Case History in

periodontics

Presentation by Dr. Harshal P Patil

Guided by Dr. P.S.Rakhewar
Dr. Lisa Chacko
Dr. Manoj Thorat
 Introduction

Recording the case history of a patient is an integral

part of Periodontics. A systematically recorded case
history provides great insight to the attitude of the
patient as well as the patients medical and periodontal
status. It helps us arrive at a diagnosis and in framing
an appropriate treatment plan.
 Demographics

Name
1. Everyone feels good when they are addressed by their name. The
purpose of asking the name of the patient is to make him feel
comfortable in order to establish a good rapport.
2. The name is also important for record purposes. It makes it easy
to identify the patient for future correspondence. It is also necessary
to have complete records in case of any medico-legal cases.
Age
1. Certain diseases are seen more commonly in certain
age groups.
 Periodontal condition Age Reason

Gingival Herpetic Children below 6 years Since the condition is contagious,

disease gingivostomatitis adults would be exposed to the
virus in their childhood and
developed immunity. Thus, it is
seen predominantly in children.
Puberty associated 11-17 years Hormonal changes increase:
gingivitis 1. Tissue response to plaque.

2. Capnocytophaga , Prevotella
intermedia and Prevotella
nigrescens which use hormones
as nutrients.
Acute necrotizing 15 30 years Seen at any age, but most
ulcerative gingivitis commonly between 15-30 years.
Children with Downs syndrome
or from low socioeconomic strata
are predisposed.
Desquamative gingivitis 40-50 years Auto-immune conditions are
common in middle aged women.
An exception is dermatitis
herpetiformis which is seen in
males between 20 to 30 years.
Periodontal Aggressive periodontitis <35 years The rate of bone loss here is 3-4
disease times faster than in chronic
periodontitis; hence, the disease
manifests at a younger age.
Chronic periodontitis >35 years Though the condition may begin
in adolescence, due to the slow
rate of progression it becomes
clinically significant after the age
of 35.
 Prognosis of the patient depends upon the age. In two patients
with the same level of disease the older patient has a better
prognosis.
For example: If a 20 year old and a 50 year old patient have
generalized 7mm pockets, the 50 year old patient has taken
much longer to lose the same amount of attachment as to the 20
year old. The 20 year old patient would lose far more attachment
by the time she is 50. Obviously the rate of destruction is more
in the younger patient and the prognosis is obviously worse.
3. Anatomic differences:
The periodontium of children exhibits the following features:

Color of gingiva Less pale than in adults due to thinness of keratinized layer which makes
the underlying vessels more visible

Surface texture Stippling is absent up to the age of 4 years

Contour Inter-dental gingiva is broad buccolingually and narrow mesiodistally to conform to
the morphology of deciduous teeth

Sulcus depth 2.1 mm 0.2 mm

Lamina dura More prominent
Periodontal ligament Wider
space

Marrow spaces of Larger

alveolar bone

Crests of inter-dental Flat and within 1 to 2 mm of cementoenamel junction

bone
The periodontium of older adults exhibits the following features:

Gingiva Thinning and decreased keratinization of epithelium

leading to decreased resistance to trauma and infection
Gingival recession due to passive eruption
compensating for attrition

Increase in collagen and decrease in cell number

Periodontal Decrease in fibroblasts
ligament Increase in elastic fibers

Width of PDL space increases with occlusal loading and

decreases in hypofunction
Cementum Increase in width by 5-10 times
Alveolar bone Presents a more irregular surface
Plaque Increased accumulation due to a greater area of the tooth
being exposed by recession, no change in microflora
Host response No change in host response but increased inflammatory
and inflammation response
Response to No change in response to non surgical and surgical therapy
treatment Greater compliance with supportive periodontal therapy
 Sex
1. Some conditions have a gender bias.
Males: Chronic periodontitis, generalized aggressive periodontitis
Females: Desquamative gingivitis
2. Conditions specific to women.
Puberty and pregnancy do not by themselves lead to gingivitis. Plaque is the cause of gingivitis and, pregnancy and
puberty merely increase the gingival response to plaque.
Puberty, pregnancy and oral contraceptives:
In all 3 conditions there is an increase in estrogen and progesterone.
Progesterone increases vascular permeability and makes the blood vessels more tortuous.
This in turn increases the inflammation in response to bacterial plaque.
Apart from this, Prevotella intermedia use progesterone as a substitute for Vitamin K as a growth factor. These
organisms are implicated in both puberty and pregnancy associated gingivitis.
Menopause: Deficiency of estrogen in menopause results in osteoporosis which is characterized by a reduction in
bone mass. Results of some studies indicate that osteoporotic patients might have a greater bone loss due to
periodontal disease than those without osteoporosis. The influence of systemic disease on periodontal bone loss was
termed bone factor concept by Irving Glickman in 1950, but this term is no longer used.
 Occupation

1. Occupational hazards.
Abrasion: Notching on incisal edges maybe seen in carpenters and tailors
who hold bobby pins and needles between their teeth.
Erosion: People who work in factories with acidic environments show
eroded teeth.
2. Stressful jobs.
There is an increase in the hormone cortisol in stressful conditions. Cortisol
suppresses the immune system and therefore, increases the susceptibility
to infections like periodontitis.
 Address

Some conditions are endemic to certain geographic locations,

for example fluorosis. Fluorosis is due to increased fluoride in
the water at the time of development of the tooth and is seen
to occur in the fluoride belts of the country. It causes enamel
hypoplasia and intrinsic discoloration of teeth.
Chief Complaint and History of Present Illness

The chief complaint of the patient should always be in his/ her own words and
should include the symptoms of the patient in a chronological order.
The history of present illness should be elicited from the patient:
1. A detailed description of the patients chief complaint including when the
symptoms started. In case of pain, nature of the pain as well as aggravating
and relieving factors should be included.
2. Apart from the symptoms mentioned by the patient, the dentist should try to
ascertain whether a periodontal problem exists by asking the patient if he has
loose teeth, bleeding gums, food lodgment, bad breath or pain in his gums.
Pain can be identified as that of pulpal or periodontal origin based on the
following:
Pulpal pain Periodontal pain

Severe, lancinating, poorly localized pain. Dull, gnawing well localized pain or pain deep in
the bone.

Increases on consuming cold/ hot food; and in Increases on chewing.

