Potency is related to the lipid solubility
of a drug and amount of drug available at a
nerve (i.e. concentration). Duration of action is
correlated with degree of protein binding. The
greater the protein binding, the longer the dura-
tion of action.
228 15 Analgesics, Anaesthetics, Anxiolytics and Glucocorticosteroids Used in Endodontics

Types and preparations properties regress before LA detaches from the

Local anaesthetics may be classified accord- sodium channel.
ing to chemical structure. All local anaesthetics There is no one LA that is suitable for all pro-
consist of an aromatic group and a tertiary amine. cedures. When choosing a LA, one needs to con-
An intermediate bond connects the two parts. sider various factors including onset, offset,
The intermediate bond may consist of either an safety profile and cost. It has been suggested that
ester or an amide. This gives rise to the classifica- for dental surgery, articaine comes closest to
tion of ester LAs and amide LAs. Examples of being the ideal LA owing to its fast onset, rapid
ester LAs include procaine (Novocaine) and metabolism, inactivation by organ- and non-
cocaine. Examples of amide LAs include lido- organ-dependent pathways, availability and
caine (Xylocaine), prilocaine (Citanest), artic- favourable safety profile.
aine (Septocaine), bupivacaine (Marcaine) and Toxicity and management
ropivacaine (Naropin). Despite the example given in the preceding
Ester LAs are metabolised by degradation to paragraph, LA toxicity cannot be only simplified
para-aminobenzoic acid (PABA), which is into an mg/kg algorithm. Various different fac-
highly antigenic and can result in allergic reac- tors affect local anaesthetic toxicity, most notably
tions. Once a PABA allergy occurs, patients site of injection (relative vascularity of site). For
may exhibit a cross reactivity to amide LAs that example, a patient may exhibit signs and symp-
contain methylparaben as a preservative. toms of LA toxicity even if only 1–2 mL of LA is
Allergic reactions to amide LAs alone is inadvertently injected into a major vessel, despite
extremely rare. being well below the calculated toxic dose.
There are a wide variety of preparations of Vascular tissue such as oral mucosa absorbs LA
LAs available. In general, LAs are prepared as a more readily than tissue with a less rich blood
hydrochloride salt, thus making them water- supply (e.g. subcutaneous tissue).
soluble. In addition, LAs for dental use often Nevertheless, toxic doses of local anaesthetic
contain preservatives (such as methylparaben or may be calculated based on lean body weight
sodium metabisulphite) and a fungicide. (see Tables 15.3 and 15.4).
Other common additives are vasoconstrictor
drugs. These include adrenaline/epinephrine, Table 15.3 Toxic dose of local anaesthetic calculated on
felypressin or octapressin. Vasoconstrictor lean body weight
drugs are added to reduce the systemic absorp- Lidocaine (plain) 4 mg/kg
tion of the LA. Depending on the LA used, this Lidocaine (with adrenaline) 7 mg/kg
potentially results in a prolongation of action. Prilocaine 6 mg/kg
In addition, for the shorter-acting LA (e.g. Prilocaine (felypressin or octapressin) 8 mg/kg
lidocaine), a larger dose may be given before Articaine 7 mg/kg
toxicity is reached. For example, the toxic Bupivacaine 2 mg/kg
dose of plain lidocaine is 4 mg/kg, whereas the Ropivacaine 3 mg/kg
toxic dose of lidocaine containing adrenaline/
epinephrine is 7 mg/kg due to the decreased Table 15.4 Systemic effects of lidocaine
systemic absorption afforded by the vaso-
Plasma concentration
constrictor. It must be noted however that for (mcg/mL) Effect
the commonly available long-acting LA (i.e. 1–5 Analgesia
bupivacaine and ropivacaine), the addition of 5–10 Light-headedness, tinnitus,
a vasoconstrictor does not change the toxic circumoral numbness/metallic
dose of the drug. With or without adrenaline/ taste
epinephrine, the toxic dose of bupivacaine is 10–15 Seizures
2–2.5 mg/kg. This is due to the strong pro- 15–25 Coma/respiratory arrest
tein binding of the LA. The vasoconstrictor >25 Cardiac depression/arrest
15.3 Local Anaesthetic Solutions
LA toxicity ultimately is directly related to
plasma concentration of the drug and manifests
itself in two major ways: cardiac toxicity and
central nervous system (CNS) toxicity.
Central nervous system effects
LA drugs are able to cross the blood–brain
barrier and act at the CNS. Typically at low
plasma concentrations, CNS excitatory symp-
toms/signs predominate such as light-headedness,
tinnitus, circumoral numbness, metallic taste in
mouth and ultimately seizures. As the plasma
concentration rises, or if there is a rapid rise in
plasma concentration, then CNS depression
(coma and respiratory depression) ensues. LA
which are more lipid soluble (i.e. more potent
such as bupivacaine) lead to CNS toxicity at
much lower doses. Certain clinical states may
make CNS more likely to occur. These include
decreased protein binding, hypercarbia and sys-
temic acidosis. Should the plasma concentration
continue to rise, then cardiac toxicity may occur.
Cardiac effects
LA drugs can lead to potentially disastrous car-
diac complications. In its mild form, LA drugs can
lead to hypotension, arrhythmias and myocardial
depression. Again, the more potent LAs such as
bupivacaine and ropivacaine are the most sinister
of these drugs as they can lead to fatal cardiac
arrest (typically ventricular fibrillation, which is
refractory to usual management) or complete heart
block. Out of the long-acting LAs, ropivacaine is
less cardiac toxic, as its affinity to the sodium
channels on the cardiac myocyte is less. The exact
mechanism of this is still not fully understood. The
dose of LA causing CNS toxicity compared to
dose causing cardiac toxicity gives rise to the con-
cept of CC:CNS ratio. Lidocaine has a CC:CNS
ratio of 7:1, whereas bupivacaine is 3:1 – thus
implying that in regard to bupivacaine, there is
only a very small margin of dose of local anaes-
thetic before cardiac toxicity occurs.
Management of local anaesthetic toxicity
The management of local anaesthetic toxic-
ity is mainly supportive and is summarised in
Table 15.5. In addition to the cardiac and neu-
ral manifestations of LA toxicity, prilocaine in
doses >600 mg can lead to methaemoglominae-
mia. Methaemoglobinaemia results in impaired
229
Table 15.5 Management of local anaesthetic toxicity
Recognise LA toxicity, stop injection of the local
anaesthetic solution and call for help
If the patient is showing mild symptoms, only then
reassure and continuously monitor until they improve.
Preparations should be made in case signs of severe
toxicity develop
Administer oxygen and ensure ventilation is maintained
and respiratory acidosis is avoided
If conscious level is deteriorating or convulsions
develop, the patient will require maintenance of airway;
this may necessitate tracheal intubation. Hundred
percent oxygen should be administered and adequate
ventilation ensured
If seizures develop, benzodiazepines can be
administered in small incremental doses
For cardiac arrest associated with local anaesthetic
toxicity, cardiopulmonary resuscitation should be
commenced using standard protocols. Cardiac
arrhythmias may be treated with lipid emulsion therapy
as per ALS guidelines. Consider Intralipid 20 %
(1.5 mL/kg) over 1 min followed by infusion at 15 mL/
kg/h. If no improvement, consider repeat bolus dose
and increasing infusion rate. Cumulative Intralipid dose
should not exceed 12 mL/kg
For further information and resuscitation cards, please
refer to the Association of Anaesthetists of Great Britain
and Ireland (AAGBI) website: http://www.aagbi.org/sites/
default/files/la_toxicity_2010_0.pdf
oxygen delivery to tissues and resultant tissue
hypoxia. Treatment is with a reducing agent such
as methylene blue.
Local anaesthesia mishaps
In addition to toxic effects affecting the cen-
tral nervous system and heart, intra-oral local
anaesthesia can result in complications.
Trismus
The inability to open the mouth can occur
2–5 days after a mandibular block has been admin-
istered. Inadvertent incorrect needle placement,
accidental penetration of muscle or puncturing of
blood vessels during administration of this block
can lead to haematoma formation and subsequent
fibrosis. Patients will often complain of marked
trismus that can last several weeks if quite severe.
Management includes reassurance and explana-
tion of possible cause. Conservative management
including use of hot packs and stretching exercises
using wooden spatulas are usually sufficient for
this condition. Rarely if the haematoma becomes
infected, then surgical referral will be needed.
230 15 Analgesics, Anaesthetics, Anxiolytics and Glucocorticosteroids Used in Endodontics
Facial nerve palsy (immediate)
Incorrect needle placement during either an
inferior dental nerve block or posterior superior
alveolar nerve block can result in a temporary
facial palsy. Patients with peripheral facial nerve
palsy will exhibit generalised weakness of the
ipsilateral side of the face, inability to close the
eyelids, obliteration of the nasolabial fold, droop-
ing of the corner of the mouth and deviation of
the mouth to the unaffected side. Management
includes reassurance and explanation with
emphasis that the weakness is temporary in
nature. An eye-patch may be advisable to avoid
ophthalmic damage.
Postinjection paraesthesia
Prolonged or permanent alteration of sensa-
tion along part or all of the distribution of either
the maxillary or mandibular branches of the tri-
geminal nerve can occur following administra-
tion of local anaesthetic. These altered sensations
can be categorised as anaesthesia (total absence
of sensation), paraesthesia (abnormal sensations
such as ‘pins and needles’) and dysesthesia
(spontaneous or mechanically evoked painful
neuropathy). They can be attributed to a number
of theories including direct trauma from the nee-
dle, intra-neural blood vessel trauma and intra-
neural haematoma formation and neurotoxicity
directly related to the local anaesthetic used.
During inferior alveolar nerve block administra-
tion, the patient may on occasion experience an
immediate electric shock sensation. This is
thought to be due to the needle contacting the
nerve trunk, which can potentially cause direct
damage to the nerve and long-lasting altered sen-
sation of various durations. The practitioner is
advised to stop the administration of the anaes-
thetic solution, and repositioning of the needle is
recommended a few millimetres away. The
patient should be warned of the potential tempo-
rary paraesthesia that can develop which should
be transient in nature but may take several weeks
to fully recover. Management of anaesthesia, par-
aesthesia and dysesthesia will require sensory
testing of the affected distribution, reassurance
and follow-up. A surgical referral may be
required in some patients to ensure prompt surgi-
cal intervention is carried out if deemed
necessary.
15.4 Topical Anaesthesia
The use and efficacy of topical anaesthesia prior
to needle insertion and injection of local anaes-
thesia has been highly variable. Nevertheless, its
use is recommended prior to all intra-oral dental
anaesthesia techniques to rest assure the patient
that the clinician is trying everything possible to
minimise any pain during treatment. Topical
anaesthetic gel formulations should be placed
over the mucosa at least 30 s to 1 min before the
injection (see Fig. 15.1).
15.5 Maxillary Infiltration
and Blocks
The pulpal sensory fibres of the maxillary teeth
are primarily carried in the anterior, middle and
posterior superior alveolar nerves, which also
supply the buccal soft tissues. Most problems
with maxillary anaesthesia can be attributed to
individual variances of normal anatomical nerve
pathways within the maxillary bone with acces-
sory pulpal innervation fibres found in the palatal
innervation supplied by the nasopalatine and
greater palatine nerves. The administration of
palatal anaesthesia is often described as a painful
experience by the patient, and direct palatal infil-
tration is difficult to administer without signifi-
cant pain or discomfort since there is little tissue
space at these sites between the mucosa and the
underlying. Using careful application of topical
anaesthesia, distraction techniques and ensuring
slow delivery of anaesthetic solution should
allow for very little to no patient discomfort.
Alternative injections using articaine in the buc-
cal vestibule alone may prove sufficient, avoiding
the palatal injection. New computer-controlled
anaesthetic delivery systems (CCLAD) are par-
ticularly proficient at eliminating or at the very
least minimising discomfort when giving injec-
tions in the palate.
Nasopalatine nerve block
Palatal anterior superior alveolar nerve block
(PASA)
The needle is placed just lateral to the inci-
sive papilla (Fig. 15.2). Once the needle has
penetrated the mucosa, initial deposition of
15.5 Maxillary Infiltration and Blocks 231

a b

Fig. 15.1 Clinical photographs demonstrating (a) anaesthesia of the mucosa prior to injection. (b) The
Xylonor topical anaesthetic pellets. One pellet contains mucosa is dried and then the topical anaesthetic pellet is
100 mg of lignocaine-based solution. Useful for topical massaged and left in situ for 30 s

a b

Fig. 15.2 (a, b) Clinical photographs and diagrams dem-
onstrating the nasopalatine block injection. The entrance
to the nasopalatine foramen is at the incisive papilla,
which may be visualised posterior to the maxillary central
incisors. The needle tip should contact the soft tissue at
the lateral aspect of the incisive papilla with a depth of
penetration of less than 5 mm. After aspiration anaesthetic
solution should be deposited at a very slow rate to mini-
mise discomfort for the patient

anaesthetic solution is injected over 10 s. the remaining solution within the cartridge is
Following this the needle is reoriented more ver- deposited. The injection will provide anaesthe-
tically to enter the nasopalatine canal a distance sia of all six maxillary anterior teeth (canine to
of 0.5–1 cm. Following negative aspiration, canine) with a single injection including soft
232 15 Analgesics, Anaesthetics, Anxiolytics and Glucocorticosteroids Used in Endodontics
tissue overlying the anterior palate (nasopala-
tine nerve distribution) and to a lesser extent the
labial gingivae.
Greater palatine nerve block
This block is used to anaesthetise the palatal
soft tissue of the teeth posterior to the maxillary
canine and corresponding alveolar bone in the
palate. The needle is inserted approximately
1 cm medial to the 1st/2nd maxillary molar on
the hard palate. The needle is advanced into the
greater palatine foramen to a depth of less than
10 mm before injecting anaesthetic solution
(Fig. 15.3).
Anterior middle superior alveolar (AMSA)
This injection is intended to provide pulpal
anaesthesia of the ipsilateral incisor, canine and
premolar teeth and their associated palatal soft
tissues. A needle is placed along the line bisecting
the premolar teeth at the point halfway between
the midline palatal suture and the free gingival
margin. Initially the needle is placed in mucosa,
and following deposition of anaesthetic solution
for 8–10 s, the needle is advanced laterally and
superiorly until bone is met. The remaining
anaesthetic solution can be administered at this
point.
a b
Fig. 15.3 (a, b) Clinical photographs and diagrams dem-
onstrating the greater palatine block injection. This injec-
tion will anesthetise the tissues of the hard palate from its
most distal aspect, anteriorly to the distal of the canine
and laterally to the midline. The entrance to the greater
palatine foramen is usually located halfway between the
Infraorbital block
This block is used to anaesthetise the 1st and
2nd premolars, canine, lateral incisor and central
incisor, corresponding alveolar bone and buccal
gingivae. It combines the MSA and ASA blocks
and will cause anaesthesia to the lower eyelid,
lateral aspect of the nasal skin tissue and skin of
the infraorbital region (Fig. 15.4). The infraorbital
margin is palpated extra-orally and the thumb
and index finger is placed in this region. The
upper lip and buccal mucosa are retracted and the
needle inserted in the area of the 1st premolar,
canine region. The needle is advanced until con-
tact is made with bone in the infraorbital region
before depositing anaesthetic solution.
Posterior superior alveolar nerve (PSAN)
block
This block is useful for anaesthetising the
pulpal tissue, corresponding alveolar bone and
buccal gingival tissue to the maxillary 1st, 2nd and
3rd molars. The needle is inserted at the height of
the muco-buccal fold between the 1st and 2nd
molars at a 45° angle to the occlusal plane superi-
orly and medially. Care must be taken in this
region due to the pterygoid plexus of veins and
risk of positive aspiration and also hematoma.
gingival margin and the midline of the palate, approxi-
mately opposite the second maxillary molar. Anatomically
this is generally 5 mm anterior to the junction of the hard
and soft palate. On penetration of the foramen, the needle
should be inserted until bone is contacted. Aspiration
should be carried out prior to slow deposition of solution
15.6 Mandibular Infiltration and Blocks 233

a b

c d

Fig. 15.4 Clinical photographs and diagrams demonstrating (a and c) Gow-Gates (GG) nerve block (b) Vazirani-
Akinosi nerve block and (d) infraorbital nerve block

15.6 Mandibular Infiltration
and Blocks
Inferior alveolar nerve block (IANB)
This technique involves blocking the inferior
alveolar nerve prior to its entry into the mandibu-
lar lingula on the medial aspect of the mandibular
ramus. The needle is inserted in the mucous
membrane on the medial border of the mandibu-
lar ramus at the intersection of a horizontal line
6–10 mm above the occlusal table of the man-
dibular teeth (height of injection) and vertical
line just lateral to the pterygomandibular raphe
(anteroposterior plane). The area of injection is
approached from the contralateral premolar
region. The nondominant hand is used to retract
the buccal soft tissue (thumb in the coronoid
notch of the mandible and index finger on the
posterior border of the extra-oral mandible). The
needle is inserted approximately 25 mm until
bone is reached. The needle is then retracted
slightly before slowly depositing anaesthetic
solution.
Gow-Gates technique
A Gow-Gates technique is indicated for use
in cases where soft-tissue anaesthesia from the
most distal molar to the midline is needed and
where conventional inferior alveolar nerve
blocks are unsuccessful. The target area is the
antero-medial border of the mandibular condylar
neck, just inferior to the insertion of the lateral
pterygoid muscle (Fig. 15.4). The injection site
intra-orally is on the mucosa on the mesial of the
mandibular ramus, just distal to the height of the
234 15 Analgesics, Anaesthetics, Anxiolytics and Glucocorticosteroids Used in Endodontics
mesio-lingual cusp of the maxillary second
molar, following a line extra-orally from the
intertragic notch of the ear to the labial commis-
sure on the same side.
Vazirani-Akinosis technique
This is a useful technique to provide anaesthe-
sia in the same area as the inferior alveolar nerve
block in patients who have infections and trismus
with limited mouth opening. The needle is
inserted into the soft tissues overlying the medial
border of the mandibular ramus directly adjacent
to the maxillary tuberosity. The needle is
advanced to a depth of 25 mm, and the hub of the
needle should be opposite the mesial aspect of
the maxillary second molar. The injection is per-
formed blindly because no bony endpoint exists,
so careful aspiration is needed before depositing
anaesthetic solution.
Long buccal nerve block
The buccal injection will anaesthetise the buc-
cal soft tissue lateral to the mandibular molars.
The needle is inserted into the tissue in the disto-
buccal vestibule opposite the second or third
molar just medial to the coronoid notch. The
needle is inserted until bone is contacted, usually
1–3 mm.
Mental nerve block
The mental nerve exits the mental foramen at
or near the apices of the mandibular 1st and 2nd
premolars. A 25- or 27-gauge short needle is
inserted at the muco-buccal fold at or just ante-
rior to the mental foramen. The bevel of the nee-
dle should be orientated towards the bone and the
tissue penetrated to a depth of between 5 and
6 mm. After aspiration anaesthetic solution can
be slowly deposited.
15.7 Supplemental Injections
Achieving profound anaesthesia during endodon-
tic procedures is a fundamental goal that can be a
challenge particularly when dealing with a ‘hot
tooth’. The term ‘hot tooth’ generally refers to a
pulp diagnosed with irreversible pulpitis with
spontaneous moderate to severe pain. When the
clinician is confronted with a case of severe irre-
versible pulpitis in which the conventional IANB
achieves lip numbness but not pulpal anaesthesia,
there are several strategies still available to the
clinician to attain good pulpal anaesthesia. It
should be reiterated that these supplemental tech-
niques are best used after achieving a clinically
successful IANB (lip numbness).
Intra-osseous injections
The intra-osseous injection technique is one
of the most successful methods amongst all sup-
plementary anaesthetic techniques used to over-
come pain. Specialised delivery systems have
been introduced for intra-osseous injections
including Stabident (Fairfax Dental Inc., Miami,
FL, USA) and X-Tip (Dentsply International Inc,
Tulsa, OK, USA). The Stabident system consists
of a 27-gauge bevelled wire that is driven by a
slow-speed hand-piece to perforate the cortical
bone. Anaesthetic solution is then delivered
through the perforation using standard anaes-
thetic solution. The X-tip system consists of a
2-part perforator/guide sleeve component also
driven by a slow-speed hand-piece. The perfora-
tor leads the guide sleeve through the cortical
bone and then is separated and removed from it.
This leaves the guide sleeve in place allowing for
positioning of a 27-gauge needle from which
anaesthetic solution can be deposited.
A point of perforation is selected to allow for
infiltration of anaesthetic solution. This point
should lie in the attached gingiva and is deter-
mined by imaging two lines running at right
angles to one another. The horizontal line runs
along the buccal gingival margins of the teeth,
and the vertical line bisects the distal interdental
papilla of the tooth in interest. The point of pen-
etration is 2 mm apical to the intersection of these
lines. If this point lies within reflected mucosa, a
point more coronal in an area of attached gingiva
is chosen. The perforator is attached to the slow-
speed hand-piece and advanced through anaes-
thetised gingivae and bone until a characteristic
‘give’ is felt. This indicates that the cancellous
bone has been perforated. The perforator is then
removed and an 8-mm short 27-gauge needle is
inserted to allow for about 1.0 mL of anaesthetic
solution to be deposited slowly over 2 min.
Limitations to the technique include active peri-
odontal disease, limited attached gingiva and
15.8 Delivery Systems
limited inter-radicular bone. Inherent risks asso-
ciated with the technique include potential sys-
temic side effects such as heart elevation and
potential damage to teeth.
Intraligamentary injections
The intraligamentary injection technique, also
known as the periodontal ligament injection, is
actually an intra-osseous injection during which
the anaesthetic solution is deposited via the peri-
odontal ligament. The solution reaches the pulpal
nerve supply by entering natural perforations
within the cancellous bone surrounding the
socket wall. The most important points regarding
this technique are the positioning of the needle
and to inject the anaesthetic agent with consider-
able force. The needle is inserted at 30° to the
long axis of the tooth and is forced to maximum
penetration until it is wedged between tooth and
crestal bone. Once the needle is correctly placed,
the anaesthetic solution is deposited under back-
pressure and is performed under resistance. Onset
of anaesthesia is rapid and achieved within 30 s
and can be immediate.
Intra-pulpal injections
This method relies on depositing anaesthetic
solution directly into the pulp chamber. It is
important to ensure that the solution is deposited
into the pulp under backpressure. Simply placing
anaesthetic solution into the pulp chamber will
not achieve adequate anaesthesia. Once an open-
ing has been made into the pulp, the needle can
be advanced into the canals until the fit is tight.
This injection is very painful and only of short
duration so should only be used as a last resort
during endodontic treatment. Once anaesthesia is
achieved, the practitioner must work quickly to
ensure that all pulpal tissue has been removed
from the coronal pulp chamber and canals. The
patient should be prewarned to expect moderate
to severe pain during the initial phase of the
injection.
15.8 Delivery Systems
Traditional local anaesthetic delivery systems
consist of a syringe (aspirating and non-
aspirating) and needles (extra-short, short and
235
long) of various gauges [24, 26, 29]. Extra-short
needles are used for periodontal ligament anaes-
thesia. Short needles are used for maxillary buc-
cal or palatal injections. A long needle is selected
for mandibular blocks or for designated posterior
maxillary blocks. A recent modification has been
to develop safety syringes to prevent the inci-
dence of needle stick injuries. In safety syringe
systems, the needle and its protective sheath are
supplied and disposed of as part of the syringe.
The entire assembly is disposed of as one unit no
longer requiring needle removal, thereby avoid-
ing resheathing.
Alternative local anaesthetic delivery systems
include electronic devices aimed at minimising
painful injections. Such systems include vibrat-
ing devices (VibraJect system, ITL Dental,
Irvine, CA, USA) and computer-controlled local
anaesthetic delivery systems (C-CLAD). The
electronic systems deliver local anaesthetic
slowly at a predetermined speed and flow, thereby
reducing discomfort in both children and adults.
Milestone Scientific (Piscataway, NJ, USA)
introduced the first C-CLAD system in 1997.
Originally known as the Wand, subsequent ver-
sions were sequentially renamed the Wand Plus,
CompuDent and STA (Single-Tooth Anaesthesia
System). Alternative products include the
QuickSleeper and Sleeper One devices (Dental
Hi Tec, Cholet, France) and the Anaeject (Nippon
Shika Yakuhin, Shimonoseki, Japan) syringes
(Fig. 15.5).
The STA system consists of freestanding unit
that contains a microprocessor, a motor that
drives a plunger and a foot control pedal. The
local anaesthetic cartridge is connected via a can-
nula to the hand-piece that holds the needle. The
STA unit has an additional feature of dynamic
pressure-sensing technology, which provides
continuous feedback to the user about the pres-
sure at the needle tip to help identify ideal needle
placement for periodontal ligament injections.
There are three operating modes including a sin-
gle slow rate of injection (0.005 mL/s), normal
mode (0.03 mL/s) and turbo mode (0.06 mL/s).
As the needle is introduced through the tissue,
the system provides continuous audible and
visual feedback alerting the clinician to the
236 15 Analgesics, Anaesthetics, Anxiolytics and Glucocorticosteroids Used in Endodontics
a b
d e
Fig. 15.5 Clinical photographs showing (a) self-aspirating needles and (b–f) the Wand (Milestone Scientific
Livingston, NJ, USA)
precise position and pressure required for suc-
cess. Activation of the unit results in micropro-
cessor control of a piston that expresses local
anaesthetic by pushing a local anaesthetic plunger
into the cartridge. The slow drip computer-
assisted delivery system dictates the flow rate
during injection aimed at creating less tissue dis-
tension and therefore pain at site of anaesthesia.
15.9 Anxiolytics
In the preceding sections, the pharmacology
and use of LAs have been extensively covered.
However, in certain situations, LA alone is
insufficient to provide adequate operating con-
ditions. In such circumstances, there may be a
need for sedation or general anaesthesia. General
anaesthesia will not be considered any further
as it should only be performed by a specialist
c
f
anaesthetist or, in certain controlled situations,
a non-specialist medical practitioner trained in
anaesthesia.
Sedation, however, is particularly coming to
the fore. The general public has begun to see the
benefits of sedation and to a certain extent have
created a growing level of expectation. It has
been reported that there are many reasons why
people choose sedation including anxiety, fear of
needles, severe gag reflex and claustrophobia
with a rubber dam. As a result, many courses
have now been developed that allow dental prac-
titioners to acquire the knowledge and skills to
perform sedation safely in an office-based prac-
tice. This chapter is not intended to be a substi-
tute for such training. Its purpose is to provide
the dental practitioner with a broad understand-
ing of what sedation entails, requirements for
safe practice, some commonly used drugs and
some novel drugs that may become more
15.9 Anxiolytics
commonplace in the future. Hopefully it also
stimulates interest, so that people may be moti-
vated to undergo further training in this field.
What is conscious sedation?
Conscious sedation is a medication-induced
state that reduces the patient’s level of conscious-
ness during which the patient can respond pur-
posefully to verbal commands or light stimulation
such as touch. The reality is that conscious seda-
tion, heavy sedation and general anaesthesia all
lie on the one continuum, with no reliable way of
determining where one ends and the next begins.
Despite it being seemingly innocuous, care must
be taken during conscious sedation as:
• The patient may lose consciousness.
• The patient’s level of sedation may rapidly
escalate to heavy sedation or GA, particularly
if multiple doses are given or a combination of
drugs is given (a multiplicative effect).
• The airway protective reflexes are diminished
increasing risk of aspiration.
• There is depression of respiration, which
could lead to hypoxia.
• There is a depression of the cardiovascular
system, particularly in the frail and unwell
patient with multiple comorbidities. This
could lead to hypotension and hypoperfusion
of key organ systems such as the brain or the
heart.
• The doses of drug are not fixed and are subject
to a wide range of individual variation based
on numerous factors such as size, age, comor-
bidities and other medications.
As a result, when preparing for ‘conscious
sedation’, one needs to prepare a patient as
though they are to have a general anaesthetic.
Whilst this may seem excessive, it does
considerably reduce risk. This involves patient
assessment, fasting, appropriate equipment
(including resuscitative equipment), adequate
personnel and a plan should a patient
deteriorate.
Patient assessment
Prior to the procedure, any patient needs to be
assessed for their suitability for sedation. This
includes a focussed history and examination
specifically for concomitant cardiac disease,
respiratory disease (including sleep apnoea),
237
neurological disease, musculoskeletal disorders
(particularly those which result in weakness of
the muscles of respiration) reflux risk, allergies,
medications and an airway assessment. The
patient then needs to be stratified according to the
American Society of Anaesthesiologists physical
status classification (see Table 15.6). In general,
dentists trained in sedation should limit practice
to ASA class 1 and 2 patients. A specialist anaes-
thetist should perform patients who are ASA 3 or
greater, whether they are under sedation or
GA. Certainly, it can be argued that ASA 4
patients should not be performed in the office-
based setting but rather in a hospital theatre.
Fasting
Fasting is an important aspect of any sedation
service as it significantly reduces the risk of aspi-
ration. The recommended guidelines for fasting
times (produced by the Australian and New
Zealand College of Anaesthetists (ANZCA) that
should be observed include 6 h for solid foods or
milk, 4 h for breast milk and 2 h for water or clear
fluids (e.g. apple juice).
Equipment
For safe oral sedation, it is mandatory to
ensure that standard equipment consisting of
oxygen with mask and nasal cannula, self-
inflating resuscitation bag and pulse oximetry is
available. However, this alone is insufficient for
intravenous sedation. In order to provide a safe
intravenous sedation service, additional equip-
ment needs to be readily available including a
range of nasal cannula and masks to deliver oxy-
gen, intravenous cannula, intravenous fluids (e.g.
0.9 % saline) with giving sets, monitoring
(including pulse oximetry, non-invasive blood
pressure, ECG, end-tidal carbon dioxide) and
suction.
Table 15.6 ASA classification of physical status
I Healthy patient
II Mild systemic disease
IIISevere systemic disease
IV Severe systemic disease that is a constant threat to
life
V Moribund patient not expected to survive with or
without operation
VI Brain dead – for organ procurement
238 15 Analgesics, Anaesthetics, Anxiolytics and Glucocorticosteroids Used in Endodontics
In addition to a defibrillator, drugs (adrena-
line, atropine, suxamethonium, Intralipid, a beta
blocker such as metoprolol, ephedrine, metaram-
inol, hydrocortisone, 50 % glucose, naloxone,
flumazenil), a range of advanced airway equip-
ment (e.g. endotracheal tubes and laryngeal
masks) and self-inflating resuscitation bag should
be available.
Various countries have guidelines regarding
conscious sedation. One such guideline is
jointly produced by ANZCA and the Royal
Australasian College of Dental Surgeons
(RACDS). This may be found on their websites
(www.anzca.edu.au or www.racds.org) and
should be consulted prior to instituting an
office-based sedation program.
Training
In order to safely conduct dental sedation and
to develop a familiarity with the myriad of equip-
ment, it is imperative that the dental practitioner
be adequately trained. There are a variety of
courses available, and practitioners should ensure
that courses are recognised by governing dental
bodies within their country of practice to ensure
that standards are met. One of the key aspects to
any course is the teaching of advanced life sup-
port (ALS). Anyone practicing intravenous seda-
tion should be proficient in ALS and advanced
airway management. In fact, all dental practitio-
ners, whether they practice sedation or not,
should be competent in basic life support (BLS)
at the bare minimum. Training for this can be
obtained from a variety of sources including Red
Cross and ambulance groups.
Personnel
It is imperative that during the sedation pro-
cess, one person be present whose sole responsi-
bility is to administer sedation and monitor the
patient. Unfortunately, in the real world, this is
frequently not achievable, and it is the procedur-
alist who has to administer the drugs. In this situ-
ation, there should be a skilled assistant to
monitor the patient’s consciousness and cardiore-
spiratory function.
The patient should be given clear verbal and
written instructions regarding preoperative and
post-operative care prior to oral sedation. Due to
the varying recovery profiles of many different
sedative agents available, the patient should be
advised not to drive, make any important deci-
sions or consume alcohol for a period of 24 h
after the appointment. This requires the patient
to have a suitable escort who must be responsi-
ble. It would be ill-advised to allow the patient
to leave the dental office unaccompanied
(Table 15.7).
Commonly used drugs
Oral
Oral sedation has the mainstay for dental prac-
titioners for numerous years. Traditionally, the
benzodiazepine, diazepam, has been used.
However, there is some evidence emerging of the
Table 15.7 A written instructions for patients having
oral sedation
Before your appointment
You can have a light meal 6 h before the appointment,
but do not have anything to eat or drink 2 h before your
appointment
Do not drink alcohol on the day of the appointment
If you are taking any medicines, take them at the usual
time unless otherwise advised
If you are taking an oral sedative, you can take it 1 h
before your appointment
Wear loose-fitting clothing and no jewellery. Remove
any contact lenses
You must be accompanied by a responsible adult, who
must remain with you in the waiting room throughout
your appointment, escort you home afterwards and
arrange for you to be looked after for the following
24 h
Report any illness occurring after the appointment
immediately, as it might affect your treatment
After your appointment
Remain at the clinic for at least 1 h after your treatment
has finished
Your escort must take you home by means other than
public transport
Rest and do not undertake any strenuous activities for
the rest of the day
If you are hungry, you can have a light meal but at
lukewarm temperatures only
Do not drive any vehicle, operate any machinery or use
any domestic appliances for 24 h after the appointment
Do not drink alcohol, return to work, make any
important decisions or sign any important documents
for 24 h after the appointment
15.9 Anxiolytics
benefits of oral ketamine, particularly for paedi-
atric dentistry.
Diazepam
Diazepam is a readily available benzodiaze-
pine that may be used as a single agent for
sedation, anxiolysis and anterograde amnesia.
It is highly lipophilic which aids in its rapid
absorption and central effects. It is highly pro-
tein bound (95 %) and is metabolised in the
liver to active metabolites (desmethyldiaze-
pam, oxazepam, temazepam) before being con-
jugated with glucuronic acid before being
renally excreted. It has a long elimination half-
life (20–45 h).
Diazepam dosage (adults) 2.5–7.5 mg/dose
Onset 10–15 min
Peak plasma concentration 60–90 min
Diazepam should be avoided in those who
have severe sleep apnoea, severe liver disease,
renal failure, acute narrow-angle glaucoma,
myasthenia gravis and pregnancy or in those who
are lactating. Extreme caution (and dose reduc-
tion) must be exercised in the elderly and the
debilitated patient.
Other oral benzodiazepines that are com-
monly used in dentistry include temazepam and
lorazepam. Lorazepam, however, has a longer
onset time and much longer duration of action
that probably makes it less suitable than diaze-
pam for dental procedures. Temazepam has a
similar onset time to diazepam but a longer time
to achieve peak plasma concentration (2.5–3 h).
Hence again, diazepam is probably more suitable
for a short procedure.
Ketamine
Ketamine is a phencyclidine derivative
that acts as an NMDA receptor antagonist
to produce dissociative anaesthesia and pro-
found analgesia. Ketamine is also a weak opi-
oid agonist. Its advantages lie in its ability to
produce potent analgesia at sub-anaesthetic
doses. It is a bronchodilator and it stimulates
the cardiovascular system due to an increase
in sympathetic tone. Compared to other intra-
venous agents, airway reflexes are relatively
239
preserved. Its disadvantages include excess
salivation and potentially disturbing dreams and
hallucinations.
Ketamine dosage (adults) 6–7 mg/kg
Onset 15–30 min
Ketamine has a particularly unpleasant taste and should
be mixed in a sweet liquid
Inhaled
Since the birth of modern anaesthesia, inhaled
nitrous oxide has been used as a sedative drug.
Since then, other inhaled drugs have emerged.
These include inhaled midazolam and xenon.
Xenon will not be considered further as it is an
anaesthetic agent, highly expensive and still
experimental. Midazolam, however, has some
real merits.
Midazolam
Midazolam is a water-soluble benzodiazepine,
whose advantage lies with its rapid onset and
short duration of action. Its pKa = 6.5, which
means at a physiological pH, 89 % is in the
unionised form and can rapidly act at the princi-
ple inhibitory neurotransmitter receptor of the
body – the GABA receptor.
Although it can be given nasally, it is princi-
pally given intravenously and occasionally orally,
although its bitter taste is often a hindrance.
Midazolam dosage 0.2 mg/kg (up to 10 mg) – mix
(oral) with a sweet drink
Dosage (intranasal) 0.3–0.5 mg/kg (up to 10 mg)
Dosage Inject 1–2 mg increments until
(intravenous) patient is tolerant of procedure.
Wait 5 min between doses
Nitrous oxide
Dentists have utilised nitrous oxide since
1844, when Horace Wells first demonstrated its
use during the extraction of a tooth. It is a colour-
less, odourless anaesthetic gas that is useful as an
inhalational sedative. It is readily available and
can be administered via a simple delivery system.
The most commonly available system is
‘Entonox’ (registered trademark of BOC) which
delivers a mix of 50 % nitrous oxide and 50 %
oxygen. Other systems are available that allow
240 15 Analgesics, Anaesthetics, Anxiolytics and Glucocorticosteroids Used in Endodontics
the practitioner to increase or decrease the nitrous
oxide/oxygen mix. It is breathed in via a demand
valve through either a mask, bite block, nasal
prongs or mouthpiece.
Nitrous oxide’s main advantages are that is
odourless, has a rapid onset and rapid offset and
provides potent analgesia. It has been used safely
for many years. Its disadvantages include being
dependant on patients being able to control and
coordinate breathing adequately in order to
obtain enough gas; it oxidises vitamin B12, thus
making it unable to act as the cofactor for methi-
onine synthase. This results in reduced methio-
nine and DNA synthesis. Even with short
exposure, megaloblastic changes may be seen on
blood film. In dental offices, where workers may
be chronically exposed to nitrous oxide, other
deleterious effects may be seen including neuro-
logical damage. Nitrous oxide is emetogenic. It
can also lead to expansion of gases in closed
spaces, thus should not be used in patients with a
pneumothorax, patients on recent diving and
patients who have recent ear operations, gross
abdominal distension or post-vitreoretinal sur-
gery (when SF6 gas may have been used).
Intravenous
The considerations and risks of intravenous
sedation have been extensively described in the
preceding sections. Nevertheless, in the hands of
well-trained professionals and with certain safe-
guards in terms of equipment, location and
patient selection, intravenous sedation is a very
safe and elegant way of providing anxiolysis,
amnesia, hypnosis and analgesia. The most com-
monly used drugs are midazolam (discussed ear-
lier), fentanyl (an opioid) and propofol (a
hypnotic).
Often the anaesthetist or sedationist gives a
combination of all three drugs. The purpose of
this is to produce balanced anaesthesia. By giv-
ing a small dose of each type of drug, the positive
effects of each drug are attained without the side
effects.
Fentanyl
Fentanyl is a synthetic opioid agonist that is
approximately 60–80 times more potent than
morphine and has a more rapid onset of action.
At low doses (<10 mcg/kg), it has a short duration
of action. Its rapid onset and offset make it very
titratable and an ideal analgesic choice as part of
a ‘sedation cocktail’. Its elimination half-life is
1.5–6 h.
Fentanyl dosage 10–20 mcg boluses every 3–5 min.
(intravenous) Maximum eight to ten doses.
Adults Effects will last 30–60 min
Fentanyl dosage 0.1 mcg/kg boluses every 3–5 min.
(intravenous) Maximum eight to ten doses
Children
Propofol
Propofol (2,6-diisopropyl phenol) is the most
commonly used intravenous anaesthetic agent for
induction and maintenance of anaesthesia world-
wide. Unfortunately it rose to infamy after the
death of the popular singer/songwriter Michael
Jackson. In low dose, and in trained hands, it can
be used as a sedative, although this was never its
primary purpose. Propofol needs to be used with
caution as it can rapidly cause cardiovascular
instability particularly in the old or infirm and
can also rapidly lead to apnoea and loss of airway
reflexes (even in sedative doses). It is presented
as a 1 % solution in a white emulsion of soya
bean oil and egg lecithin. As such, propofol
should not be given in those who have a soya
bean allergy. Egg allergy usually is not a problem
as the lecithin is derived from the yolk, whereas
the main antigenic component of eggs is the albu-
min. Nevertheless, care should be exercised.
Its advantages are it has rapid onset and less
‘hangover’ effect, it has antiemetic properties and
it produces some anxiolysis. Its disadvantages
include pain on injection safety issues as dis-
cussed and potential for abuse.
Propofol dosage (for 10–30 mg boluses or 1–3 mg/
sedation) adults kg/h infusion titrated to effect
15.10 Corticosteroids
The primary role of steroids appears to be the
regulation of the immune system, and the use of
either local or systemic steroids in endodontics is
primarily to reduce inflammation and pain.
Ledermix is a common intra-canal medicament
References
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amcinolone and 3 % demeclocycline, which are
capable of diffusing through dentinal tubules and
cementum to reach the periodontal and periapical
tissues. The use of intra-canal steroids or a corti-
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locally or systemically on endodontic posttreat-
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Clinical Hints and Tips
• Use of pre-emptive analgesia can be help-
ful for reducing post-operative pain.
• NSAIDs and paracetamol either alone or in
combination are useful for providing mild
to moderate pain relief. For cases of severe
pain, the use of an opioid combined with
either NSAIDs or paracetamol is
recommended.
• Local anaesthesia should be selected with
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241
ing the Gow-Gates mandibular nerve block,
the Vazirani-Akinosi closed-mouth man-
dibular nerve block, the PDL injection
(intraligamentary), intra-osseous and intra-
pulpal methods.
• Oral anxiolytics can be used effectively to
reduce stress and anxiety before and during
treatment and to manage preoperative and
post-operative pain.
• Local intra-canal corticosteroid–antibiotic
preparations can be useful in reducing
post-operative pain in certain cases.
• Use of oral systemic corticosteroids can be
a useful adjunct when managing hypochlo-
rite accidents.
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 Endodontic–Periodontal
Interrelationship 16

Summary
The periodontal tissues and pulp–dentine complex form an intimate
continuum through which pathological changes of either one may lead to
infection of the other. The management of such lesions can be fraught with
diagnostic and therapeutic difficulty requiring a methodical multidisci-
plinary approach. Traditional classifications of endodontic–periodontal
lesions are largely academic and based inappropriately on an attempt to
identify the primary source of infection. Treatment and prognosis of
endodontic–periodontal lesions depend on the cause and the correct
diagnosis of each tissue. It is critical to determine whether the lesion is
primarily endodontic or periodontal in origin since this will determine
which treatment plan is instigated. True combined lesions require a staged
approach with endodontic treatment initiated followed by a 2–3-month
review to reassess outcome. Appropriate periodontal therapy can then be
initiated followed by further review to assess outcome. The long-term
prognosis for such cases will be guarded requiring not only careful clinical
management but also patient motivation.

Clinical Relevance lesions of endodontic origin, palatal grooves,

A peri-apical lesion of pulpal origin may
simulate the radiographic appearance of
advanced periodontal disease and drain through
the sinus tract originating from the apex, lat-
eral or furcal accessory canal along the root
surface. This condition is not a true periodontal
pocket and must be distinguished from those of
periodontal origin. Accurate diagnosis is usu-
ally attained through careful diagnostic test-
ing including pulp vitality, periodontal probing
and radiographic examination. In addition to
fused roots, enamel pearls and vertical root
fractures can cause narrow probing defects as
well. The long-term success of a true combined
endodontic–periodontal lesion depends on a
number of crucial and key factors including the
severity and extent of the initial peri-apical and
periodontal infections, the correct treatment
planning and decision-making, the skill and
experience of the clinician(s) and the motiva-
tion of the patient, particularly with long-term
periodontal care

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 245
DOI 10.1007/978-3-319-15591-3_16, © Springer International Publishing Switzerland 2015
246
16.1 Overview of Endodontic–
Periodontal
Interrelationship
Endodontic–periodontal lesions refer to diseases,
which affect the peri-apical and periodontal tis-
sues through microbial infections arising from
the root canal system, periodontal pocket or a
combination of both. Such infections are a chal-
lenge to the clinician as far as diagnosis, progno-
sis and decision-making are concerned. In
particular, it is critically important to determine
whether the lesion is primarily periodontal or pri-
marily endodontic in origin, because the accu-
racy of diagnosis will determine whether or not
the appropriate treatment plan is instigated [1].
A number of classification systems have been
proposed resulting in confusion and controversy
due to overlapping terminology. The majority
have focused on identifying the initial source of
infection, which can be difficult. Classification
systems are necessary as they guide the diagno-
ses, which, in turn, determine prognosis and the
most appropriate sequence of treatment.
Furthermore, classification systems allow similar
clinical conditions to be evaluated in clinical tri-
als so that the evidence can be translated into
clinical practice. Discussing prognosis with
patients prior to treatment allows patients to
understand all the risks involved with a proposed
treatment and gives the opportunity to decide
whether a tooth is treated or removed [2, 3].
An excellent systematic review was recently
published highlighting the variability of defini-
tions for PE lesions as well as the small number
of controlled clinical trials [4]. PE lesions were
defined as the coexistence of a negative or altered
pulp vitality test and a probing pocket depth
(PPD) ≥6 mm (on at least one tooth for case
reports, or mean for interventional studies and
case series). The majority of publications are
case series that demonstrate successful treatment
outcomes following an accurate diagnosis and
staged treatment. These sequential treatment pro-
tocols have become the mainstay of treatment for
PE lesions. Future studies should be well-
designed, randomised, controlled, clinical trials
to reduce the publication bias inherent within the
16 Endodontic–Periodontal Interrelationship
case series with negative results less likely to be
published [5]. Within the studies analysed in the
systematic review, there was a high number of
patient dropouts (up to 27.9 %) with the outcome
of treatment not truly evaluated. Therefore, care
must be taken in treatment planning PE lesions,
as prognosis may be difficult to determine from
the outset and during treatment. Extended peri-
ods of observation may be useful in assessing the
outcome of periodontal treatment prior to a final
decision on completion of endodontic care or
placement of a full-coverage restoration [42].
In both endodontic and periodontal diseases,
the primary aetiology for causing disease is
microbial. In a classical study, the pulps of nor-
mal rats were exposed and left open to the oral
environment, resulting in pulpal necrosis, peri-
apical inflammation and peri-apical lesion forma-
tion. However, when the same procedure was
performed in germ-free rats, pulps not only
remain vital with minimal inflammation but also
dentinal repair at the exposure site occurred. The
study demonstrated that without bacteria and
their by-products, peri-apical lesions of endodon-
tic origin did not occur [6]. In pulpal disease, the
pathogens are located as biofilm within the inter-
nal walls of the root canal system, whereas in
periodontal disease, the biofilm is located on the
external root surface. Using specific PCR meth-
ods, the profiles of periodontal pathogens in
pulpal and periodontal disease within the same
tooth have been used to confirm the predominant
anaerobic species present [7]. Actinobacillus
actinomycetemcomitans, Bacteroides forsythus,
Eikenella corrodens, Fusobacterium nucleatum,
Porphyromonas gingivalis, Prevotella interme-
dia and Treponema denticola were found in all
endodontic samples, and the same pathogens
were found in teeth with chronic apical periodon-
titis and chronic adult periodontitis [7].
Several main avenues for exchange of infec-
tious elements and irritants (microbial) between
the pulp space and periodontium exist includ-
ing the apical foramen, lateral and accessory
root canals, furcation area and furcal canals,
apical delta and dentinal tubules. The apical
foramen represents the largest communication
between the pulp and the peri-apical tissues.
16.1 Overview of Endodontic–Periodontal Interrelationship
It allows the passage of endodontic bacteria
and by-products into the periodontal tissues to
form apical lesions [6]. Similarly, periodontitis
advancing towards the apex can disturb the api-
cal blood supply and lead to pulpal necrosis. In
some situations, bone loss from periodontitis
can extend beyond the root apex mimicking the
radiographic appearance of an apical radiolu-
cency caused by an infected pulp. This high-
lights the importance of combining radiographic
findings with clinical examination and sensibil-
ity tests. If there is no obvious cause for the
tooth becoming nonvital (such as caries), the
restoration should be removed to allow proper
assessment to rule out fractures or cracks. The
use of an endodontic microscope may aid diag-
nosis and also allows teeth with unrestorable
fractures to be removed prior to embarking on
treatment [8].
Lateral canals occur due to the breakdown of
Hertwig’s epithelial root sheath during root for-
mation [9]. Blood vessels running between the
dental papilla and dental follicle may be retained
and form accessory canals. Around 27 % of teeth
have lateral canals that are more commonly
found in the apical areas of the root [10]. A study
of 100 extracted human teeth found that only 2 %
of lateral canals were associated with periodontal
pockets when advanced periodontitis was present
[11]. This histological study supports the clinical
findings that only 3–4 % of teeth with advanced
periodontitis require endodontic treatment [12,
13]. If a lateral canal is exposed to the oral envi-
ronment, a chronic inflammatory lesion may
develop. Whilst pulp necrosis is possible [14], for
the majority of cases, the apical blood supply
remains intact and explains why pulp necrosis is
not common. Studies have also shown that lateral
and accessory canals do not always transverse the
entire length of the dentine and that many are
filled with connective tissue attachment rather
than blood vessels [15].
When dentine is exposed to the oral environ-
ment, through caries or a periodontal pocket,
the tubules can be penetrated by bacteria [16].
When the pulp is healthy, the outflow of den-
tinal fluid may limit bacterial penetration to the
outer 300 μm of the dentine [17]. Furthermore,
247
prolonged bacterial insult leads to a protective
pulpal reaction, formation of secondary dentine
and narrowing or occlusion of the dentine canal
at the pulp wall. The narrowing of tubules com-
bined with the outflow of dentinal fluid prevents
bacterial ingress into the pulp [17]. Therefore,
it is unlikely that periodontitis will lead to end-
odontic disease unless larger communications are
present. Root planing can mechanically dislodge
bacteria into the tubules and may explain the
presence of bacteria in dentinal tubules.
Besides these normal anatomical avenues, the
pulp and periodontal tissues may communicate
through either direct pathological pathways such
as vertical root fracture [18] and root perforation
[19] or indirectly via developmental anomalies
such as deep radicular grooves [20].
Periodontitis may have a cumulative effect on
the pulp tissue once lateral canals are exposed.
These degenerative changes may manifest as cal-
cifications, resorption or inflammation leading to
damaged pulp tissue [21]. Langeland and co-
workers demonstrated that total disintegration
might occur when all the main apical foramina
are involved [22]. In a primate study, the investi-
gators found that scaling and root planing, and
subsequent plaque re-accumulation on the
exposed root dentin, does not cause severe altera-
tion in the pulp [23]. This was confirmed in addi-
tional studies that demonstrated that the incidence
of endodontic disease in cases of advanced peri-
odontitis was small [24–26]. Some of the best
evidence arises from studies evaluating pulpal
histology of roots that were resected due to very
advanced periodontitis and bone loss near the
apex. Smukler and Tagger found that none of the
20 samples showed inflammatory changes [26].
Similarly, Haskell found very few inflammatory
cells in the pulps of resected roots. This suggests
that periodontitis does not have a significant
effect on the pulp even when bone loss is
extensive [25].
An abscess is a localised collection of pus in a
cavity formed by disintegration of tissues. The
formation of pus is termed suppuration. The end-
odontic abscess occurs after necrosis of the den-
tal pulp and subsequent root canal infection. The
periodontal abscess occurs after infection of the
248 16 Endodontic–Periodontal Interrelationship

Table 16.1 Differential diagnosis of a lateral periodontal and apical abscess

Lateral periodontal abscess Apical abscess
Pain Less severe than apical abscess Severe
Swelling More gingivally Usually over apex
Palpation tenderness More gingivally Apically
Percussion tenderness Mild or none Very tender
Timing Usually swelling before pain Usually pain before swelling
Pocket formation Yes Not always but can occur
History of trauma/previous restoration Not usually Usually
Previous symptoms of pulpitis Not usually Frequently
Radiographic appearance Marginal bone loss evident May be apical rarefaction

periodontal tissues by bacteria of the subgingival
microbiota. Dental abscesses in general expand
through tissues providing the least resistance by
forming a sinus tract (fistula). In the case of a
periodontal abscess, drainage is most likely to
take place through the periodontal pocket. In the
case of a peri-apical abscess, the spread is pri-
marily dictated by the thickness of overlying cor-
tical bone and the location of the abscess in
relation to the muscle attachments. In periodontal
health, the fistula may occasionally drain from a
peri-apical abscess along the root surface into the
gingival pocket. It is no different from a draining
sinus tract in the alveolar mucosa or attached gin-
givae. When the pocket is probed, it is narrow
and lacks width. From a diagnostic point-of-view
presentation, pulp testing procedures and peri-
odontal probing are critical to accurate diagnosis
(see Table 16.1). Insertion of a gutta-percha cone
into the sinus tract and taking subsequent radio-
graphs can help determine the origin of the lesion.
No periodontal treatment is indicated and it
should resolve following adequate endodontic
therapy [14, 27, 28].
When an endodontic infection drains through
a pre-existing periodontal pocket (periodontal
disease), the pre-existing periodontal pocket
appears more extensive because of the draining
endodontic lesion. Whilst endodontic treatment
results in periodontal healing at the base of the
pocket, periodontal treatment will be required to
treat any residual pocketing.
Animal studies have demonstrated that peri-
odontal debridement of root surfaces exposed
due to an endodontic infection results in down-
growth of epithelium and compromised healing
[29]. This relates to the removal of periodontal
ligament and cementum on the root surface dur-
ing scaling and root planing, and therefore, the
potential for reattachment is lost [30]. In more
severe cases where endodontic infection meets a
pre-existing advanced periodontal pocket, treat-
ment can be carried out in short succession. For
example, root resection may be performed if it is
felt that the periodontal infection would cause
recontamination of the apical area. However, in
most cases endodontic treatment should be
applied first.
When endodontic therapy has been completed
to an acceptable standard, there does not appear
to be any difference in the stability of marginal
bone levels [31] with more recent studies show-
ing no impact of the success of periodontal
regeneration in root-filled teeth [32]. The series
of studies by Jansson and co-workers evaluated
the impact of endodontic status in patients treated
for advanced periodontitis. Deeper periodontal
pocket depths were found in teeth with peri-
apical lesions, defined by loss of lamina dura or a
widened periodontal ligament space in teeth with
or without previous endodontic treatment. The
clinical relevance is unclear as the difference in
probing depths was less than 1 mm. When exam-
ined longitudinally, the amount of bone loss was
higher in sites adjacent to apical lesions
(0.19 mm/year. vs. 0.06 mm/year). These studies
confirm the need to treat endodontic infections
prior to periodontal treatment; however, the clini-
cian needs to be cautious not to treat a radiolu-
cency that is not associated with endodontic
infection. Review of previous radiographs and
consideration of clinical findings and diagnostic
16.1 Overview of Endodontic–Periodontal Interrelationship
a b
Fig. 16.1 (a–c) Clinical radiographs demonstrating moderate to severe periodontitis with concurrent endodontic pathology
a b
Fig. 16.2 Diagrams representing classification of
periodontal–endodontic lesions (a) Normal healthy tooth.
(b) Primary endodontic lesion (either peri-apical, lateral
tests will help reduce the risk of overtreatment
[33–35].
Endodontic–periodontal lesions are classified
according to the origin of the problem. There are
various definitions in the literature causing a
great deal of confusion [1–3, 14, 28]. Accurate
diagnosis is essential and will establish the nature
and timing of treatment. The most important fea-
ture of classifying periodontal–endodontic
lesions is whether there is communication, which
forms the basis of a true combined lesion (see
Figs. 16.1 and 16.2).
Primary periodontal lesions represent an
advanced periodontal lesion that has disrupted
249
c d
or furcal origin). (c) Primary periodontal lesion. (d) True
combined lesion. Different treatment approaches will be
dictated by origin of lesion
the blood supply to the apex of the tooth causing
it to become nonvital. This is rare with studies
reporting this to occur in 3–4 % of teeth with
advanced periodontitis [12, 24]. These lesions
have a poor prognosis due to the difficulty in
debriding the root surface near the apex and the
extent of periodontal destruction.
Primary endodontic lesions occur when an
endodontic infection causes periodontal destruc-
tion. This may be caused by drainage of an end-
odontic infection through a periodontal pocket.
Overall, these lesions have a good prognosis if
the endodontic cause can be addressed. A pri-
mary endodontic lesion can also arise due to
250
communication between the pulp and periodon-
tium following endodontic perforations, resorp-
tions and root fractures. The prognoses of these
types of lesions can be questionable.
True combined periodontal–endodontic
lesions form when there is coalescence of end-
odontic and periodontal lesions [36]. It is not
possible to accurately determine the prognosis of
the tooth at the initial examination because the
relative contribution from endodontic versus
periodontal infection is unknown. Once the end-
odontic infection has been eliminated, the resid-
ual periodontal defect that remains can guide
overall tooth prognosis. Therefore, if a true com-
bined lesion is suspected, an endodontic dressing
is placed after irrigation and debridement of the
canals. Following endodontic healing, the
periodontal pockets are reassessed to determine
feasibility of periodontal treatment in order to
retain the tooth. True combined periodontal–
endodontic lesions will require endodontic ther-
apy, periodontal treatment (possibly periodontal
surgery) and a full-coverage restoration, requir-
ing a significant investment in treatment time
and costs. This cost must be weighed up against
the patient’s wishes to keep the tooth at all costs
versus the prognosis of any tooth replacement.
An additional consideration is the difficulty to
assign an accurate periodontal prognosis [37],
and therefore, there may be a tendency to extract
periodontally involved teeth because of this
uncertainty. However, we must acknowledge the
potential for biological complications [38] with
patients with a history of periodontitis having a
higher susceptibility for peri-implantitis [39].
Bragger and co-workers also showed that one in
three patients experienced a technical implant
complication within the first 10 years of treat-
ment [40]. Patients need to be involved in the
treatment planning process so that the risk of fail-
ure is minimised.
Longitudinal tooth cracks and fractures that
principally occur in the vertical plane or long axis
of the crown and/or root can lead to particular
uncertainty in terms of diagnostic and treatment
decisions. The term ‘crack’ implies an incom-
plete break in the tooth exists, whereas the term
‘fracture’ implies an incomplete or complete
break in the tooth exists. When either a crack or
fracture has been present for a particular time
16 Endodontic–Periodontal Interrelationship
period along the long axis of the tooth, it can be
classified as a longitudinal fracture [48].
Longitudinal fractures can be occurring in
both anterior and posterior teeth as a result of
multifactorial aetiology. Predisposing factors
such as loss of healthy tooth substance due to car-
ies or trauma can increase the risks of cracks that
can propagate to fracture. Physical trauma, occlu-
sal prematurities, repetitive heavy and stressful
chewing have also been identified as risk factors
[49–51]. Complex restorative procedures includ-
ing endodontic access preparation, loss of mar-
ginal ridges, intra-canal dowel placement and
excessive dentine removal can all result in weak-
ened tooth structure increasing susceptibility to
cracks or fractures [52]. Anatomical predisposi-
tion such as narrow mesio-distal dimensions of
premolar teeth and the mesial roots of mandibu-
lar molars make these teeth more susceptible to
fracture, particularly if additional tooth structure
is removed during root canal or post preparation
procedures [53–56].
Identification of longitudinal root fractures
can be difficult. Cracks or fractures that have
been present for extended period of times may
become stained, cause pain or result in obvious
bone loss that can be diagnosed both clinically
and radiographically. Techniques available for
detection of fractures include transillumination
[55], biting devices such as the Fracfinder, meth-
ylene blue staining, magnification and illumina-
tion and radiography [57]. Clinical signs and
symptoms as well as radiographic features can
often be similar to those associated with non-
healing endodontic treatments. Certain periodon-
tal manifestations including accompanying bone
loss, pocketing and sinus tracts may be present.
Unless the crack or fracture is obviously visible
by direct inspection, then the diagnostic dilemma
of whether these features are associated with
endodontic pathology, periodontal pathology, a
true combined lesion or longitudinal fracture
remains. Nevertheless a rapid decision is required
to avoid further bone loss, which can lead to
reconstructive difficulties particularly if a dental
implant is planned in the future [58].
The American Association of Endodontists
has categorised longitudinal root fractures into
five major classes: craze lines, fractured cusp,
cracked tooth, vertical root fracture and split
16.1 Overview of Endodontic–Periodontal Interrelationship
a b
f g
Fig. 16.3 Clinical photographs and radiographs demon-
strating difficulties when diagnosing vertical root fracture.
Note (a) preoperative view of tooth 35 which had under-
gone previous root canal treatment. Clinical examination
revealed (a) a narrow 10 mm + probing profile on the lin-
gual aspect. (b–d) Following removal of the coronal resto-
ration, no obvious crack line was evident internally
despite staining with methylene blue dye. The radio-
tooth. Craze lines affect only the enamel, origi-
nate on the occlusal surface arising from occlusal
forces or thermocycling and are asymptomatic.
Fractured cusp occurs on the cusps and cervical
margins of the root resulting in acute pain on
mastication and thermal stimulus. Cracked tooth
can occur on the crown and extend into the root
developing from occlusal forces or as a direct
result of weakened tooth structure. Variable signs
and symptoms may exist. Vertical root fracture
occurs and originates in the roots with variable
signs and symptoms caused by wedging forces
within the roots (such as root canal obturation or
posts). Split tooth is a fracture through the crown
251
c d
h i
graphic appearance using conventional digital radiogra-
phy revealed no unusual peri-radicular pathology in
relation to this tooth (f). A cone-beam CT scan (e, g–i)
was arranged confirming an extensive J-shaped peri-
radicular radiolucency indicative of a probable vertical
root fracture. The patient was referred for extraction and
alternative prosthodontic replacement of this tooth
and root developing from damaging occlusal
forces or weakened tooth structure resulting in
separation of the tooth into two segments. The
tooth is typically painful on mastication [48, 50,
51, 58–60].
Radiographic determination of the presence
and extent of cracks or even vertical root frac-
tures cannot be consistently determined using
conventional plain film radiography or with the
recent advancements in cone-beam volumetric
tomography (CBVT) scans [61–63]. Axial slices
were more accurate in the detection of vertical
root fractures compared to sagittal and coronal
slices (see Fig. 16.3). The obvious sign of root
252
fracture is the radiographic appearance of root
segment separation. Strong indications in ascer-
taining the presence of a vertical root fracture
include the presence of a ‘halo’ appearance,
which is a combined peri-apical and perilateral
radiolucency in one or both sides of the root, lat-
eral periodontal radiolucency along the side of
the root or angular radiolucency from the crestal
bone terminating along the root side. In mandibu-
lar molars, radiolucency in the furcation area can
also be observed coupled with the types of radio-
lucencies described above [58, 64, 65].
Management options for cracked teeth have
the most variation due to the difficulty of accu-
rately predicting the true extension and depth of
the crack line. Treatment options for cracked
teeth with vital pulps include cuspal coverage
crown reinforcement [66] or bonded restorations
[59, 67]. If the fracture line has progressed fur-
ther down the root resulting in bacterial ingress
into the pulp chamber, then the pulp may become
nonvital requiring endodontic treatment [48, 50,
59, 68]. The prognosis for both vertical root frac-
tures and split teeth is poor, and extraction should
be considered [58–60].
Root resection is the surgical procedure by
which one or more of the roots of a multi-rooted
tooth are removed at the level of the furcation
whilst the crown and remaining roots are left in
function [69]. Endodontic indications include
root fracture or perforation, external root resorp-
tion, failed root canal treatment, root caries or
endodontic–periodontal combined lesions.
Periodontal indications include moderate to
advanced furcation involvement, severe bone loss
affecting one or more roots, severe recession or
dehiscence of a root or unfavourable root prox-
imity between adjacent teeth [70]. The prognosis
of root resection has been well documented in the
literature. Carnevale reported a group of 72
patients with 175 furcated molars, treated with
root resection and prosthetic restoration and fol-
lowed longitudinally for 10 years. At the 10-year
examination, the tooth survival rate was 93 % and
the prosthetic survival rate was 96 %. The causes
of failure were peri-apical granuloma, secondary
decay, reoccurrence of periodontitis and root
fracture [71]. Combined endodontic, periodontal
16 Endodontic–Periodontal Interrelationship
and prosthodontic measures to ensure the reten-
tion of a tooth or root(s) can be complex, time-
consuming and costly. With the increased use of
endo-osseous dental implants to replace failed or
failing teeth, the role of a root resection as part of
the treatment option has come into question.
Nevertheless, when comparing the prognosis of
root resection therapy to that of a dental implant,
Fugazzatto and colleagues reported a 15-year
cumulative success rate of 96.8 % for root
resected molars and 97.0 % for molar implants.
They concluded that molar root resection therapy
and implant therapy had a high degree of func-
tional success [72]. Such outcomes are usually
achieved with extremely motivated patients who
have been treated by experienced clinicians under
ideal conditions.
Endodontic–periodontal lesions commonly
affect teeth concurrently by pulpal and periodon-
tal infection leading to pulpal necrosis and attach-
ment loss, respectively. The long-term, successful
prognoses for these teeth depend on a number of
crucial and key factors including the severity and
extent of the initial peri-apical and periodontal
infections, the correct treatment planning and
decision-making, the skill and experience of the
clinician(s) and the motivation of the patient,
particularly with long-term periodontal care [73].
16.2 Diagnosis of Endodontic–
Periodontal Lesions
The diagnosis of periodontal–endodontic lesions
is based on a thorough history correlated with
clinical examination and radiographic findings
encompassing pulp sensitivity tests, percussion,
transillumination, probing pocket depths, mobil-
ity assessment and identification of bleeding and/
or suppurating pockets.
It is important to determine if the periodontitis
is generalised or limited to one site or tooth. The
pocket morphology can also provide a clue as to
the likely origin of the infection. A narrow peri-
odontal pocket suggests an endodontic cause or
tooth fracture. Conversely, pocket formation due
to periodontitis is broad at the gingival margin
and narrows towards the apex as the periodontal
16.2 Diagnosis of Endodontic–Periodontal Lesions
lesion advances. When a narrow pocket is found
in a tooth with a vital pulp response, it is impor-
tant to consider that narrow pockets may also be
associated with developmental grooves, fused
roots or cervical enamel projections into furca-
tion areas.
Pulp vitality tests can be used although the
results need to be interpreted carefully. Sensibility
tests determine the response of the nerve but do
not evaluate the state of the pulp’s blood supply,
which is of greater importance. Furthermore, the
results may be inaccurate in multi-rooted teeth
where the pulp status may vary between roots.
This highlights the importance correlating sensi-
bility tests with the examination and radiographic
findings.
Radiographic assessment confirms the provi-
sional diagnosis based on history, examination
and special tests. The radiograph will provide
information on the location of the lesion (apex,
crest or furcation area) and will also determine
the presence of factors that may contribute to
pulpal death, such as the presence of a deep res-
toration. Radiographic change at the apex can be
a good indicator of an infected pulp, but may not
be visible until 2–4 months after pulpal infection.
Apart from a peri-apical radiolucency, there may
also be signs of a widened periodontal ligament
or loss of the lamina dura.
Primary endodontic lesion
A tooth with a necrotic pulp draining through
the periodontal ligament into the gingival sulcus
is termed chronic apical periodontitis with sup-
puration. Although this condition mimics a peri-
odontal abscess in reality, pulpal testing will
confirm a nonvital tooth. Clinical examination
will reveal a narrow pocket as a result of a sinus
tract from pulpal origin that opens through the
periodontal ligament area. From a diagnostic per-
spective, the insertion of a gutta-percha point into
the sinus tract and radiographic evaluation should
confirm the origin of the lesion (Fig. 16.4). When
the pocket is examined, it should be narrow, lack-
ing width and isolated. A similar situation may
arise if the drainage from a necrotic pulp extends
into the furcation area from the lateral canals.
Primary endodontic lesions will usually heal
following adequate root canal treatment. The
253
sinus tract extending into the gingival sulcus area
will disappear following chemo-mechanical
instrumentation and intra-canal medication
placement. Often the patient can be reviewed
4 weeks later and resolution of the false pocket
indicative of diagnosis. Completion of endodon-
tic treatment to an acceptable standard will pre-
vent any further infection.
The astute clinician must also be aware that
there are a number of narrow sinus tract type of
probing defects associated with a tooth with a
vital pulp (see Table 16.2). Pulp testing proce-
dures are critical to accurate diagnosis, and one
must bear in mind that the same clinical situa-
tions outlined may invariably be associated with
a nonvital tooth further confounding an accurate
diagnosis.
Primary periodontal lesion
These lesions are primarily caused by peri-
odontal pathogens resulting in chronic marginal
periodontitis progressing apically along the root
surface. In most cases, pulp sensitivity testing
indicates a vital clinically normal pulp. Frequently
there will be an accumulation of plaque and/or
calculus, and the pockets will be generalised and
wider.
Periodontal prognosis is influenced by local
and systemic factors with some factors being
impossible to modify. For example, the extent of
previous bone loss and the patient’s genetic
susceptibility cannot be altered. Other risk
factors for disease progression can be modified
but rely on patient compliance and include
their smoking habit, diabetic control, plaque
control and regular attendance for periodontal
maintenance.
Determination of prognosis can be difficult
due to the multifactorial and episodic nature of
periodontal attachment loss [74]. On a tooth
level, the prognosis is influenced by initial PPD,
furcation involvement, malposition of teeth, root
proximity, tooth type/root form, mobility, poor
crown–root ratio and a parafunctional habit
without a night guard [74], but the relative
importance of each factor is unknown. When
teeth with a good prognosis are excluded
(i.e. leaving teeth with some degree of furcation
involvement, mobility etc.), these factors could
254 16 Endodontic–Periodontal Interrelationship

a b c

d e f

Fig. 16.4 Clinical photographs and radiographs demon-
strating tracking of draining sinus and periodontal
pocket associated with a necrotic tooth 46. Note (a) pre-
operative radiograph demonstrating an extensive mesial
restoration overlying the mesial pulp horn, (b) a gingival
swelling and draining sinus with associated narrow
probing profile of 10 mm +, (c) gutta-percha points
placed in the overlying sinus and pocket, (d) gutta-percha
tracing radiograph confirming suppuration and pocket
associated with distal necrotic root of tooth 46, (e) mas-
ter apical file radiograph following chemo-mechanical
preparation and (f) intra-canal calcium hydroxide
medicament

Table 16.2 Clinical situations resulting in a narrow probing defect associated with a normal vital pulp
Situation
Sinus tract draining through the
periodontal ligament of a vital tooth
Developmental grooves
Fused roots of posterior teeth
Cracked tooth syndrome
Crown–root fractures
Vertical root fractures
Enamel spurs
The sinus tract may originate from an adjacent nonvital tooth or pulpless
tooth several teeth away. Such a sinus tract could also be related to
advanced periodontal disease
Developmental grooves commonly break down as a narrow sinus tract
probing defect. The probing contours may change over time particularly
if an acute infection develops
A fusion line may result in a periodontal defect similar to that which
occurs along a developmental groove
An incomplete coronal fracture extending into the root of the tooth
An extension of enamel into a furcation or on a root surface can often
break down as a periodontal defect
16.3 Management of True Combined Endodontic–Periodontal Lesions
accurately predict a worsening of prognosis in
35 % of cases after 8 years of supportive
periodontal therapy [37].
More recent evidence suggests that systemic
risk factors may be more important [37, 74, 75].
The number of deep residual pockets (≥6 mm)
[76, 77] and a high bleeding on probing score
(above 30 %) on a subject level also suggests a
worst prognosis [77, 78]. A long-term study of
patients in periodontal maintenance (mean
22 years) showed that single-rooted teeth have a
higher chance of survival than multi-rooted teeth.
Specifically, maxillary second molars have the
worst survival rate and mandibular canines have
the highest survival rate [79]. This study also
showed that out of 600 patients, 300 did not lose
any teeth which highlights that most patients can
have a very successful outcome following
periodontal treatment. During this time, the effects
of systemic and environmental factors were not
known which may have contributed to an
increased risk of tooth loss in the downhill groups.
Smoking has an impact on periodontitis due to
an increase in the prevalence and load of subgin-
gival calculus [80], attachment loss [81] and bone
loss [82]. The risk of losing teeth increases by 2.9
times, and this worsens to 7.7 when the patient
has a hyper-inflammatory IL-1 genotype [75].
Poorly controlled diabetes also increases the
prevalence and severity of periodontal attachment
loss [83], but well-controlled diabetics have a
similar outcome to periodontal treatment [84, 85].
Collectively, the evidence suggests that a thor-
ough risk assessment, incorporating systemic as
well as tooth or site-based risk indicators, should
be completed for every patient. This assessment
can be used to guide treatment decisions with an
understanding that developing a prognosis is dif-
ficult and that it is possible to maintain teeth even
if they are severely compromised. In patients
with aggressive periodontitis, 88.2 % of ques-
tionable and 59.5 % of hopeless teeth survived
15 years with regular supportive periodontal ther-
apy [86], highlighting that early removal of peri-
odontally involved teeth is not supported. Should
a tooth require removal and replacement with a
dental implant, the patient should be informed
255
that periodontitis and peri-implantitis share the
same risk factors and that periodontal mainte-
nance is essential. Risk factor identification and
management has become a key component of
care for periodontal patients [87].
16.3 Management
of True Combined
Endodontic–Periodontal
Lesions
When an endodontic–periodontal lesion is
suspected, an overall periodontal assessment
needs to be made to ascertain the amount of
destruction in the remaining teeth. Any endodon-
tic lesion that has resulted in damage to the peri-
odontal ligament should be treated first to see if
there is any possibility of spontaneous periodontal
healing. It is therefore suggested that endodontic
treatment be initiated with a healing period
allowed prior to re-evaluation of the periodontal
pocket and periodontal treatment. Initial endodon-
tic treatment would encompass chemo-mechanical
preparation of the root canals and placement of a
long-term intra-canal medicament such as cal-
cium hydroxide. Periodontal healing and the suc-
cess of endodontic treatment of this tooth can be
monitored whilst the periodontal therapy is com-
pleted at the remaining sites in the mouth.
A difficult scenario can arise when a patient
has generalised periodontitis and an endodonti-
cally treated tooth that has a deep pocket. It is
unclear whether the pocket has occurred due to
periodontitis or due to reinfection of the root
canal because of inadequate initial treatment or
coronal leakage. Alternatively, the pocket may
have developed due to root fracture or a resorp-
tive/perforation defect. The quality of previous
endodontic treatment must be evaluated, although
this may be difficult. The clinician should be sus-
picious of a root fracture or a missed canal. A
formal assessment by an endodontist can be help-
ful in these circumstances. If there are no other
signs of endodontic failure such as pain on biting
or recurrence of a peri-apical radiolucency on
radiographs, nonsurgical periodontal treatment
256
a b
d e
g h
Fig. 16.5 Clinical photographs and radiographs demon-
strating management of a primary endodontic lesion. Note
(a) preoperative radiograph of tooth 47 showing a
J-shaped radiolucency. (b) Clinical examination revealed
a draining sinus on the mesial aspect of tooth 47. (c)
Gutta-percha was placed in the sinus and (d) radiographi-
cally tracked to the distal aspect of tooth 47. (e) Chemo-
may be initiated with a view to carrying out
exploratory flap surgery soon after.
If the restorability of the tooth is called into
question and is not suitable for endodontic
retreatment, periodontal treatment can begin and
the tooth maintained until the results of nonsur-
gical periodontal debridement is reviewed. If the
site does not heal, the area may be explored sur-
gically to identify the facture preventing heal-
ing. If a fracture is found, the tooth can be
removed and the socket debrided so that an
implant can be placed following osseous heal-
ing. In these cases, deferring extraction allows
patients with periodontitis to retain teeth in a
16 Endodontic–Periodontal Interrelationship
c
f
i
mechanical debridement revealed unusual apical anatomy
with confluence of all canals. (f) Following placement of
calcium hydroxide, intra-pulpally dressing was noted in
the overlying sinus. (g) At 4-week review appointment,
the buccal sinus had resolved, (h) mid-fill radiograph
demonstrating complex apical anatomy and (i) post-oper-
ative x-ray showing radiographic healing at 4 weeks
compromised but noninfected state so that func-
tion and aesthetics can be maintained until risk
factors for implant failure have been addressed
and implant placement is suitable. This is a valu-
able strategy in patients with advanced forms of
periodontitis as it can take time to gauge a
patient’s response to treatment and determine
overall prognosis of the dentition. This also lim-
its the impact of alveolar bone loss that occurs
once teeth are removed [41].
The treatment sequence of a combined peri-
odontal–endodontic infection is outlined below:
1. Endodontic access to determine the feasibility
of endodontic treatment (absence of cracks,
16.3 Management of True Combined Endodontic–Periodontal Lesions
a b
Fig. 16.6 Clinical radiographs and photographs demon-
strating true combined endodontic–periodontal lesion
associated with tooth 17. Note (a) preoperative x-ray
demonstrating 40–60 % horizontal bone loss and a peri-
radicular lesion, (b) preoperative intra-oral view of tooth
17 prior to (c) chemo-mechanical preparation and calcium
canal patency, tooth restorability). If deemed
satisfactory, the restoration is removed with
an orthodontic band used as an interim resto-
ration (see Fig. 16.5). The canal can be pre-
pared and an intra-canal dressing placed. A
second dressing may also be used to ensure
that the environment for periodontal healing is
not affected by endodontic infection.
2. During endodontic care, oral hygiene tech-
niques can be revised and the patient moti-
vated to achieve good plaque control.
3. The success of endodontic intervention can be
reviewed after a 4-week healing period.
Whilst there is no evidence to suggest an ideal
healing time, soft-tissue wound healing may
progresses rapidly and is likely to be complete
by 4 weeks. There is indirect evidence from
the healing of gingivectomy wounds showing
that epithelial growth occurs at a rate of
0.5 mm per day. [42]. However, 3–5 weeks are
required for the maturation of the gingival
connective tissue. [43]. A study by Proye and
co-workers evaluated the dynamics of healing
after root planing and showed that substantial
reduction in PPD occurs within 3 weeks after
a single episode of root planing. This is due to
recession and a gain in clinical attachment
[44]. Classical studies by Badersten and co-
workers highlight that periodontal healing can
257
c d
hydroxide dressing placement. (d) Review at 3 months
shows resolution of peri-apical lesion. Although the end-
odontic prognosis is good, the periodontal prognosis
remains guarded due to extensive periodontal probing and
bone loss associated with tooth 17
take up to 9 months, but most of the healing
occurs in the first 3 months. Therefore, it is a
reasonable approach to wait 3 months prior to
completing periodontal treatment once the
endodontic infection has resolved [45, 46].
4. Re-evaluation of periodontal health can be
assessed 3 months following nonsurgical ther-
apy. If residual pockets remain, a new radio-
graph is taken to assess osseous repair at the
apical region (indicating favourable endodon-
tic healing) (see Fig. 16.6). If satisfactory,
periodontal surgery can be considered. It is
best to complete all periodontal treatment
prior to completion of endodontic treatment to
guide overall prognosis. If the periodontal
healing has not been adequate, the endodontic
canals are redressed and a further healing
period observed,
5. Endodontic root filling may be completed and
a full-coverage restoration placed. Depending
on the difficulty of endodontic treatment and
the periodontal prognosis, an extended heal-
ing period may be required if there is any
doubt on the tooth’s prognosis. A cusp capped
direct restorative material can be used as a
long-term provisional restoration.
6. Periodontal maintenance is necessary with the
interval depending on the patient’s periodon-
tal risk [47].
258
16.4 Craze Lines
Craze lines commonly found in the permanent
dentition can affect both anterior and posterior
teeth. In anterior teeth, a long vertical defect may
be evident on the facial aspect of the tooth extend-
ing from the cervical area to the incisal edge. In
posterior teeth, they may extend over the marginal
ridges or buccal and lingual surfaces. The crazing
only affects the enamel and causes no clinical
symptoms. Transilluminated light from the facial
or lingual surface is not blocked or reflected
resulting in the entire tooth being illuminated.
Craze lines do not require any intervention.
16.5 Fractured Cusp
A fractured cusp is defined as a complete or
incomplete fracture that initiates from the crown
of a tooth and extends subgingivally in both a
mesio-distal and facial–lingual direction. The
marginal ridges and facial and lingual grooves
a b
e f
Fig. 16.7 Diagrams and clinical photographs demon-
strating fractured cusp. (a–d) Fractured cusps can be inde-
pendent of the root canal system or involve the root canal
system. The latter requires endodontic treatment provided
the tooth is deemed restorable. (e) Clinical presentation of
a fractured cusp associated with the MP canal of an upper
16 Endodontic–Periodontal Interrelationship
may be involved with the fracture extending to the
cervical third of the crown or root (see Fig. 16.7).
The most common cause of fractured cusps
are large restorations and extensive decay
resulting in substantial loss of sound dentine
culminating in undermined and unsupported
tooth structure. This can often lead to the devel-
opment and increased susceptibility of the tooth
to fracture. Cusp fractures tend to be shallow usu-
ally resulting in no pulpal exposure. Clinically
the patient may report brief, sharp pain on masti-
cation or temperature sensitivity, particularly to
cold. Often the pain is described as pain on
release associated with certain hard foods such as
when eating steak or breads with grains. Pain
only occurs on stimulus and symptoms may be
relieved when the cusp fractures off. Symptoms
may be reproduced using a biting test such as
closing onto a piece of cotton wool or using the
Fractfinder or tooth sleuth bite test instrument.
Pulp testing should confirm vitality.
Treatment often involves removal of the exist-
ing restoration and confirmation of a fractured
c d
g
right maxillary molar. (f, g) Following removal of the
fractured cusp, a restorability assessment is made to see
whether the tooth is deemed restorable. Additional crown
lengthening procedures may be indicated if a suitable fer-
rule is not available
16.6 Cracked Tooth Syndrome
mobile cusp. The separated cusp should be
removed and provided the tooth is restorable, i.e.
the fracture does not extend subgingivally along
the root surface near crestal bone; an appropriate
cast restoration can be placed.
The long-term prognosis for shallow cusp
fractures not involving the pulp is favourable pro-
vided a suitable cast restoration is placed to
ensure the tooth is protected. To prevent the pos-
sibility of cusp fractures, inlay restorations that
can increase the propensity to wedge should be
avoided. Adequate cuspal coverage protection
can be provided using onlay amalgam or gold
restorations that provided significant fracture
resistance particularly in patients with heavy
occlusal contacts or a history of bruxism. Bonded
restorations should be carefully placed with
incremental packing and curing to reduce poly-
merisation shrinkage that can further weaken
cusps increasing the potential for fracture in the
future.
16.6 Cracked Tooth Syndrome
A cracked tooth is a variant of the fractured cusp,
although they tend to be centred more occlusally
and extend in an apical direction with possible
pulpal involvement. It is defined as an incomplete
fracture initiated from the crown and extending
subgingivally, usually directed mesio-distally.
Aetiological factors that may predispose to
cracked tooth include the type of restoration
used to restore the tooth. Teeth restored with
amalgam and gold inlays without adequate cus-
pal coverage may be more susceptible to micro-
crack formation as a result of cuspal flexure
caused by occlusal load stress during mastica-
tion and repeated thermal expansion of the
restorative material. Restorative procedures
such as retentive threaded pin placement using a
twist drill may also result in internal stresses
that can lead to cracking or crazing of dentine.
Cracks can also occur in an unrestored tooth as
a direct result of trauma from chewing hard,
brittle substances (grains, nuts etc.).
Diagnostic tests used to confirm cracked tooth
include clinical symptoms, transillumination,
bite testing, removal of restorations and methy-
259
Fig. 16.8 Clinical photograph demonstrating multiple
internal cracks associated with a tooth diagnosed as
cracked tooth syndrome. (a) Following removal of the
overlying amalgam restoration, a mesio-distal crack line
is noted in the floor of the cavity overlying the pulp cham-
ber. Methylene blue dye is used to stain the floor of the
cavity to highlight the cracks
lene blue dye staining, tracing the track with a
bur, pulpal vitality testing and radiographic
assessment. Symptoms associated with cracked
teeth have been described as acute pain (sharp)
that occurs during mastication (or release) of cer-
tain small hard food substances that may be exac-
erbated by cold. If pulpal involvement has
occurred, then variations may occur with signs
and symptoms consistent with irreversible pulpi-
tis or pulp necrosis.
If any restorations are present, they should be
removed in the first instance to allow for direct
inspection of the tooth. Transillumination may
show a characteristic abrupt blockage of the
transmitted light. When a fracture is present, a
thin air space may be present which does not
readily transmit light. Staining the tooth with
methylene blue may also highlight the extent
and nature of the fracture although not predict-
ably. Methylene blue soaked on a cotton wool
pledget can be applied directly to the tooth under
rubber dam staining all internal walls and the
floor of the cavity (see Fig. 16.8). Once the dye
is washed away, the crack line may become
obvious. Further inspection using illumination
and magnification (preferably using a dental
260
a b
e f
Fig. 16.9 Clinical radiographs demonstrating manage-
ment of teeth diagnosed as cracked tooth syndrome. (a)
Extensive fracture extending subgingivally on the palatal
aspect of tooth 26. An obvious peri-radicular radiolucency
was noted. (b) The tooth was deemed restorable, and fol-
lowing chemo-mechanical preparation and intra-canal
calcium hydroxide medicament, an orthodontic band was
cemented in place. (c) Obturation was completed 3 months
later with significant reduction in the apical lesion. (d)
operating microscope) is useful to confirm the
presence and extent of the fracture. If irrevers-
ible pulpitis or pulp necrosis is suspected and the
crack appears to involve the pulp chamber, then
endodontic access will be necessary. Following
access preparation and coronal pulp removal,
the floor of the pulp chamber can be inspected
following dye application. Removal of the frac-
ture line in the proximal portions of the tooth or
axial walls of the cavity may further reveal the
extent of the fracture line. One must bear in
mind that complete removal of the fracture line
will not always disclose the true extent and
removal of sound tooth structure will further
16 Endodontic–Periodontal Interrelationship
c d
g h
Completed cast restoration demonstrating good marginal
integrity that will ensure success over the long term. (e)
Preoperative view of tooth 47 suspected of cracked tooth
syndrome and irreversible pulpitis symptoms. A decision
was made to carry out endodontic treatment prior to final
definitive cast restoration. (f–h) Two-stage endodontic
treatment using intra-canal medicament was carried out
with an orthodontic band in place prior to definitive
restoration
compromise both restorability and reduce tooth
strength increasing susceptibility to further frac-
ture in the future.
Periodontal probing should be routinely car-
ried out when assessing the tooth since this may
disclose the approximate depth and severity of
the underlying fracture. The presence of deep
probing may also be associated with periodontal
disease, and the absence of deep probing does not
preclude the diagnosis of cracked tooth.
Selective bite testing using a tooth sleuth or
Fractfinder is particularly helpful when the
patient reports masticatory pain either on biting
or release. Radiographic assessment is usually
16.8 Split Tooth
inconclusive in relation to crack determination
but invaluable when determining probable pulp
status of the tooth.
Determining the appropriate treatment for
teeth with unknown depth may be difficult par-
ticularly when pulpal assessment is inconclusive.
In cases where the pulp is deemed vital and not
associated with crack extension, then cuspal cov-
erage restorations with a crown or a bonded res-
toration are indicated. Krell and Rivera evaluated
27 patients who were diagnosed with vital
cracked teeth and treated with cast cuspal cover-
age restorations without endodontic intervention.
Within 6 months, 20 % of patients experienced
signs of irreversible pulpitis requiring root canal
treatment. Eighty percent of patients remained
asymptomatic at the 6-year evaluation period.
In cases where the pulp chamber is involved,
careful inspection of the floor of the pulp cham-
ber, axial walls and coronal root canal orifices
must be made. If the fracture extends through the
floor of the pulp chamber or below the level of the
alveolar bone, then treatment is hopeless and
extraction is necessary. Fracture lines extending
into the canal orifices carry a guarded prognosis at
the very least, and the patient must be made aware
of further crack propagation and root fracture
despite endodontic and restorative intervention. A
stainless steel orthodontic band should be placed
to protect the cusps and tooth until completion of
endodontic treatment and provision of definitive
cast cuspal coverage restoration (see Fig. 16.9).
16.7 Vertical Root Fracture
A vertical root fracture (VRF) is defined as a
complete or incomplete fracture initiated in the
root at any level and usually directed bucco-
lingually. It typically extends to the periodontal
ligament resulting in soft-tissue growth into the
fragment space and increased separation of the
root segments. Periodontal ligament breakdown
manifested as narrow pocketing, alveolar bone
loss and granulation tissue formation can
occur when bacteria ingress to the fracture area.
Rapid alveolar bone breakdown with either bony
261
dehiscence or fenestration can result. Clinically
commons signs and symptoms include pain to
percussion, pain on palpation, pain on mastica-
tion, mobility, swelling, isolated periodontal
defects and the presence of one or more highly
localised sinus tracts in the overlying attached
gingivae. Radiographic signs include either a
‘halo’ appearance, which is a combined peri-
apical and peri-radicular radiolucency on one or
both sides of the root, lateral periodontal radiolu-
cency along the side of the root or an angular
radiolucency from the crestal bone terminating
along the root side. Furcation involvement may
also be noted in mandibular molars coupled with
the type of radiolucencies described (see
Figs. 16.10, 16.11, and 16.12).
Treatment options for teeth diagnosed with
VRF are limited, with a poor general prognosis
requiring extraction. Destruction of the support-
ing tissues as a direct consequence of bacterial
irritation precludes any treatment other than
extraction (see Figs. 16.10 and 16.11). In poste-
rior teeth with multiple roots, hemisection or root
amputation may be indicated followed by appro-
priate restoration.
16.8 Split Tooth
A split tooth is a complete fracture that initiates
in a crown and extends to the root subgingivally
in a mesio-distal direction through both marginal
ridges and proximal surface of the tooth.
Diagnosis is made by visual inspection of the two
tooth segments with wedging forces. If the split
tooth has been present for sometime, a deep iso-
lated probing depth may be noted. Clinically the
patient may present with pain on mastication and
associated periodontal abscess. Mobility or sepa-
ration of the two fragments may be evident.
Treatment options depend on the extent of the
split and whether the tooth is deemed restorable.
Removal of the smaller split fragment will
determine whether cast restoration is amenable,
crown lengthening or orthodontic extrusion is
possible or simply the tooth is not salvageable
(Fig. 16.13).
262
a b
d e
Fig. 16.10 Clinical photographs and radiographs dem-
onstrating management of tooth 47 which presented with
(a) peri-radicular pathology, necrotic tooth and 7 mm
probing profile disto-lingually. (b) Following chemo-
mechanical preparation and intra-canal medicament,
pulpal symptoms improved with reduced mobility, pain
and tenderness. (c) The narrow probing profile did not
improve. (d) Internally a crack line was evident on the
16.9 Hemisection, Root
Amputation and Root
Resection
In the current literature, there is no uniformity in
the use of terminology on root resection tech-
niques. Hemisection usually denotes removal of
half the tooth performed in two procedures: tooth
sectioning followed by removal of one root. Root
16 Endodontic–Periodontal Interrelationship
c
disto-lingual aspect involving the floor of the pulp cham-
ber. (e) After an interim period of 3 months, symptoms did
not improve completely and there was no resolution of the
periodontal probing. The patient was informed of the like-
lihood of an incomplete vertical root fracture, and explor-
atory surgery was arranged. A buccal flap was raised and
crack line confirmed externally. The tooth was extracted
amputation refers to the removal of a root at the
furcation or apical to it, without removal of the
crown usually on maxillary molar teeth. Root
resection is generally defined as the removal of a
root without reference to how the crown is
treated.
Prior to considering root resection, the first
treatment to be performed is the endodontic
treatment. Indications for endodontic treatment
16.9 Hemisection, Root Amputation and Root Resection
a b
d e
g h
Fig. 16.11 Clinical radiographs demonstrating endodon-
tic management of tooth 35. Note (a) tooth 35 distal
bridge abutment with distal marginal defect. The patient
elected to have root canal treatment through the bridge
knowing that the restorative prognosis was questionable.
(b, c) A draining sinus was noted associated with the lat-
eral aspect of tooth 35. A peri-radicular radiolucency was
seen peri-apically and laterally (red arrows). (d) Following
chemo-mechanical preparation and intra-canal calcium
hydroxide medicament placement, the sinus resolved. (e)
The tooth was obturated using a warm vertical compac-
tion technique. (f) Sealer extrusion was noted post-opera-
tively. (g) A slight vertical infrabony defect can be seen
initially include easier access for the endodontist,
evaluation of the endodontic prognosis and the
possibility of crown build-up prior to root resec-
tion. The main objectives of this treatment are to
263
c
f
i
(yellow arrow). (h) The patient was reviewed 2 weeks
post-operatively with a reoccurrence of the draining sinus.
A gutta-percha sinus tracing was tracked to the lateral
lesion associated with tooth 35 and sealer extrusion. The
patient elected to monitor with a view to endodontic
exploratory surgery if the sinus failed to resolve. (i) At
3-month review, the buccal sinus had resolved. The mesial
infrabony defect appears to be getting larger (green
arrow). At 6-month review, a distinct mesial infrabony
defect was noted. The patient was informed of the high
probability of a vertical root fracture in relation to this
tooth and extraction was advised
carry out root canal therapy ensuring as much
tooth structure is preserved as possible. At the
completion of endodontic treatment, a retentive
core restoration should be placed with adequate
264
a b
d e
Fig. 16.12 Clinical radiographs and photographs demon-
strating vertical root fracture presentations. Note (a) preop-
erative view of tooth 47 which had undergone previous root
canal treatment and cast restoration. (a) An extensive
J-shaped peri-radicular radiolucency was noted (green out-
line) with the mesial root despite reasonable endodontic
therapy. (b) A gutta-percha sinus tracing radiograph revealed
the associated buccal sinus was related to this tooth. (c) The
tooth was extracted confirming mesial root fracture.
sealing of the coronal 1/3rd of the root canals.
Endodontic posts should be avoided since they
weaken the abutments.
Root resection can then be carried out during
the surgical periodontal phase. Access to the fur-
cation and bone is gained by flap elevation.
Particular attention is paid during the resection of
the roots to avoid damage to the inter-radicular
bone, to avoid leaving any parts of the roof of the
furcation, to avoid damage to the abutment or
possible perforation into the root canal and to
16 Endodontic–Periodontal Interrelationship
c
g
(d) Preoperative view of tooth 46 which had undergone pre-
vious endodontic treatment and cast restoration. A large
peri-radicular radiolucency was noted with the mesial root.
(e, f) A draining buccal sinus was noted with a deep peri-
odontal probing profile on the lingual aspect. An additional
lingual sinus was also noted (yellow arrow denotes draining
sinus). (g) The tooth was extracted confirming an extensive
vertical root fracture in the mesial root
create a wide enough space to allow for cleaning
when separating the roots (Fig. 16.14).
Following root resection, the remaining roots
can be surgically debrided to ensure that any
residual plaque and calculus present has been
removed. Osseous resective surgery may be
required to eliminate shallow osseous craters that
may exist around existing roots and to reduce the
bucco-lingual dimension of the alveolar process
in the area of the resected root. The flaps are then
repositioned to the level of the alveolar crest,
16.9 Hemisection, Root Amputation and Root Resection 265

a b c d

Fig. 16.13 (a) Diagram and clinical photographs and extending into the furcation. The long-term prognosis for
radiograph demonstrating split tooth. Note (b–c) Mesio- both teeth was hopeless and extraction was
distal split tooth associated with a lower mandibular recommended
molar. (d) Radiograph demonstrating a bucco-lingual split

a b c

d e f

Fig. 16.14 Diagrams showing (a–c) root resection. Note the coronal 1/3rd of the canal. Following completion of
endodontic treatment is completed prior to root resection root resection, a cast restoration is placed to prevent verti-
and suitable intra-coronal restorative material is placed in cal root fracture. (d–f) Hemisection of a molar
266
a b
Fig. 16.15 Clinical radiographs demonstrating manage-
ment of a true combined endodontic–periodontal lesion
associated with tooth 36. (a) An extensive peri-radicular
radiolucency was noted with mesial and distal apices.
Extensive bone loss was noted in relation to the distal
root. (b) The crown was sectioned and restorability
assessed. Chemo-mechanical preparation was completed
secured by interrupted sutures and periodontal
pack placed. Sutures and periodontal dressing
can be removed after 1 week, and the patient is
instructed to perform oral hygiene including the
use of interdental brushes. The provisional resto-
ration is maintained for at least 3 months to allow
for tissue maturation before proceeding to final
definitive restoration. Following the healing
phase, the endodontic–periodontal and provi-
sional prosthetic treatment is clinically and radio-
graphically re-evaluated prior to final tooth
preparation (Fig. 16.15).
Clinical Hints and Tips for Managing
Endodontic–Periodontal Lesions
• If the disease is exclusively endodontic in
origin, conventional root canal treatment
using chemo-mechanical preparation tech-
niques and intra-canal medicaments such
as calcium hydroxide will permit healing.
• When the lesion is endodontic in origin,
its drainage may occur through a peri-
odontal pocket, mucosa, gingivae or gin-
gival sulcus. The path of the fistula
should be tracked to determine the
source of the infection.
16 Endodontic–Periodontal Interrelationship
c
and an intra-canal dressing of calcium hydroxide was
placed. The tooth was provisionalised for future cast res-
toration following root resection. (c) The tooth was obtu-
rated using a warm vertical compaction technique using
AH plus cement and gutta-percha. A Biodentine restora-
tion was placed in the coronal 1/3rd of the root canals in
preparation for future resection
• If the disease involves only the periodon-
tium, then periodontal therapy comprising
of root planing and scaling, antimicrobial
agents and oral hygiene instructions should
allow for healing.
• If the two diseases are truly combined, then
primary endodontic treatment followed by
nonsurgical periodontal therapy should be
instigated. Periodontal review is carried out
thereafter to ascertain prognosis.
• When a true combined lesion is suspected
resulting in a periodontal pocket with bone
loss reaching the apical area in an unrestored
tooth, the overall prognosis is guarded. Root
resection may be a viable option in molar teeth.
• Non-endodontic pathology including root
perforation (including strip perforation and
post perforation), vertical root fracture,
cracked tooth syndrome, fused roots,
developmental grooves and enamel pearls
may mimic lesions of endodontic pathol-
ogy. Careful examination and evaluation
will be required to determine the source.
• A multidisciplinary approach will be
required for true combined endodontic–
periodontal lesions.
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85. Christgau M, Palitzsch KD, Schmatz G, Kreiner U,
Frenzel S. Healing response to non-surgical periodon-
tal therapy in patients with diabetes mellitus: clinical,
microbiological and immunological results. J Clin
Periodontol. 1998;25(2):112–24.
86. Graetz C, Dorfer CE, Kahl M, Kocher T, Fawzy
El-Sayed K, Wiebe JF, Gomer K, Ruhling A. Retention
of questionable and hopeless teeth in compliant
patients treated for aggressive periodontitis. J Clin
Periodontol. 2011;38(8):707–14.
87. Genco RJ, Borgnakke WS. Risk factors for periodon-
tal disease. Periodontol 2000. 2013;62:59–94.
 Orthodontic–Endodontic
Interrelationship 17

Summary
Successful tooth movement requires a sound knowledge base of the inter-
relationships between the tooth and periodontium. Prior insults to the
tooth and its supporting structures may affect its response and the outcome
of treatment. The need for a thorough history, examination and baseline
measurements is essential for the medical record, treatment planning and
informed consent process. The interrelationships between dental speciali-
ties and timely intervention are paramount to achieving a successful
outcome.

Clinical Relevance 17.1 Orthodontic Tooth

Orthodontic movement of the teeth will induce
some degree of pulpal inflammation. Poorly
controlled heavy forces on the teeth, previous
history of trauma or ongoing insults such as car-
ies may result in loss of pulp vitality. Combined
endodontic–orthodontic treatment planning can
benefit the overall tooth prognosis by ensuring
optimal endodontic treatment has been under-
taken. Endodontically treated teeth can be moved
orthodontically just as readily as vital teeth.
Traumatised teeth and in particular intrusive
luxation injuries may be at greater risk of moder-
ate to severe root resorption. The general dentist,
endodontist and orthodontic professional need to
ensure from history taking to execution of treat-
ment that sound methodological principles are
followed to fulfil treatment objectives ensuring a
successful outcome.
Movement and Vital Teeth
Orthodontic forces will evoke a biological
response within the dental pulp, resulting in some
degree of transient pulpal inflammation [1]. What
is of clinical significance is whether the response
evoked could lead to long-term changes to the
vitality of the tooth. The survival of the dental
pulp is dependent on the blood vessels that access
the interior of the tooth through the apical
foramen. Any changes in pulpal blood flow or
vascular tissue may have implications to the
health of the dental pulp. Use of light forces is
thought to reduce damage to the pulp and allow
time for repair [2]. In contrast, rapid orthodontic
tooth movement and heavy continuous forces are
thought to increase the risk of pulpal injury, as
undermining resorption allows increasingly large

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 271
DOI 10.1007/978-3-319-15591-3_17, © Springer International Publishing Switzerland 2015
272
increments of change, leading to alterations in
the blood vessels at the peri-apex of the tooth and
those entering the tooth apically [3].
Human studies have demonstrated pulp necro-
sis after various tooth movements such as intru-
sion [4] and extrusion [5] due to circulatory
disturbances in dental pulp. It is generally assumed
that pulpal changes and their consequences appear
to be more severe with larger orthodontic forces
[6], but sound scientific data to support this
assumption are lacking. One study found a higher
prevalence of loss of pulp vitality and root resorp-
tion on previously traumatised teeth undergoing
tipping orthodontic movements; however, the
sample size was small and heterogenous [7]. With
the available evidence, it is not possible to con-
clude that orthodontic tooth movement of trauma-
tised teeth increases the risk of pulp necrosis. A
systematic review was performed to investigate
the relationship between orthodontic force level
and pulp reaction in human teeth [8]. This rela-
tionship, which would seem to be of utmost clini-
cal importance, remains yet to be elucidated.
17.2 Orthodontic Tooth
Movement of Endodontically
Treated Teeth
A retrospective study examining 45 orthodontic
patient records treated with various orthodontic
techniques found those teeth that have under-
gone root canal treatment, including 4 teeth that
had undergone peri-radicular surgery, moved as
readily as teeth with vital pulps [9]. This pre-
sumes that there are no factors that may prevent
tooth movement, such as replacement resorption
(ankylosis) or injury to the apical periodontal
ligament that may limit its remodelling [10].
There are mixed reports of root resorption in
endodontically treated teeth subjected to orth-
odontic tooth movement. Some authors have
found increased rates [9] and others have found
reduced rates of root resorption [11]. A recent
retrospective study, where the adjacent maxillary
17 Orthodontic–Endodontic Interrelationship
incisor acted as a control, found no statistical dif-
ference between the vital control tooth compared
to the root-treated tooth [12].
17.3 Factors Affecting Root
Resorption During
Orthodontic Tooth
Movement
Orthodontically induced inflammatory root
resorption (OIIRR), or root resorption (RR), is an
unavoidable pathological consequence of orth-
odontic tooth movement [13]. RR is undesirable
because it may affect the viability of a tooth long
term; therefore, it is important to identify those
factors that may contribute to RR, in an attempt
to minimise its effects.
Andreasen defines three types of external root
resorption [14]:
1. Surface resorption, which is a self-limiting pro-
cess, usually involving small outlining areas
followed by spontaneous repair from adjacent
intact parts of the periodontal ligament
2. Inflammatory resorption, where initial root
resorption has reached dentinal tubules of an
infected necrotic pulpal tissue or an infected
leukocyte zone
3. Replacement resorption, where bone replaces
the resorbed tooth material that leads to
ankylosis
Tronstad further subdivides inflammatory
resorption, which is seen on the walls of the root
canal (internal resorption) and on the external
surface of the root (external resorption), into two
types [15]:
1. Transient inflammatory resorption occurs
when the stimulation is minimal and for a
short period. This defect is usually undetected
radiographically and is repaired by a
cementum-like tissue.
2. Progressive inflammatory resorption occurs
when stimulation is for a long period.
RR after orthodontic treatment generally takes
the form of surface resorption [14] or transient
17.3 Factors Affecting Root Resorption During Orthodontic Tooth Movement 273

inflammatory resorption [15]. Replacement resorp-
tion is rarely if ever seen after orthodontic treat-
ment. Orthodontic forces act similarly on bone and
cementum. Due to the greater resistance of cemen-
tum to resorption compared to bone, orthodontic
forces cause bone resorption, which leads to tooth
movement. However, resorption of the cementum
and dentine may also occur (see Fig. 17.1) [16].
The Malmgren index utilises a graded scale
0–4, to classify OIIRR as mild (apical RR
<2 mm) or moderate (apical RR 2 mm – 1/3 of
root length), which is seen in most orthodontic
patients [17]. Severe RR (>4 mm or a third of
the original root length) is seen in less than 5 %
of orthodontically treated teeth [18]. The use of
this index was originally described for use with
intra-oral radiography, which has inherent limi-
tations due to the two-dimensional representa-
tion of a three-dimensional structure (see
Fig. 17.2).

a b

c d

Fig. 17.1 Clinical diagram showing (a) effects of orth- at the apex, (d) which when resorbed results in external
odontic tooth movement resulting in (b) root resorption apical root resorption (Adapted form Roberts et al. [83])
lacunae that if not repaired may cause (c) a sequestration
274
1 2
Fig. 17.2 Clinical diagrams demonstrating Malmgren
root resorption index for quantitative assessment of root
resorption. Note (1) irregular root contour, (2) apical root
resorption less than 2 mm of original root length, (3) api-
The aetiological factors of RR are complex
and multifactorial. Many variables have been
suggested in the literature from individual bio-
logical variability, genetic predisposition, root
morphology, history of trauma and mechanical
factors. Regardless of genetic or treatment-
related factors, the maxillary incisors consis-
tently experience more apical RR than any other
teeth, followed by the mandibular incisors and
first molars [17]. Despite the extensive literature
that exists on this topic, there is a lack of consen-
sus on the aetiological factors, in part due to dif-
fering study designs, heterogenous and small
sample sizes and methods used for assessing root
resorption [13, 16, 17].
A systematic review attempted to elucidate
the effect of orthodontic treatment on RR [19].
Following review of 144 articles, 13 fulfilled the
inclusion criteria. A number of studies included
were conducted over a short period of time and
thus not representative of a full 18–24-month
course of orthodontic treatment. Evidence exists
that orthodontic force applied to teeth over a
short period can produce resorption lacunae
without signs of RR [20]. In addition many stud-
ies examined premolars, a tooth which quite
often does not experience significant RR. The
key findings were that teeth undergoing orth-
odontic movement had significantly more RR
compared to control teeth. Heavy forces pro-
duced significantly more RR than those treated
17 Orthodontic–Endodontic Interrelationship
3 4
cal root resorption from 2 mm to one-third of original root
length and (4) apical root resorption exceeding one-third
of original root length
with light forces and thermoplastic appliances
[21–26]. There was limited evidence that con-
tinuous force application produced significantly
more RR than discontinuous force application
[27], possibly because the pause allows the
resorbed cementum to heal and prevents further
resorption. The studies examining intrusive force
applications found significantly increased RR
rates compared with controls [21, 28]. Incisors
with clinical signs or patient reports of trauma
(but no signs of RR) had the same prevalence of
moderate to severe RR as those without trauma
[29–31]. There is a lack of high-quality evidence
on OIIRR on previously traumatised teeth with
pre-existing RR; observational data indicate a
greater chance that orthodontic movement will
enhance the resorptive process in these teeth
[16]. There is no evidence that RR is affected by
arch wire sequence or bracket system used and
little evidence that unusual tooth morphology
plays a role in increased RR. RR associated with
orthodontic treatment ceases after active treat-
ment [11].
Although RR is of concern to many general
dental practitioners and dental specialists [32],
even extensive RR does not appear to affect the
functional capacity or the longevity of the teeth.
Apical RR has been shown to be less critical on
the area of remaining periodontal support than
loss of crestal alveolar bone support, with 3 mm
of RR approximately equivalent to 1 mm of
17.4 Management of Endodontic Procedures During Orthodontic Treatment
crestal bone loss. This may explain why tooth
loss from apical shortening has not been reported
in the literature [33].
Until more high-quality clinical evidence is
published, best practice involves thorough patient
counselling at the outset of treatment. Clinically,
use of light forces is important especially for
intrusive movements. Good record keeping
including radiographs taken at baseline and after
6–9 months may detect early signs of RR. In
cases where RR has been diagnosed, there is
some evidence that a 2–3-month pause in treat-
ment with a passive arch wire decreases further
RR. If severe resorption is identified, the treat-
ment plan will need to be reassessed with the
patient. After treatment, if severe RR is shown on
the final radiographs, follow-up radiographic
examinations may be indicated until the resorp-
tion has stabilised. If it continues, sequential root
canal therapy with calcium hydroxide has been
shown to be of benefit [34].
17.4 Management of Endodontic
Procedures During
Orthodontic Treatment
During orthodontic tooth movement, both reten-
tion of a calcium hydroxide dressing in the root
canal [35, 36] and obturation of the root canal
with a definitive gutta-percha root canal filling
prior to orthodontic tooth movement [37] have
been recommended. The former recommenda-
tion is based on clinical experience and the lat-
ter is based on findings from animal studies
[38], where no significant difference was found
in resorption of the teeth managed by either
method.
In cases of external inflammatory root resorp-
tion, long-term calcium hydroxide treatment is
more effective than short-term treatment in pro-
moting root surface healing with new cementum
[39]. An increased risk of cervical root fracture in
traumatised immature teeth treated with calcium
hydroxide over prolonged periods of time during
apexification has been reported [40]. Rosenburg
et al. compared the dentine fracture strength of
teeth dressed with calcium hydroxide paste and
275
teeth obturated with gutta-percha, finding that the
micro-tensile fracture strength of dentine was
reduced by 43.9 %. This suggests the clinical use
of calcium hydroxide over a prolonged period of
time, such as what would be required over a
course of orthodontic treatment, should be
reviewed [41]. These findings support recom-
mendations of completing definitive root canal
therapy prior to a definitive course of orthodontic
tooth movement [37], with a well-cleaned and
obturated root filling with a good coronal seal
[42]. The exceptions are when a calcium hydrox-
ide dressing is required for a longer period, such
as in inflammatory resorption, or for apexifica-
tion in an immature open apex incisor, although a
single visit mineral trioxide aggregate is found to
be a predictable treatment [43].
Recommendations relating to commencement
of orthodontic tooth movement following end-
odontic intervention are based on clinical judge-
ment and experience rather than being founded
on evidence from well-designed studies. The out-
come of root canal treatment should be assessed
for at least 12 months after completion and sub-
sequently as required. A favourable outcome is
indicated by absence of pain, swelling and other
symptoms, no sinus tract, no loss of function and
radiological evidence of a normal periodontal
ligament space around the root [44].
In cases where root canal treatment has been
undertaken as a result of pulp necrosis due to
caries, orthodontic tooth movement can com-
mence immediately, in the absence of symp-
toms. Where there has been bone loss, tooth
movement should be delayed until there are
clinical and radiographic signs of some healing.
Where endodontic therapy has been carried out
following dental trauma, an interval of 1 year is
recommended prior to proceeding with orth-
odontic treatment to increase the likelihood of
complete healing and the absence of ankylosis
[36, 37]. An animal model has shown that,
although orthodontic forces applied to root-
filled teeth delays the peri-apical healing pro-
cess in comparison to obturated contralateral
incisors, it does not prevent it, with a reduced
peri-apical radiolucency visible in orthodonti-
cally moved teeth [45] (see Sect. 17.8.2). This
276
work suggests that tooth movement may be
commenced prior to complete radiographic res-
olution of peri-apical lesions.
Endodontic procedures needed during orth-
odontic treatment may prove a challenge from
diagnosis to execution of the definitive obtura-
tion. Presenting symptoms may be attributable to
tooth movement or due to a necrotic pulp.
Orthodontic bands and attachments may obscure
detection of caries clinically and radiographically
as well as prevent an accurate response with elec-
trical and thermal pulp testers. Radiographically
changes in response to tooth movement may be
misinterpreted as originating from pulpal demise.
Coronal access may be hindered in cases with
lingual attachments, an increasingly popular
appliance with an increasing adult demographic.
Apical resorption may hinder working length
determination due to destruction of the apical
constriction at the cemento-dentinal junction.
Electronic apex locators will not be accurate in
such cases. Obturation filling material may also
extend beyond the tooth where the apical con-
striction has been lost.
17.5 Orthodontics and Its Role
in Trauma
The risks and incidence of dental trauma in chil-
dren increases with age, from 5 % at age 8 to 11 %
by age 12, with boys at greater risk [46]. An
increased overjet and lip incompetency will
increase the risk [47, 48]. Prevention of trauma
forms the first line of treatment with children par-
ticipating in contact sports advised to wear protec-
tive mouth guards. However, it is important to note
that most incidences of trauma are sustained doing
activities unrelated to sport [35]. Children, who
have sustained trauma, particularly at a young age,
will often experience repeated episodes of trauma
to their teeth [49]. Timely treatment of any maloc-
clusions should be sought, although factors such
as dental health and dental development may
affect commencement of treatment.
In the event of trauma, management will vary
depending on the type of traumatic injury and the
stage of root development of the affected tooth.
17 Orthodontic–Endodontic Interrelationship
Intrusive injuries are crushing by nature and
can lead to significant damage to the tooth and its
supporting structures. Guidelines on manage-
ment of intrusion exist [50, 51]. Due to the low
occurrence of this type of injury, randomised,
controlled trials are not available. Evidence on
outcomes has been obtained from retrospective
clinical studies. Mild intrusion injuries (0–3 mm)
often require a period of observation to allow the
tooth to re-erupt. If no change is seen, orthodon-
tic repositioning should commence 2–3 weeks
after the injury. Moderate (3–6 mm) to severe
(greater than 6 mm) intrusion injuries often
require active repositioning, either surgically or
orthodontically [52]. There is no clear indication
of which option produces improved outcomes,
and the chosen method may often come down to
availability of local expertise. Due to the higher
risk of inflammatory root resorption, secondary
to pulpal necrosis in such injuries, endodontic
therapy should be instigated 2–3 weeks after the
injury when there has been complete root forma-
tion. In teeth with immature roots, these teeth
need to be monitored closely for loss of vitality.
Teeth that have been surgically repositioned will
need to be splinted for 1–2 weeks.
Other types of luxation injuries, such as extru-
sive luxation, may require repositioning and
splinting for 1–2 weeks and lateral luxation inju-
ries up to 4 weeks due to the possibility of an
associated alveolar injury [53]. If there has been
delayed presentation or no tooth mobility exists,
orthodontic repositioning is the best option to
realign the tooth. Of note is that in traumatic inju-
ries the adjacent teeth may have been subjected
to trauma, and therefore these teeth may not be
ideal for orthodontic anchorage and consider-
ation needs to be given to appliance design.
Orthodontic management of teeth that have a
history of trauma will vary depending on the
nature of the original injury. Few studies exist on
the sequelae of traumatised teeth undergoing
orthodontic treatment. The studies that exist are
often based on small numbers with a heteroge-
nous sample of injuries from which conclusions
are hard to draw. Recommended observation
times prior to instigating orthodontic tooth move-
ment are based on best practice [36, 54].
17.6 Effect of Orthognathic Surgery on Pulp Vitality
In cases of root fracture, healing with a hard
tissue callus as opposed to connective tissue is
important. To achieve healing, splinting times of
4 weeks have been advocated for apical and mid-
dle third root fractures and 4 months for fractures
of the cervical third [50]. If orthodontic tooth
movement is planned in such teeth, in those that
have healed with connective tissue, the coronal
fragment alone will move and thus the tooth will
in effect need to be treated as a tooth with a short
root. In such cases, prior to tooth movement, any
signs of coronal pulp necrosis need to be treated.
It has been recommended to wait 2 years prior to
commencing orthodontic treatment in affected
teeth [55]; however, in the absence of symptoms,
other authors have recommended a shorter period
of a year [36].
The success of a replanted tooth following an
avulsion injury is strongly dependent on time
outside of the mouth. After 60 min, even if stored
in a physiological solution or 30 min of dry time,
healing is almost always by replacement resorp-
tion. Parents and teachers are therefore encour-
aged to replace the tooth at the site of the incident
if at all possible. Once replanted, the tooth is
splinted for 7–10 days. Replanted teeth will need
to undergo endodontic treatment as soon as fea-
sible in all cases apart from open-apex teeth with
a short extra-oral time. Even in the latter case,
affected teeth need to be monitored closely for
signs of loss of vitality and appropriate endodon-
tic therapy instigated if necessary [56–59].
Orthodontic tooth movement of a replanted tooth
is possible if replacement resorption has not
occurred. It is recommended to wait a year before
commencing tooth movement to allow periodon-
tal healing to occur [36]. In a growing child, heal-
ing by replacement resorption becomes apparent
with continued vertical alveolar development of
the adjacent teeth (see Sect. 17.8.6). In an adult,
replacement resorption will be less apparent from
the clinical picture and often only detected once
orthodontic movement has commenced (see
Sect. 17.8.5).
Autotransplantation of teeth in the manage-
ment of trauma may be suitable if an upper inci-
sor is lost and there is premolar crowding. The
ideal donor tooth for an upper incisor site is a
277
lower premolar. The technique is operator sensi-
tive and relies on an atraumatic technique for
handling the donor tooth and management of the
recipient site. Once transplanted, the tooth is
splinted for 7–10 days. Endodontic therapy is
instigated in teeth that have closed apices 1–2
weeks post transplantation. Teeth that have open
apices or immature roots need to be closely mon-
itored for loss of pulpal vitality. Orthodontic
tooth movement can commence once periodontal
healing has occurred between 3 and 9 months
[60]. Autotransplanted teeth if successful will
behave as any other teeth and retain the potential
to induce alveolar bone growth. Even in cases
where replacement resorption occurs, the trans-
planted tooth will slowly resorb, maintaining
bone in the area for future replacement options.
In conclusion, orthodontic repositioning is
useful in the immediate management of traumati-
cally displaced teeth. Orthodontic tooth move-
ment is possible on previously traumatised teeth.
Certain injuries such as intrusive luxation and
avulsion may be at higher risk of negative
sequelae, such as inflammatory root resorption
and ankylosis. Good clinical and radiographic
records are essential to obtain informed consent
as well as a lengthy discussion with the patient
and family regarding the possible outcomes.
17.6 Effect of Orthognathic
Surgery on Pulp Vitality
Orthognathic surgery is used to alter the underly-
ing skeletal pattern in individuals with dento-
facial deformity or malocclusions resulting from
trauma to the maxillo-mandibular complex. An
adequate blood supply to mobilised dento-
osseous segments is crucial for the success of any
orthognathic intervention. Furthermore, this
blood supply is vital for the preservation of a
healthy pulp and periodontium [61–63].
The laser Doppler flowmeter (LDF) has been
used to evaluate changes in blood flow through
non-invasive measurement methods and to inves-
tigate vascular changes associated with orthogna-
thic surgery [64, 65]. The Le Fort I osteotomy
technique is frequently employed for altering the
278
maxillary spatial position. During this procedure,
the posterior superior alveolar vessels are tran-
sected with the palatal pedicle then becoming the
primary source of blood supply to the maxilla
[61, 63]. Studies have suggested that ischaemic
episodes in mobilised maxillary segments may
occur for a brief period after surgery. This isch-
aemic period is thought to be responsible for
potential negative sequelae, such as degenerative
pulpal changes [66]. A bilateral, sagittal split
osteotomy does not interfere with the collateral
blood supply and risk of severing the inferior
alveolar artery is small. Consequently, pulpal
changes may be less likely in mandibular osteot-
omies compared to maxillary procedures [62].
Human studies using LDF have demonstrated
a pulpal hypervascular period occurring immedi-
ately after a Le Fort I osteotomy. This is then fol-
lowed by a statistically significant reduction in
the perfusion of the pulp, which has still not
recovered 4–6 months after surgery. However, a
high variability of individual blood flow patterns
was found [67, 68]. Literature looking at segmen-
tal osteotomies has found similar findings [69].
A hypervascular episode may be of signifi-
cance to the dental pulp because of its enclosure
in a rigid shell of hard tissues, leading to a pos-
sible increase in tissue pressure and ultimately
pulpal injury or death. During the informed con-
sent process, it may be beneficial to inform
patients planned for a Le Fort I osteotomy that
there may be a small risk of loss of vitality and
discolouration of the maxillary incisor teeth
resulting in a need for root canal therapy.
17.7 Orthodontics to Aid
Restorative Procedures
Orthodontic extrusion or forced eruption of a
tooth is based on sound orthodontic and osteo-
physiologic principles [70, 71]. Ingber demon-
strated that the teeth could be erupted for crown
lengthening, altering gingival margins and level-
ling osseous defects. As teeth are extruded using
light forces, both the bone and gingiva migrate
coronally [72, 73]. Eruptive tooth movements
result in stretching of the gingival and periodontal
17 Orthodontic–Endodontic Interrelationship
ligament fibres with a consequent coronal shift of
the bone at the base of the defect as the tooth
moves occlusally [74, 75].
Teeth with deep carious margins requiring
endodontic treatment, fractured tooth margins
below crestal bone, isolated vertical periodontal
defects, lateral root perforation and unusual coro-
nal access are some situations that may benefit
from forced eruption [76]. The benefits of extru-
sion are to allow a sound tissue margin for resto-
ration and ensure the maintenance of the
biological width. In extruding the tooth for sub-
sequent restoration, it is important to ensure suf-
ficient root length remains within the bone,
leaving a minimum 1:1 crown–root ratio. Forced
eruption is increasingly been used for implant
site development in teeth with poor prognosis
with associated periodontal and osseous defects,
enhancing both hard and soft tissue defects
[77–79]. Dento-alveolar ankylosis is a frequent
complication after replantation and may not be
amenable to orthodontic extrusion. Decoronation
of ankylosed teeth in infra-position has been clin-
ically proven to preserve alveolar width and
rebuild lost vertical bone of the alveolar ridge in
growing individuals, re-establishing ideal alveo-
lar conditions prior to implant insertion once
growth has stopped. The predictable success of
decoronation also strongly supports the indica-
tion for replantation of avulsed teeth in children
even when the extra-alveolar conditions indicate
that healing might be compromised by ankylosis
[80–82].
17.8 Clinical Cases
17.8.1 Avulsion: Immediate
Replantation Adult
A 25-year-old soldier was referred for manage-
ment of his class 2 division 1 occlusion. There
was a history of trauma to the upper left central
incisor, resulting in an uncomplicated crown
fracture, which was restored. The upper right
central incisor (tooth 11) was avulsed following
the initial orthodontic assessment appointment
during a physical training session. This tooth was
17.8 Clinical Cases
stored in milk and replanted within 30 min and
underwent root canal treatment 3 days later.
On examination there was a severe skeletal 2
pattern, an incompetent lip pattern, a 12-mm
overjet and class 2 buccal segments.
The patient was counselled on the possibility of
ankylosis of the upper right central incisor (tooth
11). The treatment plan involved combined ortho-
dontics and orthognathic surgery to address the
dental and skeletal pattern. The patient com-
menced pre-surgical orthodontics and tooth 11
was bypassed initially. Active tooth movement
of tooth 11 was commenced 6 months after
replantation following establishment of periodon-
tal healing, similar to management of transplanted
a b
c d
Fig. 17.3 Clinical photographs and radiographs showing
(a) pre-treatment intra-oral view and (b) occlusal radio-
graph demonstrating no pre-existing peri-apical pathosis
279
teeth [59]. This was in contrast to best practice
which recommends a 12-month monitoring period
[36]. The patient had no clinical symptoms, and
the immediate replantation and endodontic ther-
apy indicated a more favourable prognosis for this
tooth. Good movement of tooth 11 was achieved
with no associated pathology evident (Fig. 17.3).
17.8.2 Avulsion: Immediate
Replantation Adult
A 26-year-old naval sailor was referred for man-
agement of his class 2 division 1 occlusion. There
was a history of trauma to both upper central
associated with tooth 11. (c, d) Six months post com-
mencement of pre-surgical orthodontics
280
incisors 4 years previously, resulting in avulsion
of the upper left central incisor (tooth 21) and
subluxation and a complicated crown fracture of
the upper right central incisor (tooth 11). The
avulsed tooth was stored in saliva and replanted
within 60 min. Both upper central incisors under-
went root canal treatment within a few days.
On examination there was a moderate skeletal
2 pattern, an incompetent lip pattern, a 9-mm
overjet and class 2 buccal segments with previous
loss of all first molars excluding the lower left
first molar (Figs. 17.4 and 17.5).
The patient was counselled on the poor long-
term prognosis of tooth 21 and the possibility of
ankylosis of this tooth. The treatment plan
involved combined orthodontics and orthogna-
thic surgery to address the dental and skeletal
pattern. An endodontic opinion was sought for
a b
Fig. 17.4 (a–c) Pre-treatment intra-oral clinical photographs
a b
Fig. 17.5 (a–c) Pre-treatment radiographic views.
Radiographic examination revealed Grade 3 apical root
resorption (Malmgren index) of the tooth 21 with signs of
17 Orthodontic–Endodontic Interrelationship
tooth 42, and it was felt that the peri-apical area
had resolved considerably and further endodontic
treatment was not considered necessary.
The pre-surgical orthodontic phase of treatment
progressed well with good movement of the upper
central incisors (Fig. 17.6). The patient was hit in
the mouth by a football during treatment resulting
in distortion of the upper 17 × 25 stainless steel
arch wire in the region of 21, and the tooth had
extruded [49]. An aligning arch wire was placed
and radiographic review 8 weeks later showed no
change to the appearance of this tooth from pre-
treatment views. A radiograph of 42 showed
excellent resolution of the peri-apical radiolucency
during the fixed appliance phase (Fig. 17.7).
This case highlights the importance of
informed consent. The long-term prognosis of
tooth 21 is poor. The pre-treatment position
c
c
internal inflammatory resorption and diffuse peri-apical
area. Tooth 42 had undergone RCT and had an associated
peri-apical area
17.8 Clinical Cases
a b
Fig. 17.6 (a–c) Mid-treatment intra-oral clinical photographs. Note upper incisors have responded to orthodontic
forces
a b
Fig. 17.7 (a–c) Radiographic examinations carried out 6
months post treatment commencement. Note apical short-
ening of upper left central incisor compared to pre-treat-
ment view (Grade 4 root resorption, Malmgren index) and
of the teeth would have resulted in limited treat-
ment options for replacement, given the soft tis-
sue pattern and skeletal discrepancy, potentially
resulting in further episodes of trauma.
17.8.3 Avulsion: Delayed
Replantation Adolescent
A 14-year-old male was referred for management
of his upper left central incisor (tooth 21). The
tooth had been avulsed 2 years earlier and
replanted 90 min later and endodontically treated.
The family were counselled on the possibility of
ankylosis of this tooth due to the clinical
appearance and continued vertical growth of the
adjacent teeth. Tooth 21 had previously been
restored to the level of the adjacent 11 (Fig. 17.8).
Examination revealed upper arch anterior
crowding with space loss for 21 with labial
281
c
c d
extrusion of obturation material with no associated peri-
apical pathosis. The peri-apical radiolucency associated
with tooth 42 has resolved compared to the pre-treatment
view. (d) 1 day post surgery
displacement and a 3-mm vertical step between
the incisal edges (the actual vertical discrepancy
is masked by the composite restoration).
Treatment options were discussed:
1. Restorative build-up of 21 to match incisal
level of 11. This option would accept the ante-
rior crowding and if 21 was subsequently lost
would result in requirement for pre-restorative
orthodontics to idealise space for a prosthetic
replacement.
2. Orthodontic treatment to idealise mesio-distal
space for 21 and careful mechanics to attempt
levelling. The patient was informed that this
tooth may be ankylosed and may not move
(Fig. 17.9).
The family were keen to proceed with
option 2.
Tooth 21 has not been fully levelled as demon-
strated by the gingival margin discrepancy. This
was accepted, as the patient struggled with
282 17 Orthodontic–Endodontic Interrelationship

b c d

Fig. 17.8 Pre-treatment (a–c) clinical intra-oral photo- Grade 1 root resorption (Malmgren index) and external
graphs and (d) radiographic view of tooth 21 pre-orth- inflammatory root resorption of the mesial root surface
odontic treatment. The intra-oral radiograph revealed

a b

c d

Fig. 17.9 Clinical photographs showing (a) preoperative and (b) mid-treatment views. (c, d) Note tooth 21 has
responded to orthodontic traction with crowding relieved and spacing now ideal for future replacement
17.8 Clinical Cases
maintaining good oral hygiene throughout treat-
ment, and combined with a low lip line with no
show of gingival margins on smiling, the patient
was happy. Active treatment time is 10 months.
17.8.4 Avulsion: Delayed
Replantation Adolescent
A 14-year-old female who had recently located to
the region was referred by her general dental
practitioner (GDP) for an orthodontic assess-
ment. There was a history of trauma at the age of
8, resulting in avulsion of the upper left central
incisor (tooth 21) and a luxation injury to the
upper right central incisor (tooth 11). The avulsed
tooth was stored in milk and replanted after 4 h.
On examination there was a mild skeletal 2
pattern, mild to moderate crowding of the arches
and a 10-mm overjet (Fig. 17.10). Both upper
central incisors showed signs of vitality loss. The
GDP was requested to undertake endodontic
treatment of both upper central incisors. The
GDP was unable to access the root canal of 11
due to sclerosis. Tooth 21 was endodontically
treated with a custom gutta-percha filling
although the enlarged apex and lack of apical
constriction proved challenging (Fig. 17.11).
a b
d e
Fig. 17.10 Clinical photographs demonstrating pretreatment intra-oral views of (a) right buccal segment, (b) anterior,
(c) left buccal segment, (d) maxillary occlusal and (e) mandibular occlusal views
283
The patient was re-referred following
completion of endodontic treatment. The family
was counselled on the possibility of ankylosis of
the incisors and the risks of root resorption and
accelerated loss of these teeth. Due to the crowd-
ing, the family was aware that orthodontic treat-
ment would idealise spacing for future
replacement if the incisors were lost.
Given the guarded prognosis of the upper cen-
tral incisors, a non-extraction treatment plan was
chosen to minimise forces and treatment duration
(Fig. 17.12). This case demonstrates the impor-
tance of establishing a full history, examination
and record taking to facilitate the informed con-
sent process. It also demonstrates the problems
encountered in undertaking definitive endodontic
treatment, further compounded by lack of end-
odontic input following the immediate trauma
stage.
17.8.5 Ankylosis: Late Adolescence
A 17-year-old male presented with a marked
class 2 division 1 occlusion on a skeletal 2 base
with an anterior open bite. There was a previous
history of a habit, which had stopped in his early
teens. The patient had experienced trauma to the
c
284
a b
Fig. 17.11 (a, b) Pre-treatment radiographic views. Note
apical shortening of tooth 21 (Grade 3 root resorption,
Malmgren index), lack of apical constriction and thin root
a b
d e
Fig. 17.12 (a–e) Clinical photographs demonstrating
mid-treatment intra-oral views. Note upper incisors have
responded to orthodontic forces with crowding relieved
and spacing now ideal for future replacement.
upper incisors at the age of 13. Teeth 12, 11 and
21 had undergone endodontic treatment 3–4
years following the original trauma after repeated
requests to the general dental practitioner (GDP)
(Figs. 17.13 and 17.14).
The patient was planned for a bi-maxillary oste-
otomy with a segmental maxillary procedure. The
patient was informed of the possibility of loss of
17 Orthodontic–Endodontic Interrelationship
c
canal walls indicating lack of continued root development
following original trauma. (c) Post-endodontic treatment
of tooth 21
c
f
(f) Radiographic view of tooth 21 six months post treat-
ment commencement. Note the appearance of the upper
central incisors appears relatively unchanged
the upper incisor teeth and the possibility that they
would not move with applied orthodontic forces.
Pre-surgical orthodontics was commenced
and the upper arch was bonded in sections to
facilitate segmental surgery (Fig. 17.15a–c). Oral
hygiene remained sub-optimal throughout treat-
ment. Following 3 months of active treatment, 21
and 22 showed no signs of movement despite
17.8 Clinical Cases 285

a b c

Fig. 17.13 Clinical photographs demonstrating pre-treatment intra-oral views

a b c

Fig. 17.14 (a–c) Pre-treatment radiographic views. Note a peri-apical radiolucency remains with teeth 11 and 12
however, it is reduced in size compared to pre-endodontic treatment

a b c

d e f

Fig. 17.15 Clinical photographs demonstrating (a–c) mid-treatment intra-oral views (note teeth 21 and 22 appear
ankylosed as indicated by the arch form) and (d–f) post-treatment intra-oral views
286
a b
Fig. 17.16 Mid-treatment radiographic views. Note
peri-apical radiolucency associated with teeth 11 and 21
has increased compared to pre-treatment views with
mobility evident. The patient was seen on a com-
bined clinic to re-discuss the treatment plan and
objectives. Given the proclination of the upper
labial segment, the upper first premolars were
planned for removal to facilitate space creation
for surgical setback of the anterior segment and
intrusion of the buccal segments.
The patient’s compliance was poor throughout
treatment. The upper fixed appliance was
removed and an arch-bar used intra-operatively.
A wafer was left in situ until 2 weeks post-
operative. The upper fixed appliance was
replaced, but attendance and compliance deterio-
rated and the patient was de-bonded and the
residual open bite accepted (Fig. 17.15d–f). This
case highlights the potential problems that can be
encountered when replacement resorption is
encountered and the requirement to re-evaluate
treatment objectives. The importance of informed
consent including a full discussion of all possible
negative sequelae at the outset of treatment is
vital in such cases (Fig. 17.16).
17.8.6 Ankylosis: Preadolescence
A 13-year-old male presented at the request of a
paediatric dentist for management of an infra-
17 Orthodontic–Endodontic Interrelationship
c
signs of increasing external root resorption associated
with both 11 and 21
occluding upper left central incisor (tooth 21).
The patient had been involved in trauma aged 9
whilst away on holiday when he was accidentally
kicked in the mouth during a football game.
Tooth 21 was avulsed out of the oral cavity, and
the upper right central incisor (tooth 11) had
undergone significant extrusive luxation. The
avulsed tooth was stored dry in tissue for over
30 min, followed by storage in milk until replan-
tation over an hour after the initial avulsion
(Fig. 17.17).
The paediatric dentist took over management
5 months after the original trauma. The patient
was extremely anxious and unable to tolerate any
dental treatment. After a period of acclimatisa-
tion, 11 was dressed with calcium hydroxide;
however, 21 had limited palatal access and radio-
graphic appearance indicated pulpal obliteration
and no intervention was possible (Fig. 17.17).
Tooth 21 was restored with composite to
match 11 incisal level to mask the infra-occlusion
aged 11. The patient experienced a considerable
growth spurt and the level of 21 was quite mark-
edly infra-occluded by age 13 (Fig. 17.18).
Treatment options were discussed:
1. Restorative build-up of 21 to match incisal
level of 11. This option would accept the ante-
rior crowding. In the future, there would be a
17.8 Clinical Cases
a b
Fig. 17.17 (a) Panoramic radiograph demonstrating
splinting of anterior teeth at age 9 (note upper central inci-
sors demonstrate 90 % root formation and 21 appears
intruded). Intra-oral radiographs (b) taken pre-trauma
a b
Fig. 17.18 (a, b) Clinical intra-oral photographs. Note
tooth 21 is infra-occluded and displaced labially from
arch. (c) Intra-oral radiograph at age 13. Note apical
shortening of tooth 21 (Grade 4 root resorption, Malmgren
requirement for pre-restorative orthodontics to
idealise space for prosthetic replacement of 21.
2. Extraction of 21 and orthodontic space clo-
sure with 22 planned to replace 21. 22 then
restored to resemble 11.
3. Orthodontic treatment to idealise mesio-distal
space for 21 and careful mechanics to attempt
levelling. If no movement is established, 21
will undergo decoronation [36, 80] and a pros-
thesis devised to replace 21 until the time of
definitive replacement. At the end of growth,
if an alveolar defect remains, the possibility of
orthodontic extrusion [72, 73]; if root tissue
remains, to regenerate the alveolar and soft
tissue defect prior to implant placement will
be reviewed [77–79].
Following discussion on a combined clinic,
option 3 was felt to offer the best outcome to
relieve the crowding and decoronation to pre-
serve the alveolar bone as well as attempt stimu-
lation of coronal alveolar bone [36, 80].
287
c d
(c) 1 month post -trauma (note lack of continued root
development of 21 and apical root resorption of both 11
and 21 (d) 3 months post trauma showing continued loss
of root length of both 11 and 21
c
index) and associated mesial vertical alveolar defect.
Tooth 11 demonstrates apical shortening (Grade 4 root
resorption, Malmgren index) and distal external inflam-
matory root resorption of the root surface
This case highlights the difficulties encoun-
tered in execution of ideal treatment plans in
young children who quite often have had no pre-
vious dental intervention. Given the difficulties
in eliciting compliance, the family were aware
that long-term survival of both upper central inci-
sors was guarded.
17.8.7 Lateral Luxation
A 29-year-old male soldier was referred by his
dental practitioner for an orthognathic assess-
ment. There was a history of functional appliance
therapy in his adolescent years, which was unsuc-
cessful. At the age of 26, both upper central
incisors were luxated palatally following trauma.
The luxated teeth underwent endodontic treat-
ment after the trauma. The patient reported the
teeth gradually returned to the pre-treatment
position without any orthodontic intervention.
288
a b
Fig. 17.19 Clinical photographs demonstrating pre-treatment clinical views
a b
Fig. 17.20 (a, b) Pre-treatment clinical radiographs.
Note apical shortening of tooth 21 (Grade 1 root resorp-
tion, Malmgren index), peri-apical radiolucency associ-
ated with tooth 11 and external inflammatory root
On examination there was a moderate skeletal
2 pattern, a lower lip trap, spaced upper arch, a
15-mm overjet, a deep and traumatic overbite and
class 2 buccal segments (Fig. 17.19).
The treatment plan involved combined
orthodontics and orthognathic surgery to
address the dental and skeletal pattern. The
patient was informed of the poor long-term
prognosis of the upper central incisors with
possibility of ankylosis and eventual need for
replacement.
The pre-surgical orthodontic phase of treat-
ment progressed well with good movement of the
upper central incisors (Fig. 17.20).
This case highlights the importance of
informed consent. The long-term prognosis of
the upper central incisors is poor. The pre-
treatment position of the teeth would have
resulted in limited treatment options for
17 Orthodontic–Endodontic Interrelationship
c
c d
resorption of distal root surface of tooth 11. (c) Six months
post commencement of orthodontic treatment radiograph
and (d) clinical intra-oral view. Note apical shortening of
teeth 11 and 21
replacement of these teeth if lost given the soft
tissue pattern and skeletal discrepancy, poten-
tially resulting in further episodes of trauma [49].
Clinical Hints and Tips for Managing
Orthodontic–Endodontic Cases
• With the increasing uptake of orthodontic
treatment, the expectations of what can be
achieved are increasing. The importance of an
accurate history, diagnosis and good clinical
records is fundamental to the informed con-
sent process.
• Close liaison with interdisciplinary team
members will ensure treatment plans are
achievable and ensure timely delivery of all
aspects of care.
• Involvement of the patient and family in com-
plex treatment planning decisions is vital. A
less complex plan may be more suitable for
References
some individuals following full discussion of
all alternative options.
• In cases where replacement root resorption is
suspected, careful treatment mechanics need
to be employed to avoid adverse effects to the
arch form.
• Where inflammatory root resorption is
detected prior to or during treatment, careful
monitoring is needed to check progression
with repeat radiographs at 6 months. A pause
in treatment may be beneficial to allow
healing.
• When tooth movement is not as expected, re-
evaluation of treatment objectives is necessary
with the patient and relevant interdisciplinary
team members.
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 Systemic Diseases
and Endodontics 18

Summary
Dental practitioners must be aware of common diseases affecting patients
and their implications during endodontic manipulation in order to provide
a safe and adequate endodontic therapy for these patients. Various diseases
are discussed with the relevance to endodontic procedures including
peri-operative management and outcome.

Clinical Relevance The Microorganisms of the Human Mouth: The

Endodontic manipulation can result in adverse
reactions particularly if the patient’s medical
history has pre-existing risk factors. The clinician
should not only be aware of common medical
emergencies that can arise when treating patients
but also specifically during endodontic manipula-
tion and treatment. Endodontic management in
relation to irradiated patients, pregnant patients,
and patients with pre-existing cardiac disease,
prosthetic joints, diabetes mellitus, osteoporosis,
bleeding disorders, stroke, common respiratory
disorders and latex allergies is highlighted includ-
ing all necessary precautions prior to treatment.
18.1 Focal Infection Theory
The theory of focal infection postulates that a
myriad of diseases are caused by microorganisms
(bacteria, fungi and viruses) that arise endoge-
nously from a focus of infection. In 1890, the
dentist WD Miller published his treatise:
Local and General Diseases Which Are Caused
by Them [1]. In 1900, the English physician
William Hunter reported that the preservation of
the dentition by dental treatment was a cause of a
multitude of diseases attributed to focal infection
[2]. In 1911 his remarks to medical students at
McGill University in Montreal ignited the fires of
focal infection further with unfounded reports of
gold fillings, crowns and bridges and fixed
dentures, built on and about diseased tooth roots
forming a mausoleum over a mass of sepsis to
which there is no parallel in the whole realm
of medicine and surgery [3]. In 1912 Frank
Billings formally and independently introduced
the concept of focal infection to American physi-
cians, highlighting case reports ascribing distant
infections to various pathogens and claiming
cures for these afflictions by tonsillectomies and
dental extractions as a means to removal of these
various foci of infections [4]. EC Rosenow, a
pupil of Billings, further developed the theories
of ‘elective localisation’ and ‘transmutation’,

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 293
DOI 10.1007/978-3-319-15591-3_18, © Springer International Publishing Switzerland 2015
294
whereby microorganisms could possess affinities
for certain body organs and then alter their
biological characteristics [5].
In the 1920s, Dr Weston Price published a
series of rabbit experiments and case reports
of extraordinary improvements in various
medical conditions after dental extractions [6].
Endodontics came under particular scrutiny
with advocates of Hunter, Billings, Rosenow
and West recommending that all infected non-
vital teeth should be removed rather than end-
odontically treated to prevent or cure focal
infections. Further researchers presented the
idea of microorganism’s dissemination, or their
associated toxins throughout the body formed
a focus of circumscribed infection at a particu-
lar site, which could exacerbate systemic dis-
ease or damage to a distant tissue. These ideas
were based on limited scientific research, few
controlled studies and anecdotal evidence, yet
produced a reaction that was so strong that the
teaching of clinical endodontic techniques was
stopped altogether in most American institutions
in favour of dental extractions [7]. Despite lack
of robust evidence to the contrary, there is still
an international body of dental practitioners who
refuse to perform root canal treatment, reciting
the research performed 80–90 years ago to jus-
tify their cause.
Numerous studies have attempted to deter-
mine the risk of bacteraemia associated with
lesion of endodontic origin following nonsurgi-
cal and surgical endodontics. A bacteraemia is
far more probable if root canal instrumentation is
carried out beyond the apex of the tooth rather
than maintained within the confines of the canal
[8]. A further study in 1976 investigating bacter-
aemia subsequent to surgical and nonsurgical
root canal treatment corroborated the findings of
no bacteraemia being produced if root canal
treatment was limited to within the canal. The
authors demonstrated that nonsurgical root canal
treatment resulted in a much lower bacteraemia
incidence (3.3 % due to overinstrumentation),
compared to flap reflection (83.3 %), peri-
radicular curettage (33.3 %) or tooth extraction
(100 %) [9, 10]. In the 1990s, with the advent of
18 Systemic Diseases and Endodontics
modern aseptic sampling techniques, methods of
identification using DNA probes and effective
transport mediums, further evidence has been
provided into the nature of bacteria that may be
found whether instrumentation was carried out
within the canal itself or overinstrumented. Taken
together these studies demonstrated that greater
numbers of bacteraemia result from root canal
procedures, anaerobic species were commonly
associated and even when instrumentation was
confined to the canal itself a bacteraemia was
possible [11–13].
The use of rubber dam clamps, wedges and
matrix bands has also been demonstrated as caus-
ing cumulative bacteraemia relative to tooth
extractions [14, 15]. It is reasonable to conclude
that nonsurgical endodontics may be the least
likely of dental procedures to produce a signifi-
cant bacteraemia, but antibiotic prophylaxis may
be indicated for the prevention of endocarditis in
susceptible patients according to which country
you reside in. Nevertheless, to date, no interven-
tional studies have been performed to support the
evidence that modern endodontic therapy is not
safe and effective [14, 15].
18.2 Infective Endocarditis
Damage or injury to the cardiac valves (most
commonly mitral and aortic) can result in a layer
of platelets and fibrin deposits (nonbacterial
thrombotic endocarditis or vegetation), which
can incorporate circulating bacteria and fungi
resulting in bacterial or infective endocarditis
(IE). The undoubted role of oral bacteria and in
particular the viridans group streptococci (VGS)
and staphylococci has led to the hypothesis that
oral bacteria enter the circulation during invasive
dental procedures [16].
Numerous expert committees in different
countries have proposed different antibiotic pro-
phylactic (AP) regimens for the prevention of
IE. These include the British Society for
Antimicrobial Chemotherapy (BSAC) (UK) [17],
European Society of Cardiology (Europe) [18],
American Heart Association (USA) [19] and the
18.3 Prosthetic Joints
Table 18.1 Cardiac conditions associated with the
highest risk of adverse outcomes from endocarditis
Antibiotic prophylaxis is recommended in patients with
the following cardiac conditions if undergoing a
specific dental procedure (see Tables 18.2 and 18.3)
Prosthetic heart valve or prosthetic material used for
cardiac valve repair
Previous infective endocarditis
Congenital heart disease but only if it involves:
Unrepaired cyanotic defects, including palliative
shunts and conduits
Completely repaired defects with prosthetic material
or devices, whether placed by surgery or catheter
intervention, during the first 6 months after the
procedure (after which the prosthetic material is
likely to be endothelialised)
Repaired defects with residual defects at or adjacent
to the site of a prosthetic patch or device (which
inhibit endothelialisation)
Cardiac transplantation with the subsequent
development of cardiac valvulopathy
Rheumatic heart disease in Indigenous Australians only
Infective Endocarditis Prophylactics Expert
Group (Australia) [20]. The AP guidelines for the
prevention of IE have undergone various periodic
revisions with a progressive restriction for the
indications of AP. In the UK, the National
Institute for Health and Clinical Excellence
(NICE) published new guidelines in 2008 [21],
which proposed that ‘AP against IE is not recom-
mended for people undergoing dental proce-
dures’. This proposal was applied even to the
highest-risk patients, independently of the type of
dental procedure they were undergoing.
The main argument against the administration
of AP for the prevention of distant site infections
and, specifically, of IE secondary to dental proce-
dures in patient considered to be at risk is the effi-
cacy of such regimes [22]. Daily activities such
as mastication and toothbrushing and flossing
result in a similar bacteraemia that occurs follow-
ing invasive dental procedures such as extrac-
tions [23]. Other arguments against the use of AP
for IE include the development of β-lactam anti-
biotic resistance, risk of anaphylaxis and allergy
and costs to health care systems [24].
As a result, some cardiologists remain
understandably concerned about the omission
295
Table 18.2 Dental procedures where prophylaxis is
always required
Extraction
Periodontal procedures including surgery, subgingival
scaling and root planning
Replanting avulsed teeth
Intentional reimplantation
Other surgical procedures such as apicectomy
Table 18.3 Dental procedures where prophylaxis is
required in some circumstances
Consider prophylaxis for the following procedures if
multiple procedures are being conducted, the procedure
is prolonged or periodontal disease is present
Full periodontal probing for patients with periodontitis
Supragingival calculus removal/cleaning
Placement of interdental wedges
Subgingival placement of retraction cords, antibiotic
fibres or antibiotic strips
Intraligamentary and intra-osseous local anaesthetic
injections
Rubber dam placement with clamps (where risk of
damaging gingiva)
Restorative matrix band/strip placement
Endodontics beyond the apical foramen
Placement of orthodontic bands
of AP. In general the main guidelines in Europe,
the USA and Australia continue to recommend
the administration of AP, though restricting its
indications (see Tables 18.1, 18.2 and 18.3). It
would therefore appear reasonable to adopt the
recommendations proposed by the expert com-
mittees in the country of your practice liaising
with the patients’ cardiologist to confer prophy-
laxis indicated.
18.3 Prosthetic Joints
Joint replacement is a proven cost-effective med-
ical procedure that started from hip replacements
in the 1950s expanding to include knee, ankle,
shoulder, and elbow and finger joints. Infection
following a joint replacement is a devastating
complication that can be divided into early and
late occurring. Early infections that is within the
296 18 Systemic Diseases and Endodontics

Table 18.4 Antibiotic prophylaxis recommendations for patients with hip or knee joint replacement who require den-
tal treatment
Prior to artificial joint placement
Referral to a dental practitioner to ensure the patient is dentally fit prior to joint replacement
Dental problem in the first 3 months following artificial joint placement
Urgent and aggressive treatment of any abscess. Remove the cause (extraction or endodontics) under antibiotic
prophylaxis
Provide emergency dental treatment for pain. Antibiotics are indicated if a high- or medium-risk dental procedure
performed (extraction, endodontics or subgingival debridement)
Defer nonemergency dental treatment (noninfective and no pain) until 3–6 months after prosthesis replacement
Dental treatment after 3 months in a patient with a normally functioning artificial joint
Routine dental treatment including extraction. No antibiotic prophylaxis usually required unless the orthopaedic
surgeon insists
Dental treatment for patients with significant risk factors for artificial joint infection
Significant risks factors include any immunocompromised patients such as insulin-dependent diabetes, patients
taking immunosuppressive treatment for organ transplants or malignancy, patients with systemic rheumatoid
arthritis, patients taking systemic steroids (e.g. patients with severe asthma, dermatological problems)
Consultation with the patient’s treating physician/orthopaedic surgeon is recommended prior to provision of dental
treatment
Dental treatment for patients with failing, particularly chronically inflamed, artificial joints
Consultation with the patient’s treating orthopaedic surgeon is recommended. Defer all non-essential dental
treatment until orthopaedic problem has resolved
Dental treatment for patients with previous history of infected artificial joints
Routine nonsurgical dental treatment requires no prophylaxis. Antibiotic prophylaxis is recommended for all
extractions, deep periodontal scaling and endodontics (where manipulation beyond the apical foramen is likely)
Established infection by oral organisms on an artificial joint
Urgent referral to a dentist should be made to determine and eliminate any oral cause. Aggressive treatment is
recommended with either extraction or endodontic therapy under antibiotic prophylaxis
All patients who are undergoing or have undergone joint replacement therapy should have regular dental check-ups
to ensure they are dentally fit

first 3 months following implantation primarily
relate to infection introduced at the time of the
operation, either sourced from the patient or the
surgical staff. Late infections, more than 3
months after primary implantation, are usually
secondary to bacteraemia [25].
There are a number of antibiotic prophylaxis
guidelines which have been produced by national
bodies. In July 2003, the American Dental
Association published an advisory statement in
association with the American Academy of
Orthopaedic Surgeons: ‘Antibiotic prophylaxis is
not routinely indicated for most dental patients
with total joint prosthesis but it may be advisable
to consider pre-medication in a small number of
patients who may be at potential risk of experi-
encing haematogenous joint infections’. This is a
major change in attitude by the Americans [26].
The British National Formulary has a similar
analysis, which looks at the rationale behind the
guidelines and examines the issues from a risk
management point of view. It emphasises that the
risk of antibiotic prophylaxis outweighs the risk
of joint infection. It also emphasises the need for
communication between orthopaedic surgeons
and dentists. It confirms that within broad
guidelines all patient situations are individual
and this requires individual communication,
co-operation and treatment plans [27].
The Australian guidelines agreed that antibi-
otic prophylaxis was only indicated for high-risk
dental procedures in immunocompromised
patients with joint problems (see Table 18.4).
Prior to joint replacement, all patients should be
deemed dentally fit, and an appropriate oral
review should be made to determine this. Dental
treatment during the preimplantation phase
should be aggressive to eliminate any foci of
infection. During the first 3 months following
joint replacement, if a dental infection arises, it
18.6 Osteoporosis and BRONJ
should be treated aggressively by endodontics or
extraction with appropriate therapeutic antibiot-
ics. Following this interim 3-month period once
the joint prosthesis is functioning well and is
stabilised, routine dental treatment including
extractions should be carried out without any anti-
biotic prophylaxis. Patients who are deemed high
risk of developing an infection (i.e. have already
had a previous episode of joint replacement for an
infected prosthesis or immunocompromised) may
require standard antibiotic prophylaxis. Effective
communication with the patients’ orthopaedic
surgeon is essential, and in situations where pro-
phylaxis is requested, it needs to be recorded so
that the responsibility for any adverse outcome
related to the administration of antibiotic therapy
lies with the requesting clinician [25].
18.4 Irradiated Patients
The detrimental effects of radiotherapy, chemo-
therapy and ablative surgery to the dentition and
oral health necessitate extraction of at-risk teeth.
This includes all carious and heavily restored
teeth, teeth with deep periodontal pockets and
inaccessible posterior teeth. The side effects of
radiotherapy depend on the dose, delivery (num-
ber of fractions), site and mode and can result in
xerostomia, mucositis, trismus, radiation caries
and osteoradionecrosis (ORN) developing later.
ORN is a condition of exposed, devitalised bone
for greater than 3 months in an area that has been
irradiated. This arises due to radiation-induced
free-radical species, endothelial changes, inflam-
mation, fibrosis and necrosis. The exposed bone
can then be superinfected by oral microorganisms
[28]. Endodontic treatment in the irradiated patient
may result in challenges complicated by the pres-
ence of trismus and limited inter-occlusal space
preventing ideal access cavity preparation.
Nevertheless it may be preferable to extraction,
thereby minimising the risk of ORN [29].
18.5 Diabetes Mellitus
Diabetes mellitus is a group of diseases charac-
terised by high levels of blood glucose resulting
297
from defects in insulin production, insulin action
or both. Type I diabetes, or insulin-dependent
diabetes mellitus, is an autoimmune disease that
causes the destruction of insulin-producing
β-cells in the pancreas. Type 2 diabetes, or
non-insulin-dependent diabetes mellitus is
characterised by resistance of insulin and
inadequate insulin production [30].
As a consequence, this disease promotes
hyperglycaemia, wound healing difficulties as
well as systemic and oral manifestations.
Experimental and clinical studies have demon-
strated a higher prevalence of peri-apical lesions
in patients with uncontrolled diabetes. Pulps
from patients with diabetes have the tendency to
present limited dental collateral circulation,
impaired immune response and increased risk of
acquiring infection (especially anaerobic ones) or
necrosis. With regard to molecular pathology,
hyperglycaemia is a stimulus for bone resorption,
inhibiting osteoblastic differentiation and reduc-
ing bone recovery. Patients with diabetes have
increased periodontal disease in teeth involved
endodontically and have a reduced success of
endodontic treatment in cases with preoperative
peri-radicular lesions [31, 32].
18.6 Osteoporosis and BRONJ
Osteoporosis is defined as a skeletal disorder that
compromises bone strength, predisposing a
person to an increased risk of bone fracture due
to inhibited calcium intake and mineral loss.
Osteoporosis can be classified as primary
occurring in both genders at all ages, typically
following menopause in women and occurring
later in life in men. Secondary osteoporosis is the
result of medications (glucocorticosteroids) or as
a result of diseases such coeliac disease or cystic
fibrosis.
Bisphosphonates are the primary drugs used
to treat osteoporosis by suppressing osteoclast
activity and increasing bone mineral density.
Patients treated with intravenous bisphospho-
nates have a risk of developing bisphosphonate-
related osteonecrosis (BRONJ) of the jaw. This
risk increases when the duration of therapy
exceeds 3 years. As this condition is debilitating
298 18 Systemic Diseases and Endodontics

Table 18.5 Endodontic treatment recommendations for Table 18.6 Common bleeding disorders
treating patients with risk of developing BRONJ
Coagulation Congenital
High-risk groups include patients treated with IV factor Haemophilia A and B
bisphosphonates (BP) as well as patients who have deficiencies Von Willebrand disease
been taking BPs orally for more than 3 years and who
Acquired
concomitantly present systemic issues (chronic kidney
disease, diabetes, corticosteroid therapy) Liver disease
A one-minute rinse with chlorhexidine prior to starting Vitamin K deficiency
treatment would lower the bacterial load of the oral Warfarin use
cavity aimed at decreasing any bacteraemia caused by Disseminated intravascular
soft tissue trauma from the rubber dam placement coagulation
Impaired vascularisation is a risk factor for Platelet Immune mediated
osteonecrosis so anaesthetic agents with disorders Idiopathic
vasoconstrictors should be avoided
Drug induced
Working under aseptic conditions is mandatory,
Collagen vascular disease
requiring the use of rubber dam. Disinfection of the
tooth and dam should be performed with a disinfection Sarcoidosis
solution such as 80 % ethanol for 2 min Non-immune mediated
During placement of the rubber dam clamp, particular Leukaemia
care should be taken to ensure minimal trauma or Acquired
damage occurs to the underlying gingival tissues Drug induced
Overfilling and overextension of filling material should Liver disease
be avoided to reduce the risk of adverse outcome and Alcoholism
treatment effectiveness
Vascular Scurvy
disorders Purpura
and difficult to treat, all efforts should be made to Hereditary haemorrhagic
telangiectasia
prevent its occurrence. The main triggering event
Cushing syndrome
is considered to be dental extraction. Nonsurgical Ehlers–Danlos syndrome
endodontic treatment is a safe alternative to den- Fibrinolytic Streptokinase therapy
tal extractions, but caution should be mandatory defects Disseminated intravascular
with particular attention to treatment protocols coagulation
to avoid the risk of developing BRONJ
(see Table 18.5) [33].
for the prevention of thromboembolism, myocar-
dial infarction and cerebrovascular accidents.
18.7 Bleeding Disorders Aspirin prevents thrombus formation by irrevers-
ibly inhibiting cyclooxygenase 1 in platelets,
Clinicians must be aware of the impact of bleed- thereby preventing thromboxane A2 formation (a
ing disorders on the management of endodontic potent vasoconstrictor and platelet aggregator).
patients, and proper dental and medical evalua- Patients are often maintained on low-dose aspirin
tion is essential prior to any treatment, especially therapy (75–100 mg) daily, resulting in
if an invasive dental procedure is planned. irreversible platelet function for the duration of
Bleeding disorders can be classified as coagula- their lifetime (7–10 days). Other non-steroidal
tion factor deficiencies, platelet disorders, vascu- anti-inflammatory (NSAID) drugs (ibuprofen
lar disorders and fibrinolytic defects and can be and diclofenac) also result in abnormal platelet
congenital, acquired or drug induced (see function, but once discontinued, the effects will
Table 18.6) [34–36]. last as long as the half-life of the drug. Clopidogrel
Aspirin therapy, prescribed or self- (Plavix) is commonly used for the prevention of
administered, is a leading drug used worldwide athero-thrombotic events and is often used in
18.8 Cerebrovascular Accidents
conjunction with aspirin. On cessation normal
platelet function usually recovers fully after 2
days [35].
Coumarin therapy (warfarin) is a vitamin K
antagonist which inhibits the biosynthesis of
vitamin K-dependant coagulation proteins VII,
IX, X and II (prothrombin). The activity of war-
farin is expressed using the international nor-
malised ratio (INR), which is the prothrombin
time ratio. For an individual who is not taking
warfarin, the INR would be 1.0. Warfarin is
reversed by the administration of vitamin
K. Warfarin therapy is used for either prophylaxis
or treatment of deep vein thrombosis (DVT),
atrial fibrillation and patients with prosthetic
heart valves. The therapeutic INR range is 2–3
for DVT and between 4 and 5 for patients with
prosthetic heart valves [35].
Heparin, available as standard unfraction-
ated or low molecular weight form, is com-
monly used as an antithrombotic agent and in
the treatment of thromboembolic disorders. It is
administered intravenously or subcutaneously
within the hospital setting either as inpatient or
outpatient according to route/type of heparin
used [35].
Acquired bleeding conditions such as liver
disease, alcoholism, renal failure, thrombocyto-
penia and chemotherapy will all have coagulation
and clotting disorders that may affect normal
haemostasis mechanisms [36].
Hereditary disorders include von Willebrand
disease (vWD), haemophilia A and haemophilia
B. vWD is an autosomal dominant disorder
resulting in deficient or a qualitative defect in von
Willebrand factor and in some cases deficiency in
factor VIII. This bleeding disorder commonly
results in a combined platelet plug and fibrin for-
mation defect resulting in a prolonged bleeding
time in the presence of a normal platelet count.
Haemophilia A is an X-linked recessive trait
caused by a defect or a deficiency in the activity
or the amount of factor VIII characterised by a
normal bleeding time but a prolonged activated
partial thromboplastin time (APTT). Haemophilia
B (Christmas disease) is a sex-linked recessive
299
disorder resulting in a deficiency or defective
factor IX within the intrinsic pathway of the
coagulation system [34].
Prior to undertaking endodontic treatment, it
may be necessary to liaise with the patients’
physician responsible for their care to discuss
potential management issues and to ensure that
appropriate measures have been taken to reduce
the risk of peri- and post-operative complica-
tions. In general terms, nonsurgical endodontic
treatment itself does not pose too much risk pro-
vided an atraumatic approach is taken (particu-
larly with respect to rubber dam placement) and
all instrumentation is kept within the confines of
the root canal. Local anaesthetic administration
requires special attention with the theoretical
risk of bleeding into fascial planes and haema-
toma formation, particularly when using
regional anaesthesia (inferior dental block, pos-
terior superior alveolar nerve block, lingual
infiltrations and injections). The use of infiltra-
tions and intraligamentary, intra-osseous and
intra-pulpal injections is safer. It would be pru-
dent to seek advice from the patients’ haema-
tologist prior to embarking upon any surgical
procedure and ensure that there is no significant
bleeding risk and if so appropriate cover has
been provided. Adjunctive tranexamic mouth-
washes may be indicated following surgical pro-
cedures to provide additional post-operative
cover [34–36].
18.8 Cerebrovascular Accidents
Stroke is a cerebrovascular disorder characterised
by a sudden interruption of blood flow to the
brain, causing oxygen deprivation that can result
in a sudden or rapidly progressing neurological
defect, which does not resolve within 24 h. The
effects of a stroke are principally unilateral weak-
ness, numbness and partial or complete paralysis
of the arm, leg or face on the contralateral side
of the brain. Elective and invasive endodontic
treatment should be deferred where possible
for the first 3 months after a stroke. Endodontic
300
treatment may be complicated by difficulties in
communication, mobility of the patient and risks
of anticoagulation therapy used to prevent further
thromboembolic events. Patients taking antihy-
pertensive medication may be at risk of postural
hypertension, and this should be taken into
account following prolonged periods in the den-
tal chair [30, 35].
18.9 Respiratory Disease
Chronic obstructive pulmonary disease, a combi-
nation of chronic bronchitis and emphysema, and
asthma are the most common conditions that
result in obstruction of the human airway. In
chronic bronchitis, the airway is obstructed
because of excessive mucous production and
inflammation of the smaller airways. The patient
has a chronic, productive cough on most days for
at least 3 months of the years for at least 2 con-
secutive years. Along with the cough, the patient
also experiences wheezing, shortness of breath,
exertional dyspnoea and frequent respiratory
infections. Patients are typically described as
‘blue bloaters’ to signify the cyanotic appearance
of the patient. Chronic emphysema resulting
from damage to the alveoli (usually from ciga-
rette smoking) leads to obstruction in gas
exchange. Emphysema patients are termed ‘pink
puffers’ as the effort of exhaling builds the mus-
cles of the chest to a barrel shape and air becomes
trapped in the lungs. Bronchial asthma, a reactive
airway disease, results in patients experiencing
reoccurring episodes of wheezing, coughing and
dyspnoea. An attack may last for several minutes
and then resolve spontaneously with rest or in
response to drug therapy. Mechanisms that lead
to airway obstruction include bronchial smooth
muscle spasm and constriction, inflammation
and oedema of the mucosa and excessive
mucous secretion. Several aetiological factors
may be responsible including allergies to dust,
pollen or animal dander and intrinsic mecha-
nisms triggered by emotion, stress, anxiety and
nervousness.
Dental health-care providers must be aware of
patients with compromised airway function and
18 Systemic Diseases and Endodontics
their ability to tolerate dental treatment.
Treatment may need to be altered because of
existing pulmonary disease or the medications
that are prescribed to treat them. Endodontic
treatment may be difficult or compromised due to
the patient’s inability to lie supine. Sedation
should be avoided due to the risk of respiratory
depression, and local anaesthetics should be the
drugs of choice. Care must be taken when pre-
scribing non-steroidal anti-inflammatory drugs
since some patients may experience asthma
attacks after using aspirin. Codeine-related drugs
should also be avoided since they may aggravate
bronchospasms [37].
18.10 Pregnancy
Oral health is an integral part of overall health
and no more so than in a pregnant patient.
Endodontic problems encountered during preg-
nancy should be addressed promptly and prop-
erly. A common concern has been regarding the
safety of treatment including risk of teratoge-
nicity (the ability to cause birth defects) as a
result of imaging procedures, and medications,
particularly in the first 12 weeks of gestation.
Prior to undertaking any form of treatment, the
benefits to both mother and foetus must be taken
into consideration. Any routine treatment should
be delayed if possible. Emergency endodontic
treatment should be provided, particularly if the
patient is in pain. Although radiographic imag-
ing is not contraindicated in pregnancy, the stan-
dard of care should be to take the minimum
number of images required for a comprehensive
examination. If an apex locator can be reliably
used to determine working lengths, then radio-
graphic imaging can be avoided at this stage. As
with all patients, a thyroid collar and abdominal
apron should be used. Following provision of
emergency endodontic treatment with pulpal
extirpation, subsequent cleaning, shaping and
obturation can be delayed until postpartum
where issues of radiographic imaging or use of
adjunctive medications including analgesics and
antibiotics are not so much of a concern.
Postural hypertension syndrome is a clinical
18.12 Medical Emergencies
concern, and to minimise the risk, a small pillow
can be placed under the patient’s right hip and
the head should be raised above the feet when
reclining [38].
18.11 Latex Allergy
Natural rubber latex (NRL) allergy, as a result of
sensitisation to proteins in NRL, occurs in 1–6 %
of the general population and can result from an
interaction with many dental products including
disposable gloves, dental rubber dams and bungs
in dental syringes and local anaesthetic prepara-
tions. Allergic reactions to NRL include a type I
reaction that presents as an immediate hypersen-
sitivity with itching of the skin and eyes, sneezing
and bronchospasm or anaphylaxis. Type I reac-
tions occur immediately after exposure to NRL
and can be life-threatening requiring appropriate
medical management. Type IV reactions
(delayed) usually occur 6–48 h after exposure
and may be in response to the chemicals in the
rubber manufacturing process. Appropriate pre-
cautions should be used in all patients with
known latex allergy including the use of non-
latex products such as nitrile gloves, latex-free
rubber dam and local anaesthetic in plastic car-
tridges. Vinyl rubber dam can be rapidly dis-
solved when it comes into contact with
chloroform used for re-treatment cases. Care
must be taken to avoid chloroform overflow from
within the endodontic access cavity. To date there
has only been one case report of potential hyper-
sensitivity to gutta-percha root filling material
[39, 40].
18.12 Medical Emergencies
Medical emergencies can often be prevented by
early recognition. All dentists should be compe-
tent in basic life support resuscitation. They
should be able to assess breathing and circulation
and carry out effective expired air resuscitation
(EAR), external cardiac compression (ECC) and
cardiopulmonary resuscitation (CPR) if required.
When a life-threatening emergency such as a
301
D Dangers?
R Responsive?
S Send for help
A Open Airway
B Normal Breathing?
Start CPR
30 compressions : 2 breaths
C If unwilling/unable to perform rescue breaths
continue with chest compressions
Attach Defibrillator (AED)
D as soon as available and follow its
prompts
Continue CPR until responsiveness or normal
breathing returns
Fig. 18.1 The principles of DRSABCD approach for an
acutely ill patient (Australian Resuscitation guidelines)
complete laryngeal obstruction, cardiac arrest or
bronchospasm associated with anaphylaxis
occurs, there is no time for delay and immediate
prompt diagnosis and treatment should be initi-
ated. The Australian Resuscitation Council rec-
ommends the DRABCD (check for danger, check
if the patient is responding, check the airway for
obstruction, assess breathing, assess circulation,
and attach defibrillator) (Fig. 18.1) basic sequen-
tial steps for all emergency situations. These
steps are devised to ensure that adequate delivery
of oxygenated blood to the brain occurs prior to
delivery of definitive care.
Defibrillation is the term which refers to the
termination of fibrillation. It is achieved by
administering a controlled electrical shock to the
heart, which may restore an organised rhythm,
enabling the heart to contract effectively.
Ventricular fibrillation (VF) is the most common
cause of cardiac arrest resulting in a chaotic and
rapid rhythm whereby the heart fails to contract
effectively. The provision of defibrillation using
an automated external defibrillator (AED) is the
only effective treatment for VF increasing the
chance of survival for the patient. AEDs are
sophisticated, reliable, safe and computerised
302 18 Systemic Diseases and Endodontics

Fig. 18.2 Automated

external defibrillator Unresponsive
(AED) algorithm. Continue Call for help
until victim is able to Open airway
breathe normally not breathing normally
(Australian Resuscitation Call for
Council) ambulance
Start CPR 30 compressions : 2
breaths until AED is attached

AED
Shock assesses No shock
advised ryhthm advised

I Shock
No

Immediately Return of
Immediately
resume CPR spontaneous resume CPR
30 compressions : 2 circulation? 30 compressions : 2
breaths for 2 mins breaths for 2 mins
Yes

Post resuscitation care

Table 18.7 Typical contents of the emergency drug box and routes of administration
Drug Route of administration
Oxygen Inhalation
Glyceryl trinitrate (GTN) spray (400 mg per actuation) Sublingual
Dispersible aspirin (300 mg) Oral (chewed)
Salbutamol aerosol inhaler (100 mg per actuation) Inhalation
Adrenaline injection (1:1,000, 1 mg/ml) Intramuscular
Glucagon injection (1 mg) Intramuscular/subcutaneous
Oral glucose solution/gel (GlucoGel) or alternatives include 2 teaspoons of sugar/3 Oral
sugar lumps and 200 ml milk or non-diet lucozade/Coca-Cola 90 ml
Midazolam 10 mg or 5 mg/ml (buccal or intranasal) Infiltration/inhalation

devices, which use voice and visual prompts, that
analyse the victim’s heart rhythm, determine the
need for a shock and then deliver a shock (see
Fig. 18.2).
The administration of emergency drugs is
always secondary to providing life support dur-
ing a medical emergency (see Table 18.7). It is
important to check that the drugs are within the
expiry date [41].
It is appropriate for the dentist to make estab-
lished links with the nearest medical practitioner
or facility. The dentist should administer no drugs,
other than oxygen, if he or she is not adequately
trained and confident of the diagnosis.
The predominant causes of medical emergen-
cies in dental surgeries include vasovagal syn-
cope, hyperventilation, asthma, angina pectoris,
acute myocardial infarction, cardiac arrest, epi-
lepsy, toxic effects of local anaesthetic, hypogly-
caemia (insulin-dependent diabetes), acute
airway obstruction (see Fig. 18.3) and severe
allergic reactions (anaphylaxis) [42]. Common
clinical features and treatment are discussed in
Table 18.8.
18.12 Medical Emergencies 303

Fig. 18.3 Algorithm for

Assess severity
the management of the
choking patient (Australian
Resuscitation Council) Severe airway Mild airway
obstruction obstruction
(ineffective (effective
cough) cough)

Unconscious Encourage cough

Start CPR Conscious
Continue to check
30 compressions : 5 back blows
for deterioration
2 breaths
to ineffective
5 abdominal
cough or releif of
thrusts
obstruction

Table 18.8 Predominant causes of medical emergencies in the dental setting, salient clinical features and management
protocol
Condition Clinical features (CF) and management(M)
Vasovagal syncope CF: Faintness, weakness, pallor, sweaty skin, lowered pulse, hypotension
(fainting) M: Lie horizontally, elevate feet, administer oxygen, and monitor for vital signs. Give
glucose drink on recovery
Hyperventilation CF: Dyspnoea, rapid breathing, faintness, paraesthesia of extremities, palpitations
M: Encourage slower breathing; rebreathe expired air with a paper bag
Asthma CF: Dyspnoea, cyanosis, audible wheezing, cyanosis
M: Reassure; use up to 4 metered doses of aerosol bronchodilator (salbutamol)
Angina pectoris CF: Moderate to crushing central chest pain, radiating to the left arm, neck or mandible
M: Stop treatment. Place one glyceryl trinitrate tablet 0.6 mg under tongue or spray
under tongue
Repeat dose in 5 min after first checking BP and again after 5 min if pain persists
If no improvement after 15 min, then treat as myocardial infarction
Acute myocardial CF: Chest pain similar to angina but unrelieved by 3 glyceryl trinitrate tablets over
infarction 10 min. Suspect in angina patient who says pain in much worse than usual or if this
is the first episode of chest pain
M: Call ambulance. Monitor vital signs. 100 % oxygen. Dissolved aspirin tablet and
one glyceryl trinitrate dose stat and one repeat in 5 min after checking BP
Cardiac arrest CF: Sudden unconsciousness, no breathing and no pulse
M: Call ambulance immediately. Initiate cardiopulmonary resuscitation, early
defibrillation and oxygen
Epilepsy (grand mal) CF: Patient may have an ‘aura’ or premonition that seizure is about to occur
Tonic phase – loss of consciousness; patient becomes rigid, falls and becomes cyanosed
Clonic phase – jerking movements of limbs
M: Protect from injury, monitor vital signs, oxygen and medical assistance
Decision to give medication should be made if seizures are prolonged. Midazolam via
buccal or intranasal route 10 mg for adults
Toxic effects from LA 1. Adrenaline toxicity – restlessness, throbbing headache, pallor, rapid full pulse,
palpitation
2. LA base toxicity – first CNS stimulation and then depression with convulsions
M: Basically supportive – effects should terminate rapidly
(continued)
304 18 Systemic Diseases and Endodontics

Table 18.8 (continued)

Condition
Hypoglycaemia (history
of insulin-dependent
diabetes mellitus)
Adrenal insufficiency
Acute airway obstruction
Severe allergic reaction
(anaphylaxis)
Clinical features (CF) and management(M)
CF: Slurred speech, altered behaviour, sweating, rapid pulse, apprehension, then loss
of consciousness
M: Give orange juice, glucose drink or sugar lumps at first sign which will rapidly
terminate event, i.e. loss of consciousness should never occur. If loss of
consciousness occurs, need parenteral therapy is needed (glucose or glucagon)
CF: Patient loses consciousness; the patient has a rapid, weak or impalpable pulse
and blood pressure falls rapidly; history of corticosteroid therapy/Addison’s disease
M: Lay the patient flat and raise his/her legs. Ensure a clear airway and administer
oxygen
Call an ambulance
CF: Sudden apnoea or dyspnoea cyanosis, violent coughing spasms, inability to catch
breadth
M: Try to remove cause. 5 back blows with patient’s head leaning forward. If unable
to remove, administer oxygen, and arrange transfer to hospital for bronchoscopy
CF: Asthma-like symptoms (sneezing and dyspnoea), circulatory collapse, cardiac
arrest, following drug administration
M: Call ambulance. Always check that respiratory distress is not due to other causes
Adrenaline 1:1,000 IM (1/2 ml) as injection or EpiPen
May need to repeat dose after 5 min
100 % oxygen
CPR if cardiac arrest occurs

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 Index

A propofol, 240
A beta fibres, 2 training, 238
Acute apical abscess, 6–7, 43, 45, 53–54 Apical periodontitis
Acute apical periodontitis, 6, 42–44 bacterial role, 22
Acute maxillary sinusitis, 4 dentinal tubule invasion, 25–26
Acute periodontal abscess, 7 and herpesvirus, 30–31
A delta fibres, 2 intra-canal bacteria and bacterial biofilms, 21
Allodynia, 4 microbiota, features of, 29, 30
Ameloblastoma, 58 nonmicrobial aetiological factors, 31–32
Amoxicillin, 143–145 pathogenesis, 28
Amoxiclav, 143 pulpal contamination pathways, 22–23
Analgesics, 226–227 root canal system
Ankylosis bacterial entry, 22–23
late adolescence, 283–286 bacterial interactions, 26–27
preadolescence, 286–287 microflora, spatial distribution of, 23–26
Anterior middle superior alveolar (AMSA) block, 232 nutrients, 27–28
Anterior teeth technique, 218, 220 and yeasts, 31
Antibiotics Armamentarium, 117
amoxicillin, 143 burs
amoxiclav, 143 canal preparation, 136
clindamycin, 144 cutting an access cavity, 135–136
effectiveness, 142 location of canal, 136
endodontic facial infections, management of, 84 C+ files, 119
infective endocarditis, 142–143 coloured numbering system, 118
Ledermix paste, 143–144, 146 CPITN probe, 138
local adjunctive antibiotics, 146 cutting blade design, 118
prosthetic joint implants, 143 dental magnification and illumination
Septomixine Fort paste, 143, 144 advantages, 121
systemic (see Systemic antibiotics) dental operating microscope, 122–123
tetracyclines, 144 disadvantages, 121
use of, 141 loupes, 122
Anxiolytics, 236 resolution, 122
conscious sedation, 237 DG16 endodontic probe, 138
diazepam, 239 engine-driven instruments
equipment, 237–238 controlled high-torque and low-speed motor, 126
fasting, 237 Greater Taper files, 128–129
fentanyl, 240 K3, 130
inhaled nitrous oxide, 239 LightSpeed rotary nickel–titanium instrument,
intravenous sedation, 240 127–128
ketamine, 239 ProFiles rotary nickel–titanium instrument,
midazolam, 239 126–127
nitrous oxide, 239–240 ProTaper Next, 132–133
oral sedation, 238–239 ProTaper Universal system, 129
patient assessment, 237 RaCe system, 129–130
personnel, 238 speed of rotation, 126

B. Patel, Endodontic Diagnosis, Pathology, and Treatment Planning: Mastering Clinical Practice, 307
DOI 10.1007/978-3-319-15591-3, © Springer International Publishing Switzerland 2015
308 Index

Armamentarium (cont.) Cerebrovascular accidents, 299–300

torque, 126 C fibres, 2
Vortex Blue, 130–132 C+ files, 119
WaveOne, 132 Charge-coupled devices (CCD), 170–171
Flex-R file, 118–119 Chronic apical abscess, 54
front surface reflecting mouth mirror, 136 Chronic apical periodontitis
Hedstroem file, 118, 124 acute exacerbation of, 16
instrument packs, 136–138 nonsurgical root canal treatment, 44
K-file instrument, 118, 119 peri-radicular bone resorption, 43, 46
microsurgical instruments, 134–135 with suppuration, 44–46, 54
M-Wire technology, 125–126, 132 Chronic (persistent) idiopathic facial pain (CIFP), 5, 15
obturation tray setup, 138 Ciprofloxacin, 145
rotary Ni–Ti file systems, design features of, 119–121 Clamp first technique, 217–219
sonic and ultrasonic instruments Clarithromycin, 145
applications, 133 Climax community, 28
frequency range, 133 Clindamycin, 144, 145
ProUltra or Satelec ultrasonic tips, 133 Combined occlusal trauma, 8, 9
ProUltra Piezo, 133 Commission on Dental Accreditation (CODA), 123
Start-X tips, 133–134 Condensing osteitis, 45, 47
stainless steel instruments, 123–125 Cone-beam computed tomography (CBCT), 162, 163,
torque-controlled motor set, 121 172–173
ultrasonic instrumentation, 121 Conscious sedation, 237
uniform file tape requirements, 118 Corticosteroids, 240–241
Articaine, 225 Coumarin therapy, 299
Aspirin therapy, 298 Cracked tooth syndrome, 259–261
Atypical odontalgia, 5, 15 Craze lines, 251, 258
Augmentin, 145 Creutzfeldt–Jakob disease (CJD), 89–90
Avulsion Crown-down shaping technique, 131
delayed replantation adolescent, 281–283 Crown lengthening, 109–110
immediate replantation adult, 278–281 C-shaped canal systems, 207–211
Azithromycin, 145 Cyclooxygenase enzyme (COX), 227
Cyst. See also specific Cysts
definition, 49
B radiological appearances, 52
Bay cyst, 52
Benign aggressive lesions, 52
Benign cemento-osseous dysplasia, 52 D
Benign fibro-osseous lesions, 58 Degenerative changes, tooth, 41, 42
Biofilms Dens invaginatus, 199, 202–204
bacterial condensations, 29 Dental implant failures, 112–114
definition, 28 Dental magnification and illumination
development on surface, 28, 29 advantages, 121
Bisecting-angle technique, 168, 170 dental operating microscope, 122–123
Bisphosphonate-related osteonecrosis (BRONJ), disadvantages, 121
297–298 loupes, 122
Bitewing radiography, 167–168 resolution, 122
Bleeding disorders, 298–299 Dental negligence, 69
Bolam principle, 67, 68 Dental operating microscope, 122–123
Bow first technique, 218–219 Dental records, 69–70
Buccal space, 82 Dental unit water line (DUWL) maintenance, 89
Bupivacaine, 225 Dentinal sensitivity
aetiology, 7–8
diagnostic tests, 8
C modified Bass technique, 8
Caldwell–Luc procedure, 14 prevention, 8
Canine fossa, 81 sealing dentinal tubules, 8
Cavernous sinus thrombosis, 82–83 signs and symptoms, 8
Cellulitis, 78–79 Dentinal tubule invasion, 25–26
Central giant cell granuloma, 58 Dentine hypersensitivity, 3
Cephalosporins, 145 Depth of field, 122
Index 309

DG16 endodontic probe, 138 root resection, 252

Diabetes mellitus, 297 split tooth, 261, 265
Diazepam, 239 vertical root fracture, 251, 261–264
Digital radiography, 163, 170–172 Endodontic radiology
Disinfection, 89 clinical relevance, 161
Doxycycline, 145 cone-beam computed tomography, 172–173
conventional two-dimensional radiographs, 162
digital radiography, 170–172
E instant process films, 162
Electric pulp testing (EPT), 150–151, 156–158 long-cone paralleling technique, 162
Endodontically treated teeth, 272 peri-apical lesions, 164
Endodontic diagnosis plain film radiography
cold stimulus, 150 bisecting-angle technique, 168, 170
diagnostic decision-making, 150 bitewing radiography, 167–168
electric pulp testing, 150–151, 156–158 paralleling technique, 167–169
hot stimulus, 150 peri-apical radiography, 167
laser Doppler flowmetry, 151 root canal treatment, 166
physiometric testing, 151 X-ray photons, 166
traumatised teeth, 149 radiolucent and radiopaque lesions, 175
vitality testing, 149 standard equipment, 164–166
Endodontic examination tube shift technique, 173–175
articulatory system and muscles Endodontic treatment
of mastication, 152 alternative prosthodontic replacement options,
eyes, 152 110–114
head, face and neck, 152 contraindications, 103–104
lining mucosa, 152–153 criteria, 105
lips, 152 crown lengthening, 109–110
lymph node, 152 decision-making process, 104
patient’s symptoms, 151 goal of, 103
teeth, 153–154 implant failures, 112–114
Endodontic infection control, 75 implant placement, 106
Endodontic-periodontal interrelationship long-term prognosis, 105
abscess, 247 osseointegrated dental implant, 112
animal studies, 248 peri-apical pathology, 106, 107
apical foramen, 246 periodontal assessment, 106, 108
classification systems, 246 planning, 103
clinical radiographs, 249 removable partial dentures, 111
clinical relevance, 245 root canal treatment
cracked tooth syndrome, 259–261 healing signs, 105
craze lines, 258 periodontal assessment, 106, 107
dentine, 247 restorability assessment, 105
diagnosis success rates, 104
pocket morphology, 252 tooth restorability assessment, 108–109
primary endodontic lesion, 253–254 Engine-driven instruments
primary periodontal lesion, 253, 255 controlled high-torque and low-speed motor, 126
pulp vitality tests, 253 Greater Taper files, 128–129
radiographic assessment, 253 K3, 130
differential diagnosis, 248 LightSpeed rotary nickel–titanium instrument,
fractured cusp, 258–259 127–128
hemisection, root amputation and root resection, ProFiles rotary nickel–titanium instrument, 126–127
262–266 ProTaper Next, 121, 132–133
lateral canals, 247 ProTaper Universal system, 121, 129
lateral periodontal radiolucency, 252 RaCe system, 129–130
longitudinal fractures, 250 speed of rotation, 126
longitudinal tooth cracks, 250 torque, 126
management, 255–257 Vortex Blue, 130–132
peri-apical lesions, 246 WaveOne, 120, 132
photographs, 251 Enterococcus faecalis, 29, 30
primary periodontal lesions, 249 Enucleation, 52
probing pocket depth, 246 Erythromycin, 145
310 Index

Ethico-legal issues Greater palatine nerve block, 232

Bolam principle, 67, 68 Greater Taper files, 128–129
clinical risk management checklist, 66
consultation with defence organisation, 68
culture of litigation, 69 H
dental negligence, 69 Hand hygiene
dental records, 69–70 levels of, 90
Gillick competence, 68 5 moments of, 90
good communication, 65 routine, 88
informed consent with soap and water, 91
morale and legal doctrine, 71 Healthy pulp, 36–37
principles, 70 Hedstroem file, 118, 124
patient complaints, 65 Heparin, 299
patient satisfaction, 65 Herpesvirus and apical periodontitis, 30–31
treatment High-torque control motors, 126
complications, 71–72 Hyperalgesia, 4
referral for, 71
valid consent, 66
Extra-radicular infections, 30 I
Incomplete root development, 196–199, 201–203
Infection control procedures
F automated cleaners, 89
Facial and neck space infections clinical hand contact surfaces, 88, 94
buccal space, 82 Creutzfeldt–Jakob disease, 89–90
canine fossa, 81 dental unit water system maintenance, 89, 96
cavernous sinus thrombosis, 82–83 disinfection, 89, 95
cellulitis, 78–79 enzyme cleaners, 89
fascial spaces, 79, 80 eyewear and face shields, 91–92
infratemporal fossa, 82 hand hygiene
Ludwig’s angina, 81 levels of, 90
mandibular molars and premolars, 80 5 moments of, 90
orbital cellulitis, 83 routine, 88
palatine space, 82 with soap and water, 91
parapharyngeal space, 82 immunisation policy, 94
pterygomandibular space, 82 instrument storage, 95
retropharyngeal space, 82 latex gloves, 88, 92
spread of, 78, 79 masks, 91
sublingual space, 80 mechanical and chemical-cleaning, 89
submandibular space, 81 minimal hand contact surfaces, 88, 94, 95
submasseteric space, 82 needlestick or sharps injury prevention, 88, 92–93
submental space, 80 neutral pH/mildly alkaline solutions, 89
Facial cellulitis non-latex gloves, 88, 92
definition, 78 personal protective equipment, in workplace,
management of, 84 88, 91–92
Fascial spaces, 79, 80 pre-sterilisation cleaning, 95–97
Fentanyl, 240 prevention of transmission, 87
Ferrule effect, 108 protective clothing, 92
Flex-R file, 118–119, 124 single-use instruments and prion disease, 97–99
Focal infection theory, 293–294 site decontamination, 89
Fractured cusp, 258–259 steam sterilisation, 95, 98
sterile gloves, 88, 92
sterilisation, 89
G surface barriers, 88–89, 95
Galilean loupes, 122 use of sharps devices, 88
Gates–Glidden drills, 136 vaccination, 88, 94
Gillick competence, 68 Infective endocarditis (IE), 294–295
Glucocorticosteroids. See Corticosteroids prophylactic antibiotics, 142–143
Gow-Gates technique, 233–234 Inferior alveolar nerve block (IANB), 233
Granulomatous inflammation, 52 Infraorbital block, 232–233
Index 311

Infratemporal fossa, 82 Gow-Gates technique, 233–234

Inhaled nitrous oxide, 239 inferior alveolar nerve block, 233
Intraligamentary injections, 235 long buccal nerve block, 234
Intra-oral incision and drainage, 84–85 mental nerve block, 234
Intra-osseous injections, 234–235 Vazirani-Akinosis technique, 234
Intra-pulpal injections, 235 Mandibular molar teeth, 193, 195–196, 198–201
Intra-radicular infections, 29–30 Mandibular premolar teeth, 192–193, 195–198
Intravenous sedation, 240 Marsupialisation, 52
Irreversible pulpitis, 3, 6, 38, 40, 142 Master Apical Rotary (MAR), 128
Maxillary canine teeth, 184–186
Maxillary central incisor teeth, 182–183
J Maxillary infiltration and blocks
Jaws anterior middle superior alveolar, 232
management of cystic lesions, 52 greater palatine nerve block, 232
radiolucent and mixed lesions of, 50–51 infraorbital block, 232–233
radiolucent lesions palatal anterior superior alveolar nerve block,
differential diagnosis, 53 230–232
non-healing lesions, 52 posterior superior alveolar nerve block, 232
Maxillary lateral incisor teeth, 184–185
Maxillary molar teeth, 188–191
K Maxillary premolar teeth, 186–188
Keplerian loupes, 122 Maxillary sinusitis, 12
Ketamine, 239 aetiology, 12
K3 instruments, 130 examination process, 13
management, 13–14
Maxillofacial infections, anatomical spaces
L involved, 76
Lateral luxation, 287–289 Mental Capacity Act, 68
Lateral periodontal cyst, 57 Mental nerve block, 234
Latex allergy, 88, 220 Mesio-buccal 2 (MB2) canals, 203–209
Ledermix/calcium hydroxide paste, 146 Metronidazole, 145
Ledermix paste, 143–144, 146 Microsurgical instruments, 134–135
LightSpeed rotary nickel–titanium instrument, 127–128 Midazolam, 239
Local anaesthesia (LA) Middle mesial canal, 206, 209
cardiac effects, 229 M-Wire technology, 125–126, 132
central nervous system effects, 229 Myofacial pain syndrome, 9–12
duration of action, 227
facial nerve palsy, 230
management, 229 N
mishaps, 229 Nasopalatine duct cyst, 57
noxious pain stimuli, 227 Natural rubber latex (NRL) allergy, 301
postinjection paraesthesia, 230 Necrotic pulp, 6
potency, 227 Nocturnal bruxism, 10
toxicity and management, 228–229 Non-endodontic lesions, 56
trismus, 229 ameloblastoma, 58
types and preparations, 228 benign fibro-osseous lesions, 58
Long buccal nerve block, 234 central giant cell granuloma, 58
Long-cone paralleling technique, 162 lateral periodontal cyst, 58
Loupes, 122 malignant lesions, 58
Low-torque control motors, 126 nasopalatine duct cyst, 57
Ludwig’s angina, 81 odontogenic keratocyst, 57
peri-apical cemento-osseous dysplasia, 58
Non-healing radiolucent jaw lesions, 52
M Non-narcotic analgesics, 224
Magnetostriction, 133 Non-odontogenic pain
Malignant lesions, 58 differential diagnosis, 2
Mandibular canine tooth, 192, 194 features of, 16, 18
Mandibular incisor teeth, 191–193 Normal peri-radicular tissues, 42, 43
Mandibular infiltration and blocks Normal pulp, 36–37
312 Index

O diazepam, 239
Odontoblasts, 22 equipment, 237–238
Odontogenic infections fasting, 237
dissemination, 77 fentanyl, 240
facial and neck space infections, 78–83 inhaled nitrous oxide, 239
facial cellulitis, 84 intravenous sedation, 240
fascial planes, 76–77 ketamine, 239
haematogenous spread, 77 midazolam, 239
intra-oral incision and drainage, 84–85 nitrous oxide, 239–240
principal management, 77 oral sedation, 238–239
Odontogenic keratocyst, 57 patient assessment, 237
Odontogenic (dental) pain personnel, 238
causes, 6 propofol, 240
differential diagnosis, 2 training, 238
features of, 16 corticosteroids, 240–241
Oral sedation, 238–239 delivery systems, 235–237
Orbital cellulitis, 83 local anaesthesia
Orofacial pain cardiac effects, 229
causes, 2, 3 central nervous system effects, 229
definition, 1–2 duration of action, 227
hydrodynamic theory, 2–3 facial nerve palsy, 230
prevalence, 2 management, 229
Orthodontically induced inflammatory root resorption mishaps, 229
(OIIRR), 272–275 noxious pain stimuli, 227
Orthodontic–endodontic interrelationship postinjection paraesthesia, 230
ankylosis potency, 227
late adolescence, 283–286 toxicity and management, 228–229
preadolescence, 285–287 trismus, 229
avulsion types and preparations, 228
delayed replantation adolescent, 281–283 mandibular infiltration and blocks
immediate replantation adult, 278–281 Gow-Gates technique, 233–234
clinical relevance, 271 inferior alveolar nerve block, 233
lateral luxation, 287–289 long buccal nerve block, 234
orthodontic tooth movement mental nerve block, 234
endodontically treated teeth, 272 Vazirani-Akinosis technique, 234
management of endodontic procedures, 275–276 maxillary infiltration and blocks
root resorption, 272–275 anterior middle superior alveolar, 232
vital teeth, 271–272 greater palatine nerve block, 232
orthognathic surgery, pulp vitality, 277–278 infraorbital block, 232–233
restorative procedures, 278 palatal anterior superior alveolar nerve block,
trauma, 276–277 230–232
Orthodontic tooth movement posterior superior alveolar nerve block, 232
endodontically treated teeth, 272 overview, 223–226
management of endodontic procedures, 275–276 supplemental injections, 234–235
root resorption, 272–275 topical anaesthesia, 230–231
vital teeth, 271–272 Palatal anterior superior alveolar (PASA) nerve block,
Orthognathic surgery, pulp vitality, 277–278 230–232
Orthograde root canal treatment, 50 Palatine space, 82
Orthopaedic appliance therapy, temporomandibular Paralleling technique, 167–169
disorder, 12 Parapharyngeal space, 82
Osseointegrated dental implant, 112 Percussion and palpation, 153–155
Osteoporosis, 297–298 Peri-apical cemento-osseous dysplasia, 58
Osteoradionecrosis (ORN), 297 Peri-apical condensing osteitis, 53
Peri-apical disease. See Apical periodontitis
Peri-apical endodontic lesions, 49, 50
P acute apical abscess, 53–54
Pain management case study, 59–62
analgesics, 226–227 chronic apical abscess, 54
anxiolytics, 236 chronic apical periodontitis with suppuration, 54
conscious sedation, 237 diagnosis, 52
Index 313

peri-apical condensing osteitis, 53 percussion sensitivity, 39

peri-apical fibrous scar tissue, 56 pulp tests, 39
peri-apical granuloma, 53 symptoms, 39
peri-apical pocket cyst, 54 Pulse granuloma, 31
radicular cyst, 54–57
residual cyst, 55–56
Peri-apical fibrous scar tissue, 56 R
Peri-apical granuloma, histopathological features of, 53 RaCe (reamers with alternate cutting edges) system,
Peri-apical pocket cyst, 52, 54 129–130
Periodontal pain, 6 Radial lands, 127
Persistent intra-radicular infections, 29–30 Radicular cysts, 54
Phoenix abscess, 44 categories, 51–52
Physical therapy, temporomandibular disorder, 12 cholesterol crystals, 55, 57
Piezoelectric effect, 133 definition, 49
Pioneer species, 28 pathogenesis, 55
Plain film radiography phases, 55
bisecting-angle technique, 168, 170 Radiolucent and radiopaque lesions, 175
bitewing radiography, 167–168 Radix entomolaris (RE), 195
paralleling technique, 167–169 Radix paramolaris (RP), 195
peri-apical radiography, 167 Reactionary dentine, 22
root canal treatment, 166 Referrals, for dental treatment, 71
X-ray photons, 166 Referred pain, 4
Planktonic organisms, 28 Removable partial dentures (RPDs), 111
Plaque, 28 Reparative dentine, 22
Posterior superior alveolar nerve (PSAN) block, 232 Residual cyst, 55–56
Pre-emptive analgesia, 224 Respiratory disease, 300
Pregnancy, 300–301 Retropharyngeal space, 82
Primary intra-radicular infections, 29 Reversible pulpitis, 3, 6, 37–39, 142
Primary occlusal trauma, 8, 9 Root amputation and root resection, 262–266
Professional ethics, in dentistry, 66–67 Root canal anatomy
ProFiles rotary nickel–titanium instrument, 126–127 clinical relevance, 179
Propofol, 240 C-shaped canal systems, 207–211
Prosthetic joints, 295–297 dens invaginatus, 199, 202–204
ProTaper Next (PTN) instruments, 132–133 incomplete root development, 196–199, 201–203
ProTaper Universal system, 121, 129 mandibular canine tooth, 192, 194
ProUltra Piezo, 133 mandibular first permanent molars, 182
ProUltra ultrasonic tips, 133 mandibular incisor teeth, 191–193
Pterygomandibular space, 82 mandibular molar teeth, 193, 195–196, 198–201
Pulpal and Peri-apical disease mandibular permanent canine tooth, 181
acute apical abscess, 43, 45 mandibular premolar teeth, 192–193, 195–198
acute apical periodontitis, 42–44 maxillary canine teeth, 184–186
chronic apical periodontitis, 43–46 maxillary central and lateral incisors, 181
classifications, 35 maxillary central incisor teeth, 182–183
clinical diagnostic system, 36 maxillary lateral incisor teeth, 184–185
clinically normal pulp, 36–37 maxillary molar teeth, 188–191
condensing osteitis, 45, 47 maxillary premolar teeth, 186–188
degenerative changes, 41, 42 maxillary second premolars, 181–182
irreversible pulpitis, 38, 40 MB2 canals
normal peri-radicular tissues, 42, 43 access cavity, 204–205
pulpless tooth, 41 identification, preparation and location,
pulp necrosis, 38–40 204, 206
radiographic diagnostic system, 36 mesio-buccal root, 203
reversible pulpitis, 37–39 overview, 204–205
Pulpal disease classification, 3 permanent maxillary first molar tooth, 205, 207
Pulp–dentine complex, 21–22 upper permanent maxillary molar teeth,
Pulpless tooth, 41 205, 208, 209
Pulp necrosis middle mesial canal, 206, 209
clinical radiographs, 39, 40 Vertucci classification, 180–181
occurrence, 38 vulcanised Indian rubber, 179
partial vs. complete necrosis, 39 Weine’s classification, 180–181
314 Index

Root canal system Sterile necrosis, 39

bacterial entry, 22–23 Sterilisation, 89
bacterial interactions, 26–27 Sublingual space, 80
microflora, spatial distribution of Submandibular space, 81
endodontic infection, 23–26 Submasseteric space, 82
Gram stain, 23 Submental space, 80
light microscopy, 23, 24 Supplemental injections, 234–235
morphological structure, 24–25 Surgical decompression, 52, 58–59, 61
scanning electron microscopy, 25, 26 Surgical scrub, 90
transmission electron microscopy, 24, 25 Systemic antibiotics, 142
nutrients, 27–28 amoxicillin, 144–145
treatment augmentin, 145
burs, 135–136 azithromycin, 145
healing signs, 105 cephalosporins, 145
periodontal assessment, 106, 107 ciprofloxacin, 145
restorability assessment, 105 clarithromycin, 145
success rates, 104 clindamycin, 145
Rotary nickel–titanium instrument doxycycline, 145
design features of, 119–121 erythromycin, 145
LightSpeed, 127–128 metronidazole, 145
ProFiles rotary nickel–titanium instrument, 126–127 tetracycline, 145
Rubber dam use and efficacy of, 144
anterior teeth technique, 218, 220 Systemic diseases
armamentarium bleeding disorders, 298–299
clamp forceps, 216 cerebrovascular accidents, 299–300
clamps, 215–216 clinical relevance, 293
floss, 216, 218 diabetes mellitus, 297
frames, 216–217 focal infection theory, 293–294
napkin, 215 infective endocarditis, 294–295
punch, 216 irradiated patients, 297
wedgets/OraSeal, 216 latex allergy, 301
bow first technique, 218–219 medical emergencies, 301–304
clamp first technique, 217–219 osteoporosis and BRONJ, 297–298
clinical relevance, 213 pregnancy, 300–301
latex allergy, 220 prosthetic joints, 295–297
overview, 213–215 respiratory disease, 300
split/slit dam technique, 220–221

T
S Temporomandibular disorder (TMD)
Satelec ultrasonic tips, 133 description, 4–5
Secondary colonisers, 28 examination process, 10–11
Secondary intra-radicular infections, 29–30 intercuspal position, 10
Secondary occlusal trauma, 8, 9 jaw movements, 11, 12
Self-adjusting file (SAF), 120–121 management strategies, 5
Septomixine Fort paste, 143, 144 muscle palpation, 11
Single-file reciprocation, 120 nocturnal bruxism, 10
Single-lens loupes, 122 orthopaedic appliance therapy, 12
Single-use instruments (SUI) and prion disease, 97–99 parafunctional habits, 11
Social hand hygiene, 90 patient education and self-care, 11
Sonic and ultrasonic instruments pharmacological management, 12
applications, 133 physical therapy, 12
frequency range, 133 physical trauma, 9–10
ProUltra or Satelec ultrasonic tips, 133 retruded contact position, 10
ProUltra Piezo, 133 risk factors, 5
Start-X tips, 133–134 stabilisation splint therapy, 5
Split/slit dam technique, 220–221 Temporomandibular joints (TMJs), 9–12
Split tooth, 261, 265 Tetracyclines, 144, 145
Start-X tips, 133–134 Thermal testing, 155–157
Steam sterilisation, 95 Tic douloureux. See Trigeminal neuralgia (TN)
Index
TMD. See Temporomandibular disorder (TMD)
Tooth
degenerative changes, 41, 42
pulp status, 36, 37
Topical anaesthesia, 230–231
Traumatic periodontitis, 8–9
Trigeminal neuralgia (TN)
carbamazepine treatment, 15
case study, 16–18
definition, 5, 14
diagrammatic representation, 14
examination process, 14–15
surgical management, 15
symptomatic causes, 5
Triple antibiotic paste, 146
True radicular cyst, 51–52
315
Tube shift technique, 173–175
Twisted Files (TF), 131
V
Vaccination, 88, 94
Vazirani-Akinosis technique, 234
Vertical root fracture (VRF), 261–264
Vertucci classification, 180–181
Vortex Blue (VB), 130–132
W
Warfarin therapy, 299
WaveOne rotary file system, 120, 132
Weine’s classification, 180–181