Intracanal Medicaments Treatment: Presently- single-visit treatment: vital pulp, necrotic pulp &

necrotic pulp with apical periodontal tissue involved (acutely infected or abscessed) Recommendation Vital pulp - a single visit therapy (endodontic access, chemomechanical preparation, canal obturation);
Necrotic pulp - two visit treatment: 1 visit: endodontic access, biochemo-mechanical preparation +
intracanal medical dressing + temporary filling; 2 visit: canal obturation Root canal infection mechanism:
carious pulp infected & inflamed infection pulp necrosis lost defense capability obligate
anaerobes colonize root canal spread to dentinal tubules & anatomic variables commonly in apical
third of RC periradicular lesion, not inflamed dental pulp is sterile!!! Goal: eradication of RC infection
in aseptic manner during RCT Treatment of infected root canals: antibiotics (when vascularized
periradicular tissues accessed) + chemical & mechanical procedures Endodontic treatment steps:
chemomechanical preparation, intracanal medication, root canal obturation. Chemomechanical
preparation: removal of bacteria from main root canal with mechanical action of instruments & canal
irrigation Irrigant propertiess: antibacterial Intracanal medication: against viable bacteria , destroy
remaining bacteria, limit growth of new ones, useful in apical periodontitis Properties of root canal
disinfentant: effective germicide & fungicide, non-irritating to periapical tissues, stable in solution,
prolonged antimicrobial action, remain active in presence of blood & pus, low surface tension, not
interfere with repair of periradicular tissues, not stain tooth, capable of inactivation of culture bacteria, not
induce immune response.
Classification of intracanal medicaments: Phenolic compounds Essential oils Aldehydes Halogens
Quaternary ammonium compounds Antibiotics and corticosteroids Calcium hydroxide
Phenols & their derivatives: Action: denaturation of bacterial protein and inactivation of bacterial
enzymes; toxic impact on apical periodontal tissues. Properties: loss of antibacterial action after 24 hours
due to contact with tissue fluids. Application: because phenol derivatives are vapored compounds, they
can be placed into pulp chamber to obtain bactericidal effect up to 14mm down in apical direction to
reduce harmful action on apical periodontal tissues, cresophene for 1 week in cotton pellet for necrotic
pulp Specimens: Camphorated Parachlorphenol, Camphorated Monochlorophenol -CPMC,
Camphocresol, Camphor mentol, Cresophene, Dikamfen, Endotine (parachlorphenol). Not
recommended: high toxicity, low efficacy
Essential oils Action: some antibacterial effects, severe irritant impact on periradicular tissues
Aldehydes: Action: bacterial protein denaturation effective canal desinfectant; cytotoxic; mutagenic;
carcinogenic Not recommended: high toxicity, low efficacy Specimens: Formaldehyde,
paraformaldehyde, glutaraldehyde
Halogens Chlorine in NaOCl & Iodine compounds
Iodine compounds: Action: iodine binds to bacterial proteins, has oxidative influence through oxygen
formation as the result iodine reaction with water and hydrogen iodide formation. Application: intracanal
dressing, iontophoresis. Specimens: iodine potassium iodide- IPI 2% & 4% with H2O, Lugols Solution.
Attention: possible allergy; good antibacterial effect but easily inactivated.
Quaternary ammonium compounds: Action: lower surface tension of solution, mildly effective
disinfectants
Antibiotic-Corticoids pastes:
Ledermix: is a glucocorticosteroid-antibiotic compound: 1% triamcinolone (a synthetic corticosteroid) +
3% demeclocycline (broad spectrum tetracycline). Optimal time of use: 4-6 weeks. Ledermix + Calcium
Hydroxide: 50-50 mixture does not alter pH mixture will act in similar manner to when calcium
hydroxide is used alone.
Septomixine forte: 2 antibiotics: neomycin & polymixin B sulphate +2 corticosteroids: dexamethasone +
tyrothricin. Action: inappropriate spectrum against commonly reported endodontic bacteria Not
recommended for treatment of infected root canals.
Pulpomisine (Dexadent): 2 antibiotics: framycetine B and Polimyxine B + Dexamethasone (corticoid).
Action: Antibacterial and anti-inflammatory action.
Metronidazole: nitroimidazole compound, broad spectrum of activity against protozoa & anaerobic
bacteria, strong antibacterial activity anaerobic cocci, as well as gram-negative & gram-positive bacilli, it
has bed used both systemically and topically in the treatment of periodontal disease; readily permeates
bacterial cell membrane; binds to DNA, disrupting its helical structure, very rapid cell death; excellent
activity against anaerobes isolated from odontogenic abscess but no activity against aerobes. Action:
antibacterial against anaerobic bacteria, damage of bacterial cells, change of pH in alkaline direction.
Easily inactivated. Application: 05% solution for canal irrigation during mechanical canal preparation;
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10% paste as intracanal medication for 2-3 days or in acute condition for 24 hours and change of the
dressing. Specimens: grinazole, metronidazole 10% paste.
Calcium Hydroxide: pH 12,5 - most endodontopathogens are unable to survive in highly alkaline
environment, blood, exudate & tissue fluids reduce pH & decrease its efficacy after 2-3 weeks Activity:
antimicrobial - release of hydroxyl ions in aqueous environment, facilities washing out swelling of
necrotic tissue. Antibacterial mechanism: Damage to the bacterial cytoplasmic membrane Protein
denaturation Damage to the DNA Combined with: CPMC, CHX, or IPI; increase antimicrobial
spectrum of Ca(OH)2 - additive or synergistic effects. Recommendation: Two visit treatment: First visit:
larger mechanical canal preparation- 3 files sizes over than in canal with vital pulp; it helps to remove the
most infected the root dentin; canal irrigation with antibacterial irrigants; intracanal dressing with calcium
hydroxide for 1 week (up to 3 weeks). Second visit: canal obturation, if asymptomatic tooth. Treatment:
Short-term: for 1-3 weeks intracanal dressing (temporary canal filling). Sealed temporary filling
(thickness of material layer 4-5 mm) Long-term: 3 to 12 months with the exchange of calcium hydroxide
paste in RC every 2-3 months periapical lesion; unmatured teeth (not finished root canal development)apexification; external/external resorption; re-treatment; Calcium Hydroxide points: 1. Calcium
Hydroxide Points. 2 Calcium Hydroxide Plus Points: additionally contain sodium chloride and tensides.
The tensides reduce the surface stress of liquids thereby allowing a more efficient penetration into the
dentinal tubules. Thus these points are capable of maintaining a high pH over a long period. Advantages:
minimal or no residue left, no smearing around access cavity during insertion, firm for easy insertion &
flexible enough to follow natural canal curvature, insertion of points down the apex is easy & ensures that
calcium hydroxide is released throughout the canal. 3x more Ca release than regular points, due to highly
water soluble components like tensides & sodium chloride, superior pH values & increased wettability of
canal surfaces, sustained alkaline pH for 7 days as against 3 days which was seen with calcium hydroxide
points.
Vitapex: contains: Iodoform 40,4% Calcium hydroxide 30,3% Silicone 22,4% Action: excellent
antibacterial; used in pulpectomies & infected root canal, when extruded into furcal or apical areas can
either diffuse away or be resorbed in part by macrophages, in 1-2 weeks, bone regeneration clinically &
histologically documented, used in infected root canals & pulpectomy treatment in primary teeth.
Advantages: no spatulation, radiopacity, excellent accessibility, no chemical & physical changes
Calplus - premixed Ca(OH)2 paste with iodoform with improved radiopacity & increased antimicrobial
effect
Chlorhexidine: 2% gel CHX, 2% solution CHX as canal irrigant, Points CHX.
Chlorhexidine gutta-percha points: gutta-percha matrix with 5% chlorhexidine diacetate for applying
CHX directly into canal, highly effective against bacteria, yeasts & fungi (in low concentrations), Use:
intra-canal medication & prevention of reinfection, radiopaque, easy to apply & remove.
Root canal Irrigation: Goals: Before using instruments in the root canal, it should be cleaned of the
mass of necrotic, gelatinous material comprised of pulp remnants, bacteria, and tissue fluids. Copious
irrigation with an irrigant eliminates most of this toxic material. Most instruments cut better in a wet
environment than in a dry one. Irrigation should also follow the use of each instrument, and extended
final irrigation should remove all loose debris from the canal. Removal of the smear layer just before
filling enhances the final result. Canal irrigation is performed with syringe and special designed needles.
Gelatinous mass of necrotic debris should be eliminated from the pulp canal before instrumentation.
Forcing this infected material through the apical foramen leads to acute apical periodontitis and/or an
acute apical abscess. Principles: Only irrigate under usage of rubber dam. Irrigate following the use of
each file. Canal preparation should allow for the irrigation tip to lie at two thirds of the radiographic
working length. The needle tip should not bind to the walls of the canal. Allow for adequate time in the
canal system for optimal action. Always check for leakage around the protected areas. The needle is loose
in the canal to allow backflow. Notched needle tip (inset) eliminates pressure. ProRinse irrigating needles
irrigate through a side vent. By rotating the needle in the canal, the spray reaches all regions of the canal.
This eliminates the water-cannon effect of open-end needles. Conventional irrigation: syringe + notched
needle Vibringe - sonic irrigation system - It enables activation of the irrigant solution acoustic
streaming. Activation of the irrigant improves of the canal debridement and distrupts the smear layer.
Canal irrigants: Sodium hypochlorite (NaOCl): irrigant of choice, lubricant, disinfectant, tissue
dissolvent, broad-spectrum antimicrobial activity; kill rapidly vegetative bacteria, spore-forming bacteria,
fungi, protozoa, viruses, bacterial spores different concentration: 0,5-5,25%. Full-strength NaOCl 5,25%
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dissolves both necrotic and vital pulp remnants. Half-strength NaOCl 2,6% dissolves only necrotic tissue.
Both solutions are effective antibacterial. Irrigation should also follow the use of each instrument, and
NaOCl should then be left in the canal to act as a lubricant for the next instrument. Combination: NaOCl
+ hydrogen peroxide produces a debriding, foaming action. NaOCl + CHX gluconate destroys half again
as many bacteria as NaOCl alone. Hydrogen peroxide (3% H2O2): Its alone also effectively bubbles out
debris and mildly disinfects the canal. Because of the potential for gaseous pressure from residual
hydrogen peroxide, it must always be neutralized by the sodium hypochlorite and not sealed in the canal.
10(15)-17% Ethylene Diamine Tetraacetic Acid (EDTA): EDTA buffered to a pH of 7,3. It removes only
calcified tissue, whereas sodium hypochlorite removes organic material, weak antibacterial 0,2%
Chlorhexidine gluconate: Its an effective endodontic antimicrobial agent. It possesses a broad-spectrum
antimicrobial action and a relative absence of toxicity. However, chlorhexidine gluconate is not known to
possess a tissue-dissolving property. Saline (09% NaCl). 40-50% Citric acid. MTAD (doxycycline, citric
acid, Polysorbate): Its a mixture of 3% doxycycline, 425% citric acid, and detergent (Tween-80). It has
combined chelating and antibacterial properties. It has low pH, 215. QMix: 2 in 1 solution contains a
mixture of a bisbiguanide antimicrobial agent, a polyaminocarboxylic acid calcium-chelating agent, and a
surfactant. It is effective as 17% EDTA in removal of smear layer and is highly effective as antimicrobial
agent. It kills planktonic bacteria within seconds, and it is capable of penetrating biofilms due to its
unique blend of antibacterial substance and their combined synergistic effect. Efficacy of different
endodontic procedures (% bacteria-free canals) Ultrasounds 70% bacteria free canals NaOCl 50%
bacteria free canals NaCl 0,9% - 20% bacteria free canals
Endodontic errors and mishaps: Procedural accidents: During Access preparation. During root canal
preparation. During obturation. During post space preparation. Endodontic mistakes: Access related:
treating the wrong tooth, missed canals, damage to existing restoration, access cavity perforations,
crown fracture Instrument related: ledge formation, cervical canal perforation, midroot perforations,
apical perforations, separated instruments & foreign objects, canal blockage Obturation related: over or
under-extended root canal fillings, nerve paresthesia, vertical root fractures Miscellaneous: post space
perforations, irrigant related mishaps, tissue emphysema, instrument aspiration & ingestion
A Access related:
1 Treating the wrong tooth: Causes: misdiagnosis, tooth adjacent to one scheduled for treatment was
inadvertently opened Recognition: Re-evaluation of the patient who continues to have symptoms after
treatment. When the rubber dam has been removed. Correction: Appropriate treatment of both teeth: the
one incorrectly opened and the one with the original pulpal problem. Prevention: Arrive at the correct
diagnosis. Marking the tooth to be treated. It is easily prevented- mark the tooth with a felt-tip pen.
2 Missed canals: Causes: Incorrect endodontic access.
3 Failure to remove all caries and unsupported structures: Causes: Leads to contamination and re
infection of the prepared root canal with saliva and bacteria conducting to endodontic failure. Correction:
According to the case, sometimes retreatment may be needed. Prevention: Careful remove of all caries
and unsupported tooth structure.
4 Damage to existing restoration: Causes: In preparing an access cavity through a porcelain or porcelainbounded crown, will sometimes chip. Correction: Minor porcelain chip can at time be repaired by
bounded composite resin to the crown; however, the longevity of such repairs is unpredictable.
Prevention: Placing a rubber dam clamp directly on the margin of porcelain crown is preventing damage
to the crown margin and/or fracture of porcelain. Solution: Remove the permanently cemented crown
before treatment with little or no damage to the crown. Porcelain crowns are the most susceptible to
chipping and fracture. When one is present, use a water-cooled, smooth diamond point and do not force
the stone. Do not place a rubber dam clamp on the gingiva of any porcelain or porcelain-faced crown.
5 Access cavity perforations: Searching for canal orifices perforations of crown occur: Peripherally
through the side of the crown. Floor of the chamber. Its an iatrogenic error. Recognition: Above the
periodontal attachment: the first sign of an accidental perforation will often be the presence of leakage:
either saliva into the cavity or irrigating solution into the mouth. Reason: Lack of knowledge of tooth
anatomy. Lack of attention. Misdirection of the instruments. Prognosis: Location of the perforation. Time
the perforation is open. Ability to seal the perforation. Correction: Perforations of the coronal walls above
the alveolar crest can generally be repaired intracoronally without for surgical intervention. Perforations
into the periodontal ligament should be done as soon as possible to minimize the injury to the tooths
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supporting tissues. The material used for the repair should provide a good seal and does not cause further
tissue damage. Materials used: Cavit. Amalgam. Calcium hydroxide paste. Super EBA. Glass ionomer.
Gutta-percha. Haemostatic agents. Operative error: The first of an access cavity perforation is blood in the
cavity or the patient complaining of a taste of NaOCl. This most frequently happens in the chamber floor
of molar preparations when one is searching for a third or fourth canal. When the crown is perforated into
the periodontal ligament, bleeding into the access cavity is often the first indication of an accidental
perforation. To confirm the perforation place a small file through the opening and take a radiograph. The
site of the perforation must be found, the floor of the preparation cleansed, the bleeding stopped, and
mineral trioxide aggregate (MTA) or amalgam applied to the perforation. Because MTA takes more than 3
hours to set, it should be covered with a fast-setting cement. The other canal orifices should be protected
by placing paper points or an instrument in the canals to prevent blockage. In the event MTA cannot be
immediately applied, it is best to stop the bleeding, place calcium hydroxide over the wound, place a
good temporary filling, and set an appointment with the patient, the sooner the better. The perforation area
will be dry at the next appointment; then MTA can be applied and treatment continued. Prevention:
Thorough examination of diagnostic preoperative radiographs. Close attention to the principles of access
cavity preparation: adequate size and correct location, permitting direct access to the root canals. A
thorough knowledge of tooth anatomy.
6 Crown fractures: Preparing an endodontic access cavity in a tooth, particularly in molar or premolar
with a large restoration, materially weakens the crown. Infrequently the crown fractures, either during
preparation or at a next appointment. One of the frequent causes is failure to relieve the occlusion. If the
fracture is chisel shaped and a cusp breaks off down to the periodontal ligament, the tooth can usually be
saved. If the fracture extends through the pulp chamber and down into the root, the cases is hopeless and
the tooth should be extracted. Causes: Preexisting infraction. Recognition: By direct observation.
Treatment: Tooth extraction. Prevention: Reduce the occlusion before working length is established.
Infracted crown should be supported with circumferential bands or temporary crowns.
B Instrumentation related mistakes: Under-instrumentation and over-instrumentation (cleaning and
shaping) can lead to many mishaps: Reduction of the working length. Zipping. Perforations. Injure of
periodontal tissues. Inflammation of periodontal tissues. The iatrogenic accidents such as zipping and
perforations begin with ledging during canal preparation
1 Ledge formation: Ledge is an internal transportation of the canal which prevents positioning of an
instrument to the apex in an otherwise patent canal. Causes: a. Using straight instruments in curved canal.
b. Packing debris in the apical portion of the canal. c. Rapid advancement in files sizes or skipping file
size. d. Inadequate access the operator does not have complete control over the direction of the tip of
the instrument and tip of the instrument cuts into the wall of the canal starting a ledge; newer instruments
with noncutting tips reduce this problem, because the rounded tip slips by the wall, not cut it. e. Curved
roots stiffer instruments start a ledge that can develop into a perforation; but small, flexible
instruments with noncutting tips negotiate the curves; if the instrument can no longer be inserted into the
canal to full working length, there is suspicion that a ledge has been formed; there also is a change
engaging the walls. STOP! Take a radiograph with the instrument in place. The major causes of ledge
formation include: Inadequate straight-line access into the canal. Inadequate irrigation or lubrication.
Excessive enlargement of a curved canal with files. Packing debris in the apical portion of the canal.
Recognition: When the instrument cannot reach to the full working length. There may be a loss of normal
tactile sensation at the tip of the instrument, loose feeling instead of binding in the canal. A radiograph of
the tooth with the instrument in place will provide additional information. Correction: Use of a small file,
N 10 or 15 with a small bend at the tip of the instrument. Penetrate the file carefully into the canal. Once
the tip of the file is apical to the ledge, its moved in and out of the canal utilizing ultra-short push-pull
movement with emphasis on staying apical to the defect.
2 Broken instrument: Separated instruments & foreign objects: instrument breakage is a common and
frustrating problem in endodontic treatment which occurs by improper or overuse of instruments. When
an instrument fracture occurs during root canal preparation procedures, the clinician has to evaluate the
treatment options with consideration for the pulp status, the root canal infection, the root canal anatomy,
the position and type of fractured instrument. In the root canal can break different objects, most often files
and reamers, lentulo spirals, Gates-Glidden drills and burs. It is caused by unrealistic strains placed upon
them, especially in severely curved canals and at higher rotary speeds. Symptoms: Canal blockage. Short
length of the instrument. Treatment: If a broken instrument can be grasped, it may be removed with
forceps. Use of a small tipped ultrasonic instrument to loosen and float out the broken piece. Attempt to
4

bypass it with a small file or reamer. Bypassing is made easier with a lubricant. If successful, the canal
preparation can be completed and the can filled, thus the instrument segment becomes part of the filling
material. If the fragment extends past the apex an efforts to remove it none surgically are unsuccessful,
the corrective treatment will probably include apical surgery.
3 Canal blockage: It can occur during canal enlargement. Files compact debris at the apex and working
length is shorter because the instruments are working against the packed mass at the apex. A radiograph
will confirm this suspicion. Correction is made by recapitulation starting with finer instruments and using
a chelating agent- EDTA. On the other hand, sterile dentin chips at the apex, formed during preparation,
help to block the foramen and prevent overcompaction, and stimulate cementum formation at the apex.
Injure of apical periodontal tissues: After the enlargement of the bent canal, a greater amount of dentin is
removed, and as result the previously correct working length becomes shorter and the instrument is too
long and can injure apical periodontal tissues.
Root perforations: These are usually caused by three errors: Creating a ledge and persisting until a
perforation develops. Wearing a hole in the lateral surface of the midroot by overinstrumentation (canal
stripping). Using too long instrument and perforating the apex.
Identification of perforation place: Paper points confirming strip perforation. The area of bleeding marked
on the paper point indicates the area where the strip occurred. Types of perforations:
4 Cervical canal perforations: Causes: During the process of locating and widening the canal orifice or
inappropriate use of gate-glidden burs. Recognition: Sudden appearance of blood in the cavity.
Magnification with loupes, endoscope, or microscope is useful. Correction: The bleeding is stopped and
MTA is applied to perforation. Cotton should be placed in the chamber and a good temporary filling is
placed to allow time for the MTA to set (> 3 hr). Preparation is continued at a subsequent appointment.
5 Midroot perforations: Commonly occur in the carved canal when a ledge has formed during
instrumentation, or along inside the curvature of root canal, as it straightened out. Recognition: Blood in
the canal indicates that a perforation has occurred. Management: MTA is the material of choice to close
the perforation.
6 Apical perforations: Causes: The file is not passing a curved canal. Not establishing accurate working
length. Overinstrumentation. Detection: Patient suddenly complains of pain during treatment. The canal
becomes flooded with haemorrhage. The tactile resistance of the confines space is lost. Paper point
inserted to the apex will confirm a suspected apical perforation (bleeding at the tip of paper point).
Radiographically with the instrument inside. Treatment: If the perforation create new foramen: One is
now dealing with two foramina: one natural and the other lateral. Obturation of both of these foramina
and of the main body of the canal requires the vertical compacting techniques with heat-softened guttapercha. If the perforation is caused by over instrumentation: corrective treatment include Re-establishing
tooth length short of the original length and then enlarging the canal with larger instruments, to that
length. The canal is then cautiously filled to that length. Steps: Apical perforation destroys the resistance
form, it means that the tip of the primary gutta-percha point must be blunted and fit to place so that it does
not extend beyond the orifice, even when compaction during obturation is used. Deposition tiny pack of
MTA or BIODENTINE at the apex and checking its placement radiographically. During the next
appointment after the MTA has set and plugs the apical foramen. This new plug (resistance form) allows
compaction of the gutta-percha. Later, MTA o BIODENTINE will encourage cementum formation at the
apex.
C Obturation-related mishaps: Over or underextended root canal fillings. Causes: Over extended filling:
Apical perforation. Under extended filling: Failure to fit the master gutta-percha point accurately. Poorly
prepared canal, particularly in the apical part of the canal. Recognition: When a post treatment radiograph
is examined. Correction: Underextended filling: treatment by, removal of the old filling followed by
proper preparation and obturation of the canal. Overextended filling: is more difficult. An attempt to
remove the over extension is sometimes successful if the entire point can be removed with one tug. If the
overextended filling cannot be removed through the canal, it will be necessary to remove the excess
surgically.
D Miscellaneous mishaps:
1 Irrigant-Related Mishaps: Forcibly injecting NaOCl or any other irriganting solution into the apical
tissue can be disastrous. The patient may immediately complain of severe pain. Swelling can be violent
and alarming. Symptoms: Immediately severe pain. Swelling is violent and alarming. Severity of
symptoms depends of concentration of irrigant. Paraesthesia, scarring, and muscle weakness.
Management: Antihistamines, ice packs, intramuscular steroids, even hospitalization and surgical
5

intervention may be needed. Prevention: Is the only solution. Using passive placement of a modified
needle. The needle must not be wedged in the canal.
2 Tissue Emphysema: Causes: A blast of air to dry a canal. Exhaust air from a high-speed drill directed
toward the tissue and not evacuated to the rear of the handpiece during apical surgery. Symptoms: Rapid
swelling. Erythema. Crepitus. If the air pocket breaks through into the neck region, there is a sudden
swelling of the neck, the voice sounds brassy, and the patient has difficulty breathing. If it breaks through
into the mediastinum, a crunching noise is heard on auscultation. Death can follow. Prevention: Use paper
points to dry the canal. Do not blow air directly down an open canal.
3 Instrument Aspiration and Ingestion: Prevention: Always use a rubber dam. Procedure: If instrument
aspiration or ingestion is apparent, the patient must be taken immediately to a medical emergency facility
for examination, and the dentist must accompany the patient. This examination should include
radiography of the thorax and abdomen. It is helpful if the dentist takes a sample file along so the
radiologist has a better idea of what to look for. The results may be disastrous. Be prepared for a session
in a court.
Radiographs Types: 1) Intraoral radiographs in periapical projection: Paralleling technique: film is
placed parallel to long axis of tooth; film is exposed to X-rays. Which are perpendicular to its surface,
requires special film holders. Bisecting angle technique: x-rays pass perpendicular to angular bisector by
long axis of tooth and x-ray film, no film holder is required. 2) Digital radiography: Advantages:
Reduced exposure to radiation. Increased speed of obtaining image. Possibility for digital enhancement.
Storage as digital data in computers. Ease of transmissibility. Elimination of manual processing steps.
Digital image enhancement. Inversion. Contrast. Pseudocolor. Flash light. Magnification. Measurement of
angle of root curvature. Linear measurement. Diagnostic Radiographs: ideally, paralleling angle
technique, high quality, no forshortening or elongation , they help in proper diagnosis of case, &
determining prognosis by comparison with post-operative & follow up radiographs. Working
radiographs: with bisecting angle technique, used for determining position of instruments, taken without
removing rubber dam Intraoral images: Examination of dentition and associated structure. Number,
sequence, appearance, root structure. Crown-caries, defective enamel. Interproximal areas and
restorations. Bone rarefication. Describing lesion: Size: Measure lesion with a ruler; if you must
estimate, use surrounding structure as guide. Measure in two dimensions, width and high in mm. Shape:
Regular shape like round, triangular, rhomboid. Irregular shape. Location: Localized or generalized.
Unilateral or bilateral. Where is lesion in relation to other structures & anatomic landmarks. In terms:
Mesial, distal. Inferior, superior. Posterior, anterior. Density: Is lesion radiopaque, radiolucent or mixed
density? Remember that opacity is relative to adjacent structure. If lesion is of mixed density, describe
appearance. Borders: Well or poorly demarcated. Punched out (no bone reaction). Corticated (thin opaque
border). Sclerotic (wide, uneven opaque border). Hyperostetic (increased density of trabecylation).
Internal architecture: Is lesion uniform? Internal structure such as septae or loculations (numerous small
compartments). Effect on adjacent structures: Is lesion causing: Resorption. Displacement. Scalloping.
Effacement. Destruction. Space occupying lesions displace other structure. Remodeling. Expansion.
Thinning/thickening.
Morphology and function of periradicular tissues Periodontal tissues: PDL, cementum, alveolar
process
Periodontal Ligament (PDL): ~ width 0,2mm; dense fibrous connective tissue that occupies periodontal
space between root of tooth & alveolus, derived from dental follicle; above alveolar crest - continuous
with connective tissues of gingiva; apical foramen it is continuous with dental pulp. Composition:
Collagenous fibers: running from the cementum to the alveolus. Blood vessels: forming loops and
amortizes a pressure onto the tooth. Nerves: the sensory coming from the nerve V and are associated with
mechanoreception; the autonomic nerves are associated with the supply of the periodontal blood vessels.
Cells: fibroblasts, cementoblasts and cementoclasts; osteoblast and osteoclast; epithelial cells- the rest of
Malassez and defense cells- macrophages. Mast cells, eosinophils. Sharperys fibers of PDL:
Dentoalveolar crest fibers. Horizontal fibers. Oblique fibers. Apical fibers. Gingival fibers. Interseptal
fibers.
Functions: supports tooth in alveolar socket & provides physiological mobility of tooth, amortizes action
of mastication forces, contributes in permanent reconstruction of cementum, mediates in receiving of
sensory agents.
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Cementum: thin layer of calcified tissue covering dentin of root, derived from inner layer of dental
follicle, no blood vessels & nerves, between 10&70 years of life cementum layer increases 3-fold.
Composition: Inorganic material: 65% calcium phosphate (hydroxyapatite), Organic material: 23%
(collagen, proteins), Water: 12% Classification: Cellular: apical region, cementoblasts, cementoclasts,
fibers. Acellular: cervical region, fibers. Functions: give attachment to collagen fibers of PDL, help in
maintenance of root integrity, involve in tooth repair & regeneration.
Alveolar process: Classification: Compact: cortical and cancellous. or Spongy. Composition: Inorganic
material: 65% carbonated hydroxyapatite. Organic material: 25% proteins, collagen, cells (osteoblast,
osteocytes, osteoclasts). Water: 15%. In dental socket, tooth surrounded by thin layer of compact bone in
which are numerous openings - alveolar sieve. Through alveolar sieve, at acute inflammation of apical
periodontal tissues, exudate penetrates & reaches spongy bone. Bone is covered by periosteum, well
innervated fibrous tissue. Normally invisible in radiograph, but in pathology gains osteogenic property
periosteal reaction. Function: continuous remodeling & adaptation to changing functional situations due
to resorption & proliferation (stratification): Norm: balanced processes. Pathology: osteoclasts activity
increased osteoporosis or osteolysis of bone. At enhanced osteoblasts activity/inhibition of
physiological process of destruction osteosclerosis occurs
Diseases of apical periodontal tissues - pathological processes, which involve PDL & bone of alveolar
process. Healthy apical periodontal tissues barrier. Inflamed periodontal tissues systemic diseases
Periradicular lesions: consequence of pathologic changes in dental pulp & root canal system, that harbor
numerous irritants. Irritants can initiate formation & progression of periradicular lesions. If transient
irritants - inflammatory process is short-lived & self-limiting. If excessive amount of irritants or persistent
exposure - nonspecific & specific immunologic reactions can cause destruction of periradicular tissues.
Causative factors of periradicular lesions: infective: mostly bacterial. Non infective.
Periradicular lesions of pulpal origin: Irritants: Irritation of pulpal or periradicular tissues
inflammation. Classification: Living irritants: various microorganisms and viruses. Non-living irritants:
mechanical (trauma), thermal, and chemical irritants. Mild to moderate injuries of short duration
reversible tissue damage recovery Persistent and/or severe injuries irreversible changes in pulp
periradicular lesions Living irritants: bacteria, bacterial toxins, bacterial fragments, viruses; they egress
apically from root canal system into periradicular tissues inflammation & tissue alteration by
immunological reaction. Gangrenous pulp - anaerobic bacteria (65-90%): Bacteroides intermedius,
denticola, gingivalis, endodontalis, buccae. Eubacterium, Actinomyces. Non-living irritants: Mechanical
irritants: Occlusal trauma: tooth has vital pulp & reveals significant mobility Traumatic occlusion:
premature contact with opposing tooth widened periodontal spaces; alveolar bone loss due to
periodontal disease. Iatrogenic trauma: gutta-percha point overfilled pain & inflammation Spreading
ways of periradicular tissues infection: from main root canal, from gingival pocket, through lateral canal
or perforation, via blood.
Acute Apical Periodontitis: Symptoms: Symptoms of pulpitis or necrosis + pain on bite, Clinical
examination: Pain on percussion, may or may not respond to pulp vitality testing X-ray: Thickening of
periodontal ligament space, no periradicular radiolucency. Treatment: RCT.
Chronic Apical Periodontitis: Symptoms: Asymptomatic or slight discomfort. Clinical examination:
Little or pain on percussion, no response to pulp vitality testing X-ray: Interruption of lamina dura or
apical radiolucency Treatment: RCT.
Acute Apical Abscess (closed): Symptoms: Severe discomfort, swelling, fever, some degree of mobility,
tenderness of cervical & submandibular LNs Clinical examination: Swelling in mucobuccal fold & facial
tissues adjacent to tooth, pain on bite, percussion & palpation, no response to pulp vitality testing, X-ray:
Radiolucent lesion (localization). Anything from widened PDL to periradicular radiolucency Treatment:
RCT, drainage (antibiotics).
Suppurative Apical Periodontitis (open): Symptoms: Asymptomatic (drain), swelling Clinical
examination: Fistula, swelling, no response to pulp vitality testing, no pain on bite on percussion X-ray:
Radiolucent lesion (localization with gutta-percha). Treatment: RCT.
Classification of apical periodontal tissues diseases, acc. to Polish Textbook: Acute Chronic,
Serous or Purulent | Chronic Exacerbation Acute | Serous Purulent | Chronic Fibrous or
Granulous | Fibrous Granulous | Granulous Cystitis or Purulent | Cystitis Purulent
7

Ingles classification of periradicular lesions: Symptomatic (acute) Apical Periodontitis SAP.

Asymptomatic (chronic) Apical Periodontitis AAP. Apical Abscess.AA
Symptomatic Apical Periodontitis (SAP): localized inflammation of PDL in apical region. Causes:
irritant diffusing from inflamed or necrotic pulp, egress of irritants: bacteria, bacterial toxins, disinfecting
medications, debris pushed into periradicular tissues, physical irritation of periapical tissues, impact
trauma. Pain: intensity comparable to advanced acute pulpitis, but lasts longer, constant, gnawing,
pounding, throbbing pain, tooth elevated in its socket. Examination: No pulp reaction to stimuli (necrotic
pulp), pain on percussion, painful to touch, supraocclusion Radiograph: widened PDL, no radiolucency
Treatment: Give long-acting block anesthesia. Relieve occlusion in opposite arch if possible. Opening of
tooth gives release; even small amount of fluid gives immediate relief.Endodontic access & chemomechanical preparation of canal. Intracanal dressing with antibiotic & corticoid. Place small dry cotton
pellet in chamber & thin temporary filling; re-check occlusion. If pain unbearable at night, instruct patient
how to remove temporary filling, watching in mirror & using safety pin bent at right angle; relieve
pressure. Give antibiotics & NSAIDs: ibuprofen. RCT should not be undertaken until all acute symptoms
subsided. Asymptomatic Apical Periodontitis (AAP): Granuloma& Cyst: may be preceded by SAP or
apical abscess, frequently asymptomatic. Causes: inadequate RCT, gradually release of noxious agents
with low-grade pathogenicity or in low concentration by necrotic pulp Symptoms: non-significant pain,
little or no pain on percussion, if AAP perforates cortical plate of bone, palpation of superimposed tissues
may cause discomfort; negative pulp response for electrical or thermal stimuli (necrotic pulp)
Radiograph: periradicular radiolucent changes ranging from thickening of PDL & resorption of lamina
dura to destruction of apical bone resulting in well-demarcated radiolucency Local effects: Bone &
periodontal ligament replaced by inflammatory tissue, destructive & healing processes occur
simultaneously in asymptomatic apical lesions. Extent of lesion depends on potency of the irritants within
RC system & activity level of defensive factors in this region. Balance maintained asymptomatic. If
causative factors overcome defensive elements symptomatic periradicular lesion superimposed on
asymptomatic one - phoenix abscess. Systemic Effects: it is not a focus of systemic diseases via immune
complexes, but SAP systemic immunologic reactions & some systemic disease. Condensing osteitis Chronic Facial Sclerosing Osteomyelitis: radiographic variation of AAP Inflammation stimulates
osteoclastic & osteoblastic activities; predominant osteoblastic (formative) activity; unknown reason,
possibly special balance between host tissues & RC irritants; localized overproduction of apical bone;
low-grade inflammation of periradicular tissues. Location - observed around apices of mandibular
posterior teeth with pulp necrosis or chronic pulpitis. Symptoms: various - associated with variety of
pulpal & periradicular lesions, may be asymptomatic or sensitive to stimuli, may or may not respond to
electrical & thermal stimuli. Radiograph: well-circumscribed radiopaque area around 1 or all of roots;
often indicative of chronic pulpitis; radiopaque changes return to normal after successful RCT, additional
bony trabeculae formed, marrow spaces reduced to minimum. PDL space visible,despite increased
radiopacity of nearby bone. Periradicular granuloma: mass of chronically inflamed granulation tissue of
apex of non-vital tooth, may arise after acute condition like periapical abscess becomes quiet or de novo;
lesion is not static; may transform into periapical cyst or undergo acute exacerbation. Pain: painless, or
relatively painless Examination: negative pulp vitality test (pulp necrosis by trauma or caries).with
transillumination tooth appears darker than its neighbour, percussion is of little value Radiograph: welldefined periapical lesion, variable size, external resorption usually not destroyed root end, loss of lamina
dura. Histology: Predominantly of granulation inflammatory tissue with many small capillaries,
fibroblasts, numerous connective tissue fibers, inflammatory infiltrate, & usually connective tissue
capsule. Capsule is replacing periodontal ligament, apical bone, & sometimes root cementum & dentin;
infiltrated by plasma cells, lymphocytes, mononuclear phagocytes &occasional neutrophils. Lesion shows
inflamed granulation tissue containing a dense lymphocytic infiltrate mixed with PMNLs
(polymorphonuclear leukocyter), plasma cells & macrophages. Epithelial rests of Malassez may be seen
within granulation tissues. Cholesterol clefts may be seen along with associated multinucleated giant
cells. Areas of extravasation of RBCs and hemosiderin pigmentation are also common. Conditions: low
virulence bacteria in canal, well controlled by layers of periapical inflammatory lesion, can spring into
violence if virulent bacteria take over & phoenix abscess develops, or it may develop into an apical cyst.
Treatment: RCT, surgery not necessary, curettage to speed up healing Periradicular cysts: inflammatory
process stimulates epithelial resting cells of Malassez, cystic cavity filled with cholesterol & fluid
develops around apex, may grow by expansion from fluid, may become infected Examination:
radiograph, may be unnoticed until starts moving teeth (pathognomonic) or becomes infected & abscess
8

develops; does not respond to thermal or electric stimulation; may be slightly discolored in
transillumination; negative percussion, but if grown to size where it perforates cortical plate may be
palpated. Radiograph: round or ovoid radiolucency with sclerotic border; if infection supervenes, margin
becomes indistinct like in granuloma. Histology: Central cavity lined by incomplete & ulcerated stratified
squamous epithelium; lumen contains pale eosinophilic fluid & occasionally some cellular debris.
Connective tissue capsule surrounding epithelium contains cellular & extracellular elements of
periradicular granuloma. Inflammatory cells are also present within epithelial lining of this lesion.
Presence of dental epithelium-lined cavity filled with fluid or semisolid material. Treatment: RCT &
periapical surgery Differential diagnosis: Periapical granuloma. Periapical cemento-osseous displasia
(early lesion) Types of periapical (radicular) cysts: Apical, Lateral, residual radicular cyst Classification
of cysts acc. to WHO: 1. Odontogenic: A. Developmental Odontogenic keratocyst (primodial cyst)
Dentigerous (follicular) cyst Eruption cyst Lateral periodontal cyst Gingival cyst of infants (Epstein
pearls) Gingival cyst of adults Glandular odontogenic cyst; sialo-odontogenic cyst Orthokeratinized
odontogenic cyst B. Inflammatory Radicular (periapical) cyst: apical, lateral, residual Paradental cyst 2.
Non-odontogenic: Nasopalatine (incisive canal) duct cyst Nasolabial (nasoalveolar) cyst Apical
Abscesses: localized collection of pus in cavity formed by disintegration of tissues: Symptomatic &
Asymptomatic Symptomatic Apical Abscess (SAA): sudden egress of bacterial irritants, accompanied by
exudate formation within lesion. Cause: rapid influx of microorganism, or their products, from root canal
system. Pain: in pain, fever, increased WBCs, not as painful as SAP, pressure from accumulation of
exudate within confining tissue severe pain Swelling: Gentle palpation reveals early swelling. Spread
of lesion toward surface, erosion of cortical bone & extension of abscess through periosteum & into soft
tissues is usually accompanied by swelling & some relief. Swelling localized, but may become diffuse &
spread widely (cellulitis); depends on virulence & incubation period of involved bacteria, & hosts
resistance. Location of swelling determined by relation of apex of involved tooth to adjacent muscle
attachments. Tooth examination: No pulp reaction to stimuli (necrotic pulp). Percussion: varying degrees
of sensitivity to percussion and palpation. Redness of mucosa & later pointing of abscess. Clinical:
Initial stage: tenderness of affected tooth. Later: pain becomes intense with extreme sensitivity to
percussion. Extrusion of tooth from its socket. Systemic findings: fever, chills Radiograph: No gross
radiographic changes may be noted at first, but later in the process, rapid bone loss shows up as
radiolucency. Therefore, the x-ray picture varies from no obvious signs of pathosis through a thickening
of the periodontal ligament space to a frank periradicular lesion. Spread of inflammatory response into the
cancellous bone results in apical bone resorption; since inflammation is not confined to the periodontal
ligament but has spread to the bone, the patient now has an acute osteitis. Course: Immunologic or noimmunologic inflammatory responses contribute to the breakdown of the alveolar bone and cause
disruption of the blood supply, which, turn, produces more soft and hard tissue necrosis. The suppuration
process finds lines of least resistance and eventually perforates the cortical plate; when it reaches the soft
tissue, the pressure on the periosteum is relieved, usually with a reduction of symptoms. Once this
drainage through bone and mucosa is obtained, supportive apical periodontitis or an asymptomatic
periradicular abscess is established. Treatment: Early stages drain canal with slight opening with
reamer, if it doesnt work antibiotic therapy; frequent hot rinses, once abscess becomes fluctuant, incision
& drainage is employed to drain abscess, once whole area quiets down, RCT may be completed.
Asymptomatic Apical Abscess (AAA): Features: abscess from low virulence; long-standing fistulous
draining abscess continuously or intermittently by draining sinus tract, drained into oral cavity as stoma
on oral mucosa but occasionally extraorally as fistula on skin of face, cutaneous fistula; exudate can also
drain through gingival sulcus of involved tooth, mimicking a periodontal lesion with pocket,
asymptomatic patient often tolerate condition for months or even years, may also develop acute
exacerbation, the so-called phoenix abscess Examination: If draining fistula is present, process is quite
apparent. One should probe fistulous track with a gutta-percha point, using a radiograph as a guide. Often
what is thought to be the obvious tooth may not actually be the culprit. Pulp test reveal the necrotic pulp.
Radiographs: diffuse radiolucency, sometimes of enormous size. Treatment: RCT. Often fistula stops
draining after 1st visit, abscess area heal to new bone. Surgery root apex is chewed-up by
inflammatory resorption. Open apex- difficult to obturate; so, surgery & root-end filling. Removing all
chronic inflammatory cells from region - speed up healing. Apical Scar (Fibrous Scar): Variation in
healing process. Norm - surgical site fills with blood clot- organizes, mineralizes & remodels like
surrounding bone. Occasionally it fails, patient asymptomatic, no treatment.
9

Resorption of dental root - physiologic or pathologic factors leading to loss of hard dental tissues &
bone tissue.
Classification of root resorption Based on nature: Pathologic: seen in both, deciduous and permanent
dentition. Physiologic: seen in deciduous dentition. Based on anatomical occurrence of region: Internal.
External: Apical, Lateral, Cervical Based on causes: Local. Inflammation: External & Internal Pressure:
Orthodontic, Tooth movement, Tumor, Cyst Replacement or dentoalveolar ankyloses. Systemic.
Idiopathic.
Resorption process: In physiologic condition the mineralized dental tissue of the permanent teeth are not
normally resorbed. They are protected in the root canal by the predentin and the odontoblasts and on the
root surface by the precementum and the cementoblasts. In pathologic condition, if the predentin or the
precementum becomes mineralized or in case of precementum is mechanically damaged or scraped offthe osteoclast- like cells will colonize the mineralized or denuded surface and resorption will develop.
However, resorbing cells require continuous stimulation during phagocytosis, and stimulation by a
denuded dentin or cement surface is not sufficient to support the resorptive process for long. Therefore, a
phagocytic colonization of denuded areas of the root will be transient without additional stimulation of
the cells, and repair with cement- like tissue will occur both in the root canal and on the root surface. This
type of resorption is named a transient root resorption. Phases: 1. An injury (mechanical or chemical) to
the protective tissues covering the root (precementum or predentin) which initiates the resorption process.
2. A continued stimulation of the resorptive process by either infection or pressure.
External resorption: Pathologic loss of tooth structure resulting in a defect in the root and adjacent bone,
it is initiated in the periodontium. Etiology: Chronic inflammation of periradicular tissues. Necrotic pulp.
Mechanical injury- trauma. Tooth replantation. Orthodontic treatment. Impacted teeth. Internal bleaching.
Idiopathic- unknown cause.
Histologically: Scalloped border lined with osteoclasts.
Radiographically: Defect is rough. Asymmetric. Moth-eaten appearance.
Types according to causative agents:
Inflammatory: periradicular lesions always result in resorption of both bone and tooth, and after
replantation of the tooth. Root resorption supported by infection can occur: In the root canal internal
resorption. On the tooth surface external resorption and cervical resorption. Depending on whether
the bacterial stimuli come from the gingival sulcus or from the root canal.
External inflammatory resorption: A commonly occurring complication following displacement of the
teeth (after luxation and avulsion, injuries leading to a disruption of the pulpal blood vessels at the apical
foramina and to ischemic pulp necrosis). It can be initiated by mechanical trauma resulting in the removal
of cementoblasts, precementum, and sometimes cementum in areas of the root surface. The resorptive
process is then maintained by bacterial products from the infected root canal which provide the necessary
continuous stimulation of the resorbing cells. If the resorptive process progress, the tooth may be destroy
completely in a few months Due to tooth traumatic injure: mechanical stimulation of osteoclasts to
support a progressive resorption is seen, for example, in root-fractured teeth there sharp edges of the root
fragments are selectively resorbed. Only when fragments are well rounded and cause no further tissue
irritation will the resorption stop Pulpal infection root resorption: following infection, the presence of
bacteria in the dentinal tubules is the stimulating factor of the osteoclastic inflammatory response that
takes place in the dentin bone. Treatment: Ca(OH)2 is placed in the canal for 6-12 months or MTA.
Diagnosis: radiographically, there is a radiolucency on external root surface and adjacent bone or on
internal root canal walls.
External Cervical Resorption: Periodontal infection root resorption: external root resorption that occurs
after injury of the precementum below the epithelial attachment, and contamination by bacteria from the
sulcus. Consequently, resorbing cells penetrate into the damaged areas of the root, causing resorption
inside the root and in the adjacent alveolar bone. Initially, this does not penetrate into the root canal but
may do so at later stages. Radiographically: a single radiolucency in the dentin at crestal bone level.
Treatment: surgically expose the resorptive area and remove the granulation tissue, followed by
restoration with resin composite or amalgam. The root canal treatment in necessary only if canal is
perforated.
Post traumatic injury: following severe traumas (avulsion or intrusion), healing with cementum may not
be possible. Therefore, bone comes into contact with the dentin without an intermediate protective layer
(cementum) and the dentin becomes part of the normal bone remodeling process. Causes: Trauma.
Idiopathic.
10

Clinically: The ankylosed tooth lacks physiologic mobility, has metallic percussion sound, and may be in
infraocclusion.
Radiographically: There is no PDL. No radiolucent areas. The root becomes replaced by bone
Treatment: there is not. Treatment of idiopathic resorption: Use the same method as for inflammatory
resorption. Prognosis depends on extent and location, sometimes unpredictable. Prevention: The goal with
severe traumas such as avulsions is to minimize damage to PDL cells by either immediately replanting the
tooth into the socket, or placing the tooth into a suitable storage media until the tooth can be replanted.
Cervical tooth resorption: damage of epithelial attachment, it begins on root surface and may extend and
form the chamber and canal perforations.
Pressure: in the permanent teeth the pressure resorption may be seen during: Teeth eruption, especially of
maxillary canines and mandibular third molars. The presence of certain tumors impinging on the roots of
the teeth. Orthodontic movement of the teeth, usually in the form of apical resorption and a shortening of
the roots. Pressure resorption may be quite destructive if diagnosed late on. However, the resorptive
process will be arrested when the stimulation of the resorbing cells stops. Orthodontic teeth movement:
apical root resorption resulting from pressure applied during orthodontic movement. Teeth are
asymptomatic and vital. Most root resorption is minimal and ceases after the appliances are removed.
Treatment: discontinue orthodontic treatment. Endodontic treatment is not necessary. Impacted
tooth/tumor pressure: pressure applied from erupting permanent teeth (mainly canines and mandibular 3rd
molars) or tumors causes resorption of adjacent roots. The teeth affected are most often vital and
asymptomatic. Radiographically: resorptive area is next to the impacted tooth or tumor. Treatment:
surgery.
Replacement resorption/ ankylosis: pathologic loss of tooth structure with the ingrowth of bone into the
defect fusion of bone to cementum or dentin Causes: trauma, idiopathic Following severe traumas
(avulsion or intrusion), healing with cementum may not be possible.Therefore, bone comes into contact
with the dentin without an intermediate protective layer (cementum) and the dentin becomes part of the
normal bone remodeling process. Clinically, the ankylosed tooth lacks physiologic mobility, has metallic
percussion sound, and may be in infraocclusion. Radiographically, there is no PDL, and no radiolucent
areas, and the root becomes replaced by bone. No treatment
Surface/transient: Physiologic process causing small superficial defects in the cement and dentin that
undergo repair by deposition of new cement. Pathologic process is initiated by a denudated area of the
root surface and supported by mechanical irritation, increased pressure in the tissue or infection of the
root canal and tubules of the crown and root dentin. Usually too small to be detected on a radiograph and
without clinical importance.
Internal resorption: associated with a long-standing chronic inflammation in pulp,occurs sometimes
during chronic pulpitis or due to injure as a result of damage of the odontoblasts layer. The predentin is
mineralized and becomes sensitivity on the action of the osteoblast-like cells. The loss of dentin (dentin
decay is called as the resorption lacuna) in more or less regular shape is occurred, which is filled by
granular tissue. The dental pulp is changed into the granulation tissue with presence of giant cells.
Predisposing factors: Unknown, the process appears to be associated with a pulpal inflammation.
Features: Preceded by disappearance of the odontoblastic layer of cells, followed by an invasion of
macrophage- like dentin-resorbing cells. Internal resorption is usually asymptomatic and is discovered on
routine radiographs. The resorptive process may progress slowly, rapidly or intermittently with periods of
activity and inactivity. Mechanism: Pulp stimulated by irritants Inflammation. Undifferentiated cells of
pulp become osteoclasts and macrophages. Dentinal resorption.
Types: Surface/transient: is associated with a long-standing chronic inflammation in the pulp. It occurs if
the odontoblasts in an area of the root canal are destroyed so that the predentin becomes mineralized. No
detectable radiographically.
Inflammatory: (internal granuloma, internal progressive resorption, pink tooth, pink spot). The
enlargement of the dental cavity size in oval shape lacuna. Often in pulp chamber is necrotic pulp,
however, the early performed root canal treatment can inhibit the resorption progression. In case of the
progressive internal resorption, the resorptive activity is sustained by infection of necrotic tissue coronally
in the root canal. Etiology: chronic pulpitis, disorders of blood circulation followed by a trauma, vital
pulpotomy with calcium hydroxide. Unknown reason: idiopathic resorption. Histologically: the dental
pulp is changed into granular tissue with presence of giant cells, which resorb dentin. Location: Type
A&B- non perforated, Type C- perforated Type A: resorption in dental crown. The only clinical symptom
11

can be a pink spot, which is the result of shining the richly vascularization granular tissue through the thin
enamel without supporting dentin. On the radiograph the ampulla enlargement of chamber is observed.
Type B: resorption in root canal wall. Type C: perforation of root dentin by granulation tissue. Diagnosis:
occasionally radiograph taken. When the resorption decay is spread from labial or lingual root canal
surface it is difficult to distinguish the internal resorption from external one based on radiograph. The
affected teeth for a long time normally react on thermical and mechanical agents, asymptomatic course; in
case of perforating resorption dental pulp is infected and necrotic. Management: Non-perforated (A,B): 1.
Pulp removal and canal preparation: Coronal access modified or enlarged to allow greater penetration of
the NaOCl. Copious irrigation with (NaOCl). Ultrasonic instrumentation coupled with high volume
flushing. Interim CaOH if difficult to remove at 1st visit. 2. Canal obturation: Small or moderate defect:
use vertical compaction with warm gutta-percha, thermoplasticized gutta-percha, or pressure syringe
injection. Large defect: use same techniques with more pressure required. Near perforation: use same
techniques with avoid excessive pressure, use CaOH-based root canal scaler. Perforated (C): Determined
of perforation: Clinically: Continue hemorrhage after all the pulp has been removed. Blood in paper pints
at side. Radiographically: Lateral radicular lesion at resorptive defect. Nonsurgical repair: defect is far
apical to epithelial attachment. Technique: Calcium hydroxide paste into the canal until a hard-tissue
barrier is formed, then obturation with MTA. Surgical repair: making a flap, area is curetted, cleaned and
obturated with an alloy, composite resin, glass ionomer restoration or MTA. Perforating: a
communication between the root canal and the periodontal ligament due to a perforation of the root by
progressive internal resorption. It can be misdiagnosed as cervical external resorption when the
perforating internal resorption is located in pulpal chamber. Replacement: irregular widening of dental
cavity is observed. Histologically: dental pulp metaplasia into bone tissue is found.
Resorption:
INTERNAL
EXTERNAL
Margins
Smooth and well-defined
Rough & mouth-eaten
Symmetric
Symmetrical
Asymmetrical
Canal anatomy
Altered + size
Unaltered
The relationship of the canal to the The relationship of the defect to the
X-ray projection: different
defect will remain the same,
canal will shift as the horizontal angle
horizontal beam angles
regardless of the angle
of the beam is altered
Identification and differentiation:
Internal: regular, round, outline of canal is distorted, centered
External: irregular, moth eaten outline of canal is normal, off center
External resorption
Type
Differential diagnosis
Treatment
Prognosis
Transient Small excavation is separated from No treatment is necessary Excellent
Surface
bone by periodontal ligament
Pulp is responsive
Pressure
Pulp is responsive
Correction and
Excellent when etiologic
Resorption stops when pressure is discontinuance or
pressure is discontinued
discontinued
pressure
No RCT
Type
Differential diagnosis
Replacement There is no periodontal space at the
- Ankylosis resorptive site
Margins of the defect are irregular
Canal maintains regular form
Pulp responsiveness may vary
depending on etiological injury
Inflammator There is a radiolucency next to the
y
resorption
Margin of the resorption varies from
smooth to ragged but is not
comparable to the irregular defect of

Treatment
Prognosis
No predictable direction Poor
of therapy
RCT usually neccesary
owing to etiologic injury
RCT

Excellent

12

ankylosis
Multiple angulation x-ray films will
shift lesion when superimposed over
pulp.
Canal maintains original form, tissue
may be fluctuant or a fistula may be
present owing to nonresponsive pulp.
Internal resorption
Type
Differential diagnosis
Intracanal
Ampullar enlargement of pulp
resorption with chamber or canal
no external
Resorptive pulp during active
perforation
phase
Intracanal
Ampullar enlargement extends to
resorption with periodontal tissues
infraosseus
There is a radiolucency at site of
perforation
perforation
Pulp is nonresorptive
Tissue may demonstrate
fluctulance or fistula

Treatment
RCT

Prognosis
Excellent

Root canal debridement Far to excellent

Ca(OH)2 paste inserted depending on the quality
into canal until tissues
of obturation of the canal
repair occurs
space and resorptive
MTA inserted at the site defect
of resorption
Well condensed filling of
the canal and resorptive
defect
Type
Differential diagnosis
Treatment
Prognosis
Intracanal
Ampullar enlargement extends to RCT- root canal treatment Depends on location
resorption with or near the oral environment
& surgical repair
surgical access and
supraosseus
Periodontal breakdown extends
periodontal defect will
perforation
to perforation
repair
Pulp is nonresorptive
Tissue may demonstrate
fluctulance
Extracanal invasive resorption
Type
Differential diagnosis
Treatment
Prognosis
Extracanal
There is an irregular radiolucency RCT; Debridement of
Poor to good depending
invasive
within the tooth, often
defect through coronal on the quality to debride
resorption
superimposed over pulp canal
access opening with
the defect and the quality
Radiolucency becomes more
slow-speed round bur
of the filling
regular in advanced stage
Filling with loose mix of
Canal maintains original form
silver alloy, composite or
Pulp remains responsive
GI or better with MTA

13