the supine position due to increased pulpal
pressure.
 Past Dental History
This should include whether the patient has previously visited the dentist and the reason for the same.
1. If the patient has visited the dentist before, it shows that he/ she has a greater awareness and
motivation towards dental treatment.
2. If the patient gives a history of extractions, then it is important to find out whether the teeth
extracted were carious or mobile. Past history of periodontal disease is a risk factor for periodontal
breakdown in the future.
3. If the patient has got his/ her teeth restored, the quality of these restorations should be checked.
Overhanging restorations can cause plaque accumulation and under-filled proximal restorations can
lead to food impaction, both of which are predisposing factors of periodontal disease.
Ask for history of syncope, bleeding and hypersensitivity
4. Complications seen during previous treatment.
Syncope: Syncope is the transient loss of consciousness due to reduced blood supply to the brain.
The most common cause is anxiety towards dental treatment. There is an increase in the levels of
catecholamine which lowers peripheral resistance, causes peripheral pooling of blood and reduces
cerebral blood flow. Signs and symptoms before the onset syncope include weakness, nausea,
sweating, pallor, dizziness and low pulse pressure.
To treat syncope the patient should be made to lie down in a supine position with the legs raised to
increase the venous return to the heart and blood to the brain. When the back of the chair is reclined
such that the head of the patient is lower than his feet it is called Trendelberg position. Apart from
this tight clothes should be loosened and a patent airway maintained.
A patient who gives a history of syncope at the previous dental visit should be well motivated for
future procedures and if necessary pre-anesthetic medications such as sedatives maybe prescribed
prior to treatment.
 Drug allergies: Some patients are hypersensitive to local
anesthetic agents. It is important to find out about
hypersensitivity to penicillin or local anesthetics before
initiating dental treatment
 Medical history
Ask for history of diabetes mellitus, cardiovascular problems, bleeding disorders, liver problems
and medications.
Diabetes mellitus: Periodontal disease has been described as the sixth sign of diabetes by Loe
H. in 1993.
1. Periodontal findings
Hirschfeld has mentioned the following periodontal symptoms associated with diabetes:
a. Enlarged gingiva
b. Sessile or pedunculated polyps
c. Polypoid gingival proliferations
d. Abscess formation
e. Periodontitis
f. Loosened teeth
Presence of multiple periodontal abscesses is the most characteristic finding of Diabetes
mellitus.
 Apart from the these findings diabetics have increased gingival bleeding, deep periodontal
pockets, rapid bone loss and tooth loss.
Diabetics are three times as likely as non-diabetics to develop destructive periodontal disease. This
is because of the effect of diabetes on bacterial pathogens,
function of neutrophils and
altered collagen metabolism.
a. Bacterial Pathogens: Due to increased glucose in blood and gingival crevicular fluid there is an
increase in mainly the black pigmented species which includes Porphyromonas gingivalis, Prevotella
intermedia and Campylobacter rectus.
b. Neutrophil Function: Glucose metabolism is necessary for the production of ATP which is a source
of energy for all cells. Therefore, in diabetics cell function is affected and neutrophils have impaired
chemotaxis, phagocytosis and adhesion.
c. Altered Collagen Metabolism: Regular collagen turnover is necessary to maintain tissue integrity.
In diabetics Advanced Glycation End (AGE) products attach to collagen and render it less soluble and
less likely to be repaired. This damaged collagen remains in the tissues longer and breaks down
easily in the presence of periodontal disease.
2. Two way relationship of diabetes and periodontitis: Infections such as periodontitis increase the
tissue resistance to insulin, reduce uptake of glucose by the cells and thus, increase the glucose
concentration of blood. Therefore, treating periodontitis will help in improving the glycemic control in
diabetic patients.
Complications on the dental chair with diabetic patients-
The most common complication on the dental chair is that of hypoglycemia or decreased blood glucose.
Increased incidence is seen in well-controlled diabetics taking insulin or sulfonylurea agents. It is important
to ensure that the patient has had his meal before the dental treatment.
If a patient goes into hypoglycemia on the dental chair (usually at glucose levels <60mg/ dl) , then the
treatment should be discontinued and the patient should be given either juice or 4 teaspoons of sugar.
Unconscious patients can be given 25ml of 50% dextrose or 1mg glucagon intravenously.
Cardiovascular problems:
Hypertension
a. Time of treatment: Blood pressure is usually highest mid-morning, therefore it is better give the patient
an afternoon appointment.
b. Use of adrenaline: Using local anesthesia without adrenaline will minimize its anesthetic action and
cause the release of endogenous adrenaline. Therefore, adrenaline should be used along with the local
anesthetic agent but the concentration should not exceed 1:100,000.
c. Levels at which treatment is possible: All dental procedures can be performed up to a blood pressure of
160/ 100, non-surgical techniques may be performed up to a level of 180/ 110 and after this only
emergency care maybe undertaken.
d. Drugs: Calcium channel blockers used to treat hypertension can lead to gingival enlargement. Therefore,
it is essential to document drug history in these patients.
Myocardial infarction and angina pectoris
Patients having suffered from ischemic heart disease should avoid dental treatment for 6
months. Anginal episodes on the dental chair should be treated by administration of
nitroglycerin (sublingual) and oxygen.
Patients with cardiac pacemakers
Older pacemakers are unipolar and get disrupted by ultrasonic and electrosurgery units.
Thus, the use of these equipments should be avoided in these patients. However, newer
pacemakers are bipolar and unaffected by equipment generating an electromagnetic field.
Infective endocarditis
The presence of bacteria in the blood is called bacteremia. This can trigger infective
endocarditis in a patient who gives a history of the same. Dental procedures can cause
bacteremia and prophylactic antibiotics need to be given in patients at risk for infective
endocarditis.
Usually amoxicillin is given at the dosage of 2g, 1 hour before the procedure and in
patients allergic to amoxicillin Azithromycin or Clarithromycin maybe prescribed at a
dosage of 500 mg, 1 hour before the procedure.
Bleeding disorders and liver disease
Liver disorders are of importance as the liver is responsible for production of pro-coagulant factors and
metabolism of certain drugs. Coagulation tests such as Prothrombin time and Partial Thromboplastin time
should be carried out before initiating periodontal therapy and medications should be prescribed with
caution.
Drug history
1. Drugs which directly affect the periodontium
Examples of medications affecting the periodontium are:
a. Drugs such as calcium channel blockers (nifidipine), anticonvulsants (phenytoin) and immunosuppressants
(cyclosporine) can lead to gingival enlargement.
b. Oral contraceptives cause an exaggerated response to local factors.
2. Drugs which increase bleeding tendency
Patients on salicylates (aspirin) or anticoagulants (heparin, warfarin) will have increased bleeding. It is better
to take an opinion from the physician regarding drug discontinuation during the periodontal procedure.
3. Drug interactions
Metronidazole should be avoided in patients consuming alcohol or patients on warfarin or lithium. Similarly,
ciprofloxacin should be avoided in patients taking theophylline, caffeine or warfarin.
Apart from these factors medical history is also important because certain drugs are contraindicated in
certain conditions such as Ibuprofen in asthmatics, Diclofenac sodium in patients with gastritis and Pencillin
in patients with known hypersensitivity to the drug.
 Family history

Ask if family members too have periodontal problems.

Genetic defects have been implicated in both chronic and aggressive periodontitis,
hence, it is important to know whether the patient gives a positive family history.
Polymorphisms in genes coding for Interleukin 1, TNF , FcgR and Vitamin D
predispose patients to periodontitis and are called genetic markers.
Knowledge of family history becomes particularly essential in aggressive
periodontitis which is known to have familial aggregation. Thus, family members
especially younger siblings, of the patient with aggressive periodontitis should be
examined for the signs of the disease, educated about preventive measures, and
monitored closely.
Personal history
Habits:
Ask for history of smoking and alcohol consumption.
A study by Tomar SL and Asma S in 2000 (as a part of Third National Health and Nutrition
Examination Survey or NHANES III) showed that subjects smoking greater than 30 cigarettes
per day are 4 times more likely to have periodontitis and former smokers were 1.68 times
more likely. Therefore, smoking is a known risk factor for periodontal disease. Smokeless
tobacco too has been associated with localized attachment loss and recession.
A current smoker is said to be one who has smoked atleast 100 cigarettes in his lifetime and is
currently smoking
A former smoker is one who has smoked 100 cigarettes in his lifetime but is not currently
smoking.
Heavy smokers are those who smoke more than or equal to 20 cigarettes per day while those
people smoking less than 20 cigarettes per day are considered as light smokers.
Cigarette smoke contains various injurious substances and includes a particulate and a
gaseous phase.
Particulate phase: Nicotine, Tar, Benzene, Benzopyrene.
Gas phase: Carbon Monoxide, Ammonia, Dimethylnitrosamine, Formaldehyde, Hydrogen
Cyanide, Acrolein.
The effects that smoking has on the periodontium are:
a.Physiologic effects: Microvasculature is altered in smokers.
Nicotine stimulates the sympathetic nervous system which further leads to vasoconstriction.
This leads to decrease in bleeding on probing, gingival crevicular fluid flow, subgingival temperature and
clinical signs of inflammation.
b. Microbiologic effects: There is no change in the amount of plaque but there is a change in the bacteria present in
it.
Grossi et al. in 1996 have showed that Tannerella Forsythia was 2.3 times more likely to be there in smokers
than in non smokers.
Hafajjee AD and Socransky SS in 2001 have shown an increase in the Orange and Red Complexes in smokers.
Increased colonization of these periodontal pathogens is seen in shallow pockets and therefore, there is an
increased prevalence of periodontal destruction.
c. Immunologic effects: The alterations in the host response causing increased periodontal breakdown are
Nicotine causes functional changes in neutrophil chemotaxis, phagocytosis and oxidative burst and thus, affects
the innate response.
The humoral response is also affected by the reduced production of the IgG2 antibody.
Concomitantly, there is increased production of tissue destructive agents such as Tumor Necrosis Factor a,
Prostaglandin E2, elastase and collagenase.
d. Effect on calculus formation: Pindborg found a positive correlation between smoking and calculus deposition.
They reported more pipe smokers than cigarette smokers have supragingival calculus. The reasons given for this
are that pH of pipe smokers is more, and because pipe smokers circulate the smoke around the mouth.
e. Response to periodontal therapy: In smokers there is less pocket depth reduction and less gain in clinical
attachment levels following both surgical and non surgical periodontal therapy. Smokers also showed poor results
in procedures such as guided tissue regeneration and use of bone grafts. GTR membranes were exposed and less
pocket reduction was achieved following placement of Demineralized Freeze Dried Bone Allograft.
.
 The smoking history of the patient should include the following details:
a. Number of years for which the patient is smoking.
b. Number of cigarettes smoked each time.
c. Number of times in a day that the patient smokes.
d. In a former smoker it is important to know how many years he smoked for and
how many years it has been since he quit smoking.
e. In case of smokeless tobacco it is important to know the form in which it is used
and which part of the mouth it is placed in.
Smokers should be motivated to quit smoking in the Phase I or Etiotropic phase
of periodontal therapy. The smoking cessation program has the following steps:
Chronic alcoholism can cause cirrhosis of the liver, which can increase the
bleeding tendency during periodontal instrumentation. This is the reason for
recording any history of chronic alcoholism
Oral Hygiene Habits
Frequency of tooth brushing
By finger / brush/ other
Manjan/ Tooth paste
Method Horizontal / vertical
 Extra oral examinations
Symmetry of the face: Gross asymmetry of the face maybe
observed in the following conditions:
1. Cysts and tumors of the jaw
2. Facial fractures
3. Dentoalveolar abscess
4. Hemi-atrophy or hemi-hypertrophy
5. Bells Palsy
Lymph node examination
If a node is palpable, record site, size,
texture, tenderness, fixation to
surrounding tissues etc

Local infections: pericoronitis,
periodontal/pericoronal/periapical
abscess/lesions, ANUG, apthous ulcers,
acute herpetic gingivostomatitis,
malignancy

Systemic infections: syphilis, TB,
Bacterial/fungal/parasitic infections,
malignancy, HIV, lymphomas,
leaukaemias
 TMJ examinations

Temporomandibular joint:
Lips:
Whether the lips are competent or not should be checked
while the patient is relaxed. If the patient is asked to close his
lips, he might forcefully close it and it becomes difficult to
differentiate between potentially competent and competent
lips.
Incompetent lips are usually associated with mouth
breathing. In these patients gingiva appears erythematous
and shiny especially in the maxillary anterior region. This
change has been attributed to surface dehydration.
 Test to check mouth breathing

1. Mirror test
2. Butterfly test
3. Water holding test
 Intraoral examination
Soft tissue examinations
Parts of oral mucosa:
Buccal mucosa: Lesions of lichen Planus, leukoplakia, erthyroplakia and oral submucous fibrosis
maybe seen on the buccal mucosa.
Physiological alterations that maybe seen include cheek bite (linea alba buccalis) and ectopic
sebaceous glands (Fordyces granules).
Labial mucosa: Vesicles and ulcers on the labial mucosa may be due to Herpes labialis. The scaling
appointment in these patients should be rescheduled and caution should be used during patient
examination since the condition is contagious. When it spreads to the clinicians finger the lesion is
called herpetic whitlow.
Floor of the mouth: Mucous retention cysts (Ranula) might be present in the floor of the mouth.
Tongue: The tongue has quite an irregular surface which offers ideal niches for sheltering bacteria and
retaining desquamated cells and food remnants.
Tongue coating is particularly seen in case of hairy tongue (lingua villosa) or fissurated tongue (lingua
plicata). This tongue coating is responsible for oral malodor. Tongue cleaning should be advocated in all
patients to avoid halitosis.
 examination
Periodontal indices
Oral hygiene index
Plaque index: Silness and Loe, Quigley Hein
Gingival index: Loe and Silness
Periodontal Index: Russells index, Ramfjords index, CPITN
index
 ORAL HYGIENE INDEX SIMPLIFIED
( John C. Greene & Jack R. Vermillion, 1964 )
DEBRIS INDEX
SCORE CRITERIA
0 No debris or stain present
Soft debris covering not more than one-
1 third of tooth surface, or presence of
extrinsic stains without other debris
regardless of surface area covered
2 Soft debris covering more than one-
third, but not more than two thirds, of
the exposed tooth surface.
3 Soft debris covering more than two
thirds of the tooth surface.
CALCULUS INDEX
SCORE CRITERIA
0 No calculus present
1 Supragingival calculus covering not more
than third of the exposed tooth surface.
Supragingival calculus covering more than
one third but not more than two thirds of
2 the exposed tooth surface or the presence
of individual flecks of subgingival calculus
around the cervical portion of the tooth or
both
Supragingival calculus covering more than
3 two thirds of the exposed tooth surface or a
continous heavy band of subgingival
calculus around the cervical portion of the
tooth or both.
 INTERPRETATION OF SCORES

FOR DI/CI FOR OHI-S

GOOD 0 0.6 GOOD 0 1.2

FAIR 0.7 1.8 FAIR 1.3 3.0

POOR 1.9 3.0 POOR 3.1 6.0

 PLAQUE INDEX
( Silness P. & Loe H , 1964 )

Interpretation


SCORE CRITERIA
EXCELLENT 0


0 No plaque present

GOOD 0.1 0.9
A film of plaque adhering to the free gingival
margin and adjacent area of the tooth. The
1 plaque may be seen in situ only after
application of disclosing solution or by using
FAIR 1.0 1.9
the probe on the tooth surface.
Moderate accumulation of soft deposits within

2 the gingival pocket, or the tooth and gingival
margin which can be seen with the naked eye.

POOR 2.0 3.0

3 Abundance of soft matter within the gingival pocket
and/or on the tooth and gingival margin
 GINGIVAL INDEX
( Loe H. & Silness J , 1963

SCORE CRITERIA


0 Absence of inflammation/normal gingiva INTERPRETATION OF SCORES



MILD GINGIVITIS 0.1 1.0
1 Mild inflammation, slight change in colour,
slight edema; no bleeding on probing.

2 Moderate inflammation; marked glazing, MODERATE GINGIVITIS 1.1 2.0
redness edema and hypertrophy. Bleeding
on probing.
SEVERE GINGIVITIS 2.1 3.0
3 Severe inflammation; marked redness and
hypertrophy ulceration. Tendency to
spontaneous bleeding.
 SULCUS BLEEDING INDEX (SBI)
Muhlemann H.R and Son S. in 1971

SCORE CRITERIA
0 Normal-appearing gingiva, no bleeding upon probing.
1. No colour or contour changes, but bleeding on probing.
2. Bleeding on probing, colour change(reddening),no edematous contour changes.
3. Bleeding on probing, colour change, mild inflammatory edema.
4. Bleeding on probing, colour change, severe inflammatory edema.
5. Spontaneous bleeding on probing, colour change, very severe inflammatory edema
with or without ulceration.
Gingival bleeding index (Ainamo and Bay, 1975)
The gingival bleeding index is based on recordings from all four tooth surfaces of all
teeth.
Recorded as
Bleeding present +
Bleeding absent -

Gingival bleeding index is calculated as a percentage of affected sites.

USES:
It is useful for experimental studies and in practice on routine basis in individual
patients.
ADVANTAGES:
Simple and easy to use.
LIMITATIONS:
Does not discriminate areas of bleeding as mesial, distal, facial, lingual surfaces .
 PERIODONTAL INDEX
(Rusell A.L, 1956)

ADDITIONAL RADIOGRAPHIC CRITERIA

SCORE CRITERIA FOR FIELD STUDIES FOR CLINICAL STUDIES
Negative. There is neither overt inflammation in
0 the investing tissues nor loss of function due to Radiographic appearance is essentially
destruction of supporting tissues. normal.
Mild gingivitis. An overt area of inflammation in
1 the free gingival does not circumscribe the
tooth.
Gingivitis. Inflammation completely
2 circumscribes the tooth, but there is no
apparent break in the epithelial attachment.

4 Used only when radiographs are available There is early notch like resorption of alveolar
crest.
Gingivitis with pocket formation. The epithelial
attachment has been broken and there is a There is horizontal bone loss involving the
pocket (not merely a deepened gingival crevice alveolar crest, upto half of the length of the
6 due to swelling in the free gingiva). There is no tooth root.
interference with normal masticatory function;
the tooth is firm in its socket and has not
drifted.
There is advanced bone loss involving more
Advanced destruction with loss of masticatory than half of the tooth root or a definite
8 function. The tooth may be loose, may have infrabony pocket with widening of periodontal
INTERPRETATION OF SCORES

Clinically normal supporting 0 0.2

tissues
Simple gingivitis 0.3 0.9
Beginning destructive 1.0 1.9
periodontal disease
Established destructive 2.0 4.9
periodontal disease
Terminal disease 5.0 8.0
Gingival status
The gingiva is the part of the oral mucosa that covers the alveolar processes of the jaws and surrounds
the necks of the teeth. It is divided into marginal, attached and interdental areas.
Color
The normal color of the gingiva is coral pink.
Factors which determine gingival color include:
1. Thickness of epithelium
2. Degree of keratinization
3. Vascular supply
4. Pigmentation
The changes in the color of the gingiva in inflammation are:
Reddish pink: This is due to increased blood vessels and reduced keratinization
Bluish red: Blue color of tissues is always associated with reduced oxygen supply; similarly gingiva turns
bluish red because of venous stasis and anoxemia
localization of these changes in color help in diagnosis:
ANUG marginal involvement
Herpetic gingivostomatitis diffuse
Chemical irritation patch like

Chemical burn Aspirin

Metallic pigmentation:
Black line on gingiva-Bismuth, arsenic, mercury

Bismuth induced black line

Lead: Burtonian line bluish red/deep blue
Silver: violet marginal line

 Cause: absorbed metals are precipitated in perivascular areas as metallic sulfides

into the subepithelial connective tissue.
Pigmentation only occurs in areas of inflammation (since increased permeability of
irritated blood vessels permit seepage of metal into surrounding tissues)
Site: gingiva, inner surface of lips, at the level of occlusal line in cheeks, lateral
border of tongue
Treatment: Removal of local irritating factors; discontinuity of metal containing
drugs; topical application of concentrated peroxide to oxidize dark metallic sulfides.

Pigmentation
Endogenous
Melanin which is increased in the
following systemic condition:
Addisons disease (adrenal dysfunction)
Peutz Jeghers syndrome (intestinal
polyposis)
Albrights syndrome (fibrous dysplasia)
Von Recklinghausens disease
(neurofibromatosis)
Bilirubin (Jaundice)
Iron (Hemochromatosis)
Blood dyscrasias like anemia,
polycythemia, and leukemia
Exogenous
Metallic pigmentation due to bismuth, arsenic,
lead and silver:
Pigmentation occurs when inflammation leads
to increased vascular permeability and there is
precipitation of metallic sulfides into the
connective tissue. Therefore, the treatment
consists of scaling.
Tobacco
Coloring agents in food and lozenges
Amalgam tattoo or implantation of amalgam
into the gingiva
 ORAL PIGMENTATION INDEX
( Dummett, 1966 )

SCORE CRITERIA INTERPRETATION OF SCORES

0 No pigmentation
0 No clinical pigmentation ( pink tissue
)
0.03 1 Mild pigmentation
1 Mild clinical pigmentation ( mild light
brown tissue ) 1.03 2 Moderate pigmentation

2 Moderate clinical pigmentation 2.03 3 Heavy pigmentation
( moderate brown tissue )

3 Heavy clinical pigmentation ( deep
brown to black tissue )
Size
The size of any matter depends on what it is made up of; the size of the gingiva is
determined by the sum total of:
1. Cells
2. Intercellular substance
3. Vascular supply
Increase in the size of the gingiva is called gingival enlargement and is classified based on its
etiology as:
Inflammatory Acute : Abscess
Chronic : Plaque induced gingivitis
Drug induced Antiepileptic agents: Phenytoin
Calcium channel blockers: Nifidipine
Immunosuppressants: Cyclosporine
Associated with systemic conditions Conditions in which the reaction to plaque is
Associated with systemic disease increased leading to gingival enlargement:
Pregnancy, puberty, plasma cell gingivitis,
pyogenic granuloma and scurvy
Enlargement is due to the disease itself
irrespective of the plaque, for example due to
leukemia, Wegeners granulomatosis or
sarcoidosis
Neoplastic Benign: Fibroma, papilloma, giant cell
granuloma
Malignant: Carcinoma, malignant melanoma
False enlargement Due to underlying bone lesion: Tori, Pagets
disease, fibrous dysplasia, cherubism, osteoma,
osteosarcoma
Cue to underlying dental tissue: prominence of
enamel during tooth eruption
 Inflammatory gingival enlargement has been graded by
Bokencamp et al in 1994 as:
Grade 0: No sign of enlargement
Grade I: Enlargement of interdental papilla
Grade II: Enlargement of papilla and marginal gingiva
Grade III: Enlargement covering three quarters or more of the
crown
New Clinical Index For Gingival Overgrowth [Eva Ingles
1999]
Grade 0:
No overgrowth; firm adaptation of the attached gingiva to the underlying bone. Slight
granular appearance & a knife edged papilla present toward the occlusal surface with
increase size of gingiva
Grade 1:
Early overgrowth as evidenced by an increase in density of gingiva with marked stippling &
granular appearance.
The tip of the papilla is rounded & probing depth is </= 3mm
Grade 2:
Moderate overgrowth, manifested by an increase in size of papilla & rolled margins.
The contour is still concave or straight with buccolingual dimension of up to 2mm. The
papilla is retractable
Grade 3 :
Marked overgrowth, represented by encroachment of gingiva onto the clinical crown.
The contour is convex with buccolingual dimension of 3mm or more.
The probing depth is > 6mm & the papilla is clearly retractable
Grade 4:
Severe overgrowth, characterized by a profound thickening of gingiva with a large
percentage of the clinical crown covered. The papilla is retractable & the probing depth is >
6 mm & bucco lingual dimension is approximately 3mm
 Consistency
Normal consistency of the gingiva is firm and resilient due to:
1. Collagenous nature of the lamina propria; and
2. Contiguity with the mucoperiosteum of the alveolar bone.
It is checked with the help of blunt end of the Instrument.
In gingivitis the consistency maybe soft and edematous due to edema, inflammatory cell infiltration
and degeneration of connective tissue elements.
Since gingivitis is a chronic inflammatory condition the outer wall may show repair in the form of
increased fibrosis and keratinization. In these cases the gingiva appears pale pink and firm in
consistency though the inner lining of the sulcus is still atrophic or ulcerated. Here the presence of
bleeding on probing helps us arrive at the diagnosis of gingivitis irrespective of outer changes in color
or consistency.
 Contour
The contour of the gingiva is scalloped with knife edge margins.
Gingival contour depends upon the following factors:
1. Shape of the teeth
2. Alignment of the teeth in the arch
3. Proximal contact
4. Dimension of gingival embrasure
Contour is accentuated in labially placed teeth and the gingiva is thickened in lingually placed teeth. Besides these
physiologic variations in contour, in areas of diastema the interdental papilla is missing and the gingiva is firmly adherent
to the underlying bone.
Normal gingiva follows scalloped outline. Accentuated scalloped outline where recession is present.
In gingivitis the knife edge is lost. The marginal gingiva is rounded and the interdental papilla is blunt.
Other inflammatory changes include:
Stillmans cleft is an apostrophe shaped area of recession or triangular indentation on the gingival margin.
McCalls festoon is a thickened band of gingiva or life preserver shaped enlargement of the gingiva most commonly in the
cuspid region. These lesions were earlier attributed to traumatic occlusion but are now known to be due to inflammation.
 Surface texture

The attached gingiva and central portion of the interdental papilla

show an orange peel appearance called stippling. This is best
visualized by drying the gingiva. Stippling appears by 5 years of
age and disappears again in old age.
Cause of stippling: alternate rounded protuberances and
depressions in the gingival surface due to the projection of the
connective tissue papilla into the epithelium.
Function of stippling: functional adaptation of the gingiva.
Stippling is reduced in inflammation and increased in drug induced
gingival enlargement
 Position

The normal position of the gingival margin is 1mm above the

cementoenamel junction.
When the level of the gingival margin is below the CEJ it is
called recession. It is defined as the exposure of the root
surface due to apical migration of the gingival margin.
Classifications of recession:
1. Sullivan and Atkins, 1968
Shallow, narrow
Shallow, wide
Deep, narrow
Deep, wide
2. PD Miller, 1985
Class I: Marginal tissue recession not extending beyond the mucogingival junction.
There is no loss of interdental bone or soft tissue.
Class II: Marginal tissue recession extends to or beyond the mucogingival junction.
There is no loss of interdental bone or soft tissue.
Class III: Marginal tissue recession extends to or beyond the mucogingival junction.
There is loss of interdental bone and soft tissue or tooth malposition
Class IV: Marginal tissue recession extends to or beyond the mucogingival junction.
There is severe interdental bone and soft tissue loss or severe tooth malposition.
Cause of recession:
1. Ageing
2. Improper brushing habits horizontal technique, use of
toothpowder or using a hard bristled brush
3. Inflammation
4. High frenal attachment
5. Labially placed teeth
6. Congenital defects such as thin bone margins and dehiscence.
7. Pressure from denture clasps
8. Pressure from orthodontic bands
9. Following periodontal surgery
10. Overhanging restorations
Width of Attached gingiva
Definition: It is the distance between MGJ and the projection on the external surface of the bottom of the gingival sulcus or
the periodontal pocket.

Width of keratinized gingiva= Attached gingiva + Marginal gingiva

Width of attached gingiva=Total width of Gingiva from the margin to the MGJ - Pocket depth

Methods of determination:
Tension test (when stretching of lip or cheek induces movement of the free gingival margin, gingiva is considered
inadequate).
Pushing adjacent mucosa coronally with a dull instrument.
Painting mucosa with Schillers Potassium Iodine solution.

In maxillary anteriors: 3.5 - 4.5 mm

mandibular anteriors: 3.3 3.9 mm
In premolars (maxillary): 1.9 mm
In premolars (mandibular): 1.8 mm
Tension test
Application of tension at the MGJn by retracting cheek, lip & tongue (upwards, outwards & downwards) to tighten alveolar
mucosa and test for the presence of attached gingiva.
Area of missing attached gingiva is revealed when alveolar mucosa and frenum are connected directly to free gingiva.
PURPOSE:
To detect adequacy of AG
To locate frenal attachment and their proximity to free gingiva
To identify MGJn

PROCEDURE:
Facial: Retract cheeks and lips laterally away . Watch MGJn. Move the lips up, down and across, creating tension
at MGJn.
Lingual: Hold mouth mirror to tense mucosa of floor of mouth, gently retract side of tongue so MGJn is clearly
visible.
OBSERVATIONS:
Blanching at MGJn
Frenal attachment
Recession
Movement of free gingival margin; AG
Amount of attached gingiva
This is the distance from the projection on the external surface of the bottom of gingival sulcus or pocket to
the mucogingival junction. Keratinized gingiva includes marginal gingiva.
Assessing width of attached gingiva
Determined by subtracting the sulcus pocket depth from the total width of gingival (gingival margin to
mucogingival line)
Tension test
Kopczyk RA (1974); Glickman (1964)
Purpose
To detect adequacy of width of attached gingiva
Locate frenal attachment and their proximity to the free gingiva
To identify promptly the mucogingival junction
Procedure
Facial
Retract cheeks and lips laterally by grasping the lips with thumb and index finger, watch at the
mucogingival junction.
Move the lips and cheeks up and down and across, creating tension at the mucogingival junction
Lingual
Hold the mouth mirror to tense the mucosa of the floor of the mouth, gently retracting the side of
the tongue, so that the mucogingival junction is clearly visible.
Request the patient to move the tongue to left, right, up to touch the palate.
Observation
Blanching at mucogingival junction
Frenal attachments
Areas of apparent recession where there is very little keratinized gingiva and the base of the sulcus or pocket is
near the mucogingival junction
Areas where color, size, loss of slipping, smooth shininess or other characteristic indicates need or careful probing
to determine amount of attached gingiva.
Area where tension pulls the free gingiva from the tooth, indicating no attached gingiva.
Frenal attachment has been described by Placek. M, Skach M, Mrklas L (1974)
Mucosal attachment refers to the attachment of the frenum to the mucogingival junction
Gingival attachment refers to the attachment of the frenum within the attached gingiva
Papillary attachment refers to the attachment of the frenum within the papilla
Papilla penetrating attachment refers to an attachment of the frenum passing through the papilla while inserting
into the attached gingiva (of the palate)
Pull syndrome Placek et al (1974)
Detaching movement of marginal gingiva transferred from the lip by the frenum has been termed pull syndrome.
 Bleeding on probing
: Bleeding on probing is an objective sign indicating periodontal disease.
Other signs such as changes in color or consistency are subjective and might be
interpreted differently by different examiners.
The presence of bleeding on probing and exudation indicate that the disease is active.
Absence of bleeding on probing is a good prognostic indicator as it correlates with
periodontal stabiltiy.
Method to check for bleeding on probing: Running the probe. It might take 30 to 60
seconds for the bleeding to become apparent.
Reduced bleeding on probing: Smokers
Local Chronic Chronic gingivitis and
periodontitis
Acute ANUG
Injuries: Mechanical, chemical
and thermal
Systemic Bleeding disorders Hemophilia, Christmas
disease, Thromocytopenia,
Leukemia
Hypoprothrombinemia, Scurvy,
Hormonal changes Pregnancy, puberty, patients
on oral contraceptives,
diabetes mellitus
Medications Salicylates (aspirin) and
anticoagulants (heparin,
warfarin)
Exudation

Certain changes are observed in the sulcular epithelium due to chronic inflammation. Neutrophils enter
the epithelium from the connective tissue and release hydrolytic enzymes which kill bacteria and
degrade the adjacent epithelial cells as well. On applying digital pressure on the lateral aspect of the
gingival margin the pus consisting of dead and live Neutrophils, dead and live bacteria and
desquamated epithelial cells is expressed as an exudate. Therefore, this exudate does not correlate with
the pocket depth but is merely a lateral wall change which indicates that the disease is active.
Abcess
An abscess is a localized accumulation of pus. It is different from exudation as it is well contained.
Classifications:
1. Single or multiple. Multiple periodontal abscess is common in diabetics.
2. Occurring in the supporting tissues or occurring in the gingiva
Classification by Meng, 1999
Gingival abscess: In previously healthy sites and caused by impaction of foreign bodies.
Periodontal abscess: In relation to a periodontal pocket, either acute or chronic.
Pericoronal abscess: In relation to an incompletely erupted tooth.
Differences between acute and chronic
abscess are:

Acute Chronic
Appears as an ovoid swelling and Presents a sinus opening
the gingiva is red, edematous,
smooth and shiny
Accompanied by throbbing pain, Usually asymptomatic. There might be
tenderness on palpation, tooth dull, gnawing pain.
mobility, enlarged lymph nodes,
fever and malaise.
 Differences between gingival and
periodontal abscess
Gingival
Limited to marginal gingiva and
interdental papilla
Caused by bacteria being carried deep
into the tissues when a foreign substance
like a toothbrush bristles is forcefully
embedded in the gingiva
Periodontal
Usually involves attached gingiva
Caused due to the localization of inflammation
because of one of the underlying resons:
1. Extension of infection to lateral wall of
pocket
2. Extension of infection deep into the
supporting periodontal tissues.
3. In the deep end of a spiral or complex pocket
4. Incomplete removal of calculus leads to
shrinkage of the gingival wall and occludes the
opening of the pocket.
5. Due to perforation through the root during
endodontic therapy
Differences between periodontal and
periapical abscess
Periodontal
Periodontal pocket is present
Tooth is vital
Pain is usually dull and localized
(easy to localize due to the
presence of tactile fibers in the
periodontal ligament)
Tender on lateral percussion
Usually not visible on the
radiograph
Periapical
Caries is present
Tooth is non-vital
Pain is severe and difficult to localize
(difficult to localize as pulp basically
consists of only pain perceiving fibers)
Tender on vertical percussion
Appears as a periapical radiolucency
 Periodontal examination

Periodontitis is defined as an inflammatory disease of the supporting tissues of

the teeth caused by specific microorganisms or groups of specific
microorganisms resulting in progressive destruction of the periodontal ligament
and alveolar bone with pocket formation, recession, or both.
Periodontal pocket
Definition: The periodontal pocket is defined as a pathologically deepened
gingival sulcus.
Method to check for pocket: Walking the probe. Probing should be done using a
standard force of 25 grams (Armitage et al 1977). The probing force applied is
equivalent to the capillary pressure.
 Classification:
Based on involvement of supporting periodontal tissue
Gingival (Pseudopocket) Periodontal pocket
No loss of supporting tissue, pocket is There is loss of supporting periodontal tissues
formed due to gingival enlargement and
coronal migration of the gingival margin

Based on surfaces involved

Simple Compound Complex/ Spiral

Pocket involves only one surface Pocket involves Pocket starts on one surface,
more than one follows a tortuous course to
surface involve another tooth surface

Based on relationship with bone

Suprabony (supracrestal/ supraalveolar)
Base of the pocket is coronal to the crest
of the alveolar bone
Horizontal bone loss
Interproximally, transseptal fibers are
arranged horizontally
Facially and lingually, periodontal
ligament fibers follow a horizontal course
Infrabony (subcrestal/ intraalveolar)
Base of the pocket is apical to the crest of the
alveolar bone
Angular bone loss
Interproximally, transseptal fibers are arranged
obliquely
Facially and lingually, periodontal ligament
fibers follow an angular course
 Clinical features associated with a pocket:
1. Bluish red marginal gingiva
2. Rolled edge separating gingival margin from the tooth surface
3. Gingival bleeding
4. Suppuration
5. Tooth mobility
6. Diastema formation or extruded teeth
7. Pain deep in the bone
Level of attachment and pocket depth:
Pocket depth is measured from the gingival margin to the
base of the pocket whereas level of attachment is from the
CEJ the base of pocket. It is more reliable to assess level of
attachment as it is from a fixed point (CEJ). The gingival
margin might move coronally due to inflammation and then
apically once the inflammation subsides.
Dimensions of the periodontal probe:
Different shapes and sizes of periodontal probes yield different penetration depths into periodontal tissues. Periodontal
probes with a point diameter of 0.4-0.5 mm have been used successfully. Most probes are circular in cross-section. The
probe should be thin enough to reach the true attachment level under healthy conditions, with JE and resistant
connective tissue, but will penetrate the less resistant, inflamed connective tissue in diseased pockets and over-
estimate loss by 0.5-1.0 mm. A thicker periodontal probe will not reach the true attachment level. A thin blade-shaped
probe will give the most accurate result, but to access all the sites, it has to be able to be rotated 360 (Axelsson,
1982).

Probing force
0.75N of probing force has been found to be well tolerated and accurate.
Probing forces:
The probe is inserted along the long axis of the tooth into the pocket with gentle (approximately 25 g) force until
resistance is met. 25-g of force is necessary to indent the pad of the thumb about 1-2 mm. In clinical application, what
would be considered gentle insertion force, do not penetrate apical termination of JE. According to some authors,
forces of 0.75 N have been well tolerated & accurate [Van der Velden, 1979]. The tip of the probe has been assumed to
identify the level of the most apical cells of the dentogingival epithelium. This, however, is not the case always (Saglie
et al, 1975; Polson, 1980).

Probe penetration depends on tissue inflammation. In health, probe tip penetrates most coronal intact fibres of
connective tissue attachment (0.3 mm) into JE [Listgarten et al, 1976]. There may be over-estimation (probe may
penetrate beyond apical termination of dentogingival epithelium due to inflammation) or under-estimation (reduction
in inflammation after successful therapy with concomitant deposition of new collagen prevents complete penetration of
probe) of the true pocket.
 Probing technique

The probe is inserted parallel to vertical axis of tooth and walked circumferentially around each
surface of each tooth to detect the areas of deepest penetration.
To detect interdental crater the probe should be placed obliquely from facial and lingual surfaces to
explore the deepest point of the pocket located beneath the contact point
Probing technique:
Probe is to be placed parallel to vertical axis of tooth and walked circumferentially around each
surface.
Gutta percha points or calibrated silver points with radiographs can also be used.

 In clinical practice, conventional periodontal probes are widely used to obtain two important
measurements: probing depth (PD) and clinical attachment loss (CAL).

PD is defined as the distance from the gingival margin to the base of the probeable crevice.

Probing depth measurements are clinically important since they provide a useful overall assessment of
the depth of periodontal pockets which are the principal habitats of periodontal pathogens.
In addition, PD measurements can be rapidly recorded and give a good assessment of the distribution of
periodontal problems within a given patient. They are an essential component of a complete periodontal
examination
Positioning of the probe:
Manual probing is subject to measurement error because of variations in the angulation and site of
insertion of the probe and because of the difficulty in obtaining a fixed landmark as a reference point.
The probe should be kept as parallel as possible to the long axis of the root.
The tip should continuously follow the root surface, to prevent penetration of the pocket epithelium and
connective tissue, resulting in underestimation of attachment loss.
Each tooth is examined at 6 locations: MB, B, DB, DL, L, and ML. The probe may be angled approx. 10 in
interproximal areas.
Level of attachment
Clinical attachment level the level of attachment is the distance between the base of the pocket
and the cemento-enamel junction.
Determining the level of attachment
When gingival margin is located on the anatomic crown, the level of attachment is determined by
subtracting from depth of the pocket the distance from gingival margin to the cemento-enamel
junction. If both are same loss of attachment is 0.
When the gingival margin coincides with the cemento-enamel junction, the loss of attachment
equals the pocket depth.
When gingival margin is located apical to the cemento-enamel junction, the loss of attachment
will be greater then pocket depth, therefore the distance from cemento-enamel junction to
gingival margin should be added to the pocket depth.
Vertical probing attachment loss (PAL)/Clinical attachment loss (CAL):
CAL is the distance from the cementoenamel junction to the base of the probeable crevice.

Gingival margin is located on anatomic crown: CAL= PD (gingival margin to CEJ)

Gingival margin coincides with CEJ:CAL=PD
Gingival margin is located apical to CEJ, i.e. recession: CAL= PD + (gingival margin to CEJ)

 In single-rooted teeth, LOA occurs only vertically. In multirooted teeth, loss of attachment
can also occur horizontally, indicating furcation involvement.

Changes in CAL can be due only to gain or loss of attachment & afford a greater/better
indication of the degree of periodontal destruction. Shallow pockets attached at the apical
third of root are more destructive than deep pockets attached at the middle third of root.

CAL assessments are more difficult to accurately measure, but they give a better overall
estimate of the amount of damage to the periodontium than do PD measurements. In
prospective studies, CAL measurements are the most valid method of assessing treatment
outcomes.

Probing depth as well as loss of attachment (LOA) can be measured by manual probing or
by more sophisticated, automated, computer-linked, pressure-sensitive periodontal
probes.
Alveolar bone loss
The alveolar bone levels are evaluated by clinical and radiographic examination.
Transgingival probing (sounding) helps to provide information of bone architecture. Area is
anaestheitized the probe should be walked along the tooth-tissue interface so that the operator
can feel the bony topography. The probe can also be passed horizontally through tissue to
provide more three dimensional information (thickness, height, shape).
Radiographic evaluation
Access
Bone condition
Tooth condition
Root anatomy
BONE SOUNDING/TRANSGINIVAL PROBING:
In order to arrive at a correct diagnosis with respect to the alveolar bone level, presence of
angular bony defects and interdental osseous craters, etc, sounding may be done.
Procedure:
Local anaesthesia
Tip of probe is inserted into the pocket and forced through supraalveolar connective tissue to
make contact with the bone and the distance from CEJ to bone level is assessed.
 Hard Tissue examinations

Number of teeth present

Caries/decayed
Missing
Filled
Stains/ deposits
Wasting disease - Attrition/ erosion/ abfraction
Occlusion
 Teeth present
Various nomenclature systems are used as follows:

Zsingmondys and palmar method: 87654321 12345678

87654321 12345678

Universal system: 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
32 3130 29 28 27 26 25 24 23 22 21 20 19 18 17
FDI system: two digit system :
18 17 16 15 14 13 12 11 21 22 23 24 25 26 27
28
48 47 46 45 44 43 42 41 31 32 33 34 35 36 37
38
 Stains and calculus:

+ - satins and calculus involving only cervical portions of tteth

++ - stains and calculus extending upto middle third of the
tooth
+++ - stains and calculus involving more than two third or
involving whole of the facial or lingual surface
Classification intrinsic and extrinsic
 Occlusion type of angles malocclusion should be mentioned
here.
Caries/decayed ,
missing tooth
filled tooth
 Wasting diseases of
teeth
Wasting is defined as any gradual loss of tooth substance
characterized by the formation of smooth, polished surfaces,
without regard to the possible mechanism of this loss.
The most systematic classification is given by Grippo, who
define four categories of wasting of tooth i.e.
Attrision-
Abrasion
Erosion-Also called corrosion, erosion is a sharply defined,
wedge-shaped depression in the cervical area of the facial
tooth surface."
Abfraction
 Attrition. Attrition is occlusal wear resulting from functional
contacts with opposing teeth. Such physical wear patterns may
occur on incisal, occlusal, and approximal tooth surfaces.
Occlusal or incisal surfaces worn by attrition are called facets.
shiny, smooth, and curviplanar facets are usually the best
indicator of ongoing frictional activity.
If dentin is exposed, a yellowish brown discoloration is
frequently present
 Abrasion. Abrasion refers to the loss of tooth substance induced by
mechanical wear other than that of mastication.
Abrasion results in saucer-shaped or wedge-shaped indentations with a
smooth, shiny surface. Abrasion starts on exposed cemental surfaces
rather than on the enamel and extends to involve the dentin of the root.
A sharp ditching" around the cementoenamel junction appears of to the
soft cemental surface compared with the hard enamel surface.
Toothbrushing with an abrasive dentifrice and the action of clasps are
common causes of abrasion; brushing is the much more prevalent cause'
abrasion of the incisal edges results from habits such as holding objects
(e.g., bobby pin, tacks) between the teeth.
 Erosion-Also called corrosion, erosion is a sharply defined,
wedge-shaped depression in the cervical area of the facial
tooth surface.
The surfaces are smooth, hard, and polished.
In the early stages, it may he confined to the enamel, but it
generally extends to involve the underlying dentin as well as
the cementum.
the etiology of erosion is not known. Suggested causes
include decalcification by acidic beverages' or citrus fruits and
the combined effect of acid salivary secretion and friction.
 Abfraction. A recently studied mechanism of tooth wear,
abfraction results from occlusal loading surfaces causing
tooth flexure and mechanical microfractures and tooth
substance loss in the cervical area.`
Clinical pictures of attrision abrasion
and erosion
FOOD IMPACTION:
Is the forceful wedging of food into the periodontium by occlusal force
It can be vertical and horizontal.
Vertical- open contact & Contour of occlusal surface
(due to marginal ridges & grooves):
as teeth wear down- flat surface- wedging effect of opposing cusp.
Plunger cusp: Cusp that tend to forcibly wedge into interproximal
embrasures.

Horizontal or lateral food impaction- in caes of enlarged gingival

embrasure
lateral pressure from lips, cheeks and tongue: forces food interproxim
Classification of Factors Causing Food Impaction: (Hirschfeld 1930)5
Class I: Occlusal wear
Class II: Loss of proximal contact
Class III: Extrusion beyond the occlusal plane
Class IV: Congenital morphological abnormality
Class V: Improperly constructed restorations

Interdental bone defects: Pressure & irritation from food impaction

contribute to inverted bone architecture.
Sequelae of food impaction:
Feeling of pressure & urge to dig
Vague pain that radiated deep in the jaws
Gingival inflammation
Bleeding
Foul taste
Gingival recession
Abscess formation
Sensitivity to percussion
Destruction of alveolar bone
Root caries
Proximal Contacts

Normal proximal contacts do not allow any food impaction in between the teeth.
The interdental papilla fills the space up to tooth contact in normal conditions. However due to
periodontal disease there is loss of interdental soft tissue and bone levels.
Due to this, the position of interdental papilla recedes from its normal position.

Classification according to Nordland and Tarnow (1998):

Normal: The interdental papilla occupies the entire embrassure space apical to the interdental
contact
point / area.
Class I: The tip of the interdental papilla is located between the interdental contact point and
the level of
the CEJ on the proximal surface of the tooth.
Class II: The tip of the interdental papilla is located at or apical to the level of the CEJ on the
proximal
surface of the tooth but coronal to the level of the CEJ midbuccally.
 Classification of interdental embrasures, by Perry and Schmid
(1996)
Type I embrasure: The gingival papilla fills up the embrasure
space completely.
Type II embrasure: The gingival papilla partially fills the
embrasure space due to papillary recession.
Type III embrasure: The embrasure space is not filled. The
gingival papilla has receded extensively or it is completely lost.
Pathologic migration
Definition: Tooth displacement that results when the balance among the factors
that maintain physiologic tooth position are disturbed by periodontal disease.
It should be differentiated from physiologic migration or drifting. Due to proximal
and occlusal wear the tooth moves occlusally and mesially throughout life, this
shortens the arch by around 0.6cm from midline to third molar by the age of 40.
This is called physiologic migration.When it occurs in the occlusal direction it is
termed extrusion.
it may be present as extrusion,facial flaring,rotation diastema and drifting of
affected teeth, mostly show combined form.

Causes:
1. Weakened periodontal support
2. Pressure from granulation tissue
3. Trauma from occlusion
4. Tongue thrusting
TRAUMA FROM OCCLUSION:
Definition: When occlusal forces exceed the adaptive capacity of the tissues, tissue injury results. The resultant injury is termed TFO.

Types: Primary and Secondary

Clinical features:

Excessive tooth mobility; pain

Infrabony pockets
Pathologic migration
Gingival recession
Stillmans cleft/McCalls festoon
Food impaction
Wearing of teeth & appearance of facets
Hypersensitivity of teeth
Tenderness of TMJ & muscles of mastication
Smudging of articulating paper
Dull percussion note
Vibrations from fremitus

Radiographic features:
Widening of PDL space
Lamina dura thickened
Vertical/ angular bony destruction
Radioluscence & condensation of alveolar bone
Buttressing bone
Root resorption

Methods of determination:
Fremitus test:
It is the measurement of the vibratory pattern of the teeth when the teeth are placed in the contacting positions and movements are made.
To measure fremitus, dampened ungloved index finger is placed along the buccal and labial surfaces of maxillary teeth (or the tooth in question) & the
patient is asked to tap the teeth together in maximum intercuspation (CO) & grind systematically in the lateral excursive movements (lateral fremitus).
Vibrations are perceived. It is easier to detect fremitus in the maxillary teeth than the mandibular teeth.

By Ingreval
Class I fremitus: Mild vibrations or movements detected
Class II fremitus: Easily palpable vibrations but no movements detected
Class III fremitus: Movements visible with naked eye

Occlusal registration strips/articulating paper

Auditory test: In centric relation, there is a distinct ringing sound during tooth contact. But in TFO, with deflection present, sound is dull and imperceptible

Fremitus
Fremitus means the palpable vibration or movement, in dentistry it refers to the vibratory patterns of the teeth.

Procedure
Seat the patient up right and head stabilized against headrest index finger is firmly placed over the cervical third each maxillary tooth in succession
starting with most posterior tooth on one side and moving around the arch patient is requested to click the posterior tooth.
Record by tooth number where vibration is felt and the teeth where actual movement is noted

N = normal (no vibration)

+ = one degree fremitus
Only slight vibration can be felt
++ = two degree fremitus
Tooth is clearly palpable but movement is barely visible.
+++ = Three degree fremitus
Movement is clearly observed visually

Significance
Tooth with fremitus has excess contact, premature contact.
Well distributed posterior contact
Coupled contacts between opposing teeth
Smooth excursive movement without interfere
TOOTH MOBILITY:
The movement of a tooth in its socket as a result of an externally applied force. Tooth mobility is seen as one
of the measures useful in evaluatinvalue depends on the observerss skill and experience.

Causes:
g the health of the periodontal tissues (Prichard, 1979). The most common clinical method used to examine
tooth mobility is to press the tooth in a horizontal or vertical direction with a finger, or with the handle of the
blunt ends of two metal instruments (Prichard, 1979). This method is imprecise and its Local Factors:
Bone loss/loss of tooth support (periodontitis, TFO, endodontic problems)
Hypofuction
Periapical pathology, cysts or tumors
After periodontal therapy [Nyman & Lindhe (1976), Persson (1981)]
Orthodontic forces; heavy fuctional loads (from prosthetic appliances)
Parafunctional habits (bruxism, clenching)
Pathologies (tumours, cysts, osteomyelitis)
Traumatic injuries to dentoalveolar unit
Tooth morphology

Systemic causes:
Age: progressively increases
Sex & Race: females>males; Negroes more
Menstrual cycle: Friedman (1972) observed increased horizontal tooth mobility during 4 th week of menstrual
cycle.
Oral contraceptives (Dorothy, 1981)
Stress
Nutritional deficiency
Pregnancy (Mobility increases from 2nd to 8th month progressively)
Circadian rhythm (more during early morning & progressively decreases)

 Tooth mobility indices:

Millers index (1938)
I: first distinguishable sign of movement
II: movt. of tooth which allows crown to deviate within 1mm of its normal
position
III: easily noticeable & allows tooth to move more than 1 mm in any
direction or to be rotated or depressed in the socket

Modified Millers index

Scores: 0, , 1, 1, 2, 3 are utilized

Prichards index (1972)

1: Slight mobility
2: Moderate mobility
3: Extensive mobility in a lateral or M-D direction combined with vertical
displacement in alveolus
4: Signs can be used for added refinement

Tooth mobility measuring devices:

Periodentometer (Muhleman, 1951)
Persson & Svensons devices (1980)
Periotest (Schultz, 1987) [It helps in objective assessment of tooth mobility. The tooth is
rapidly percussed 16 times (four times per second) and then the rebound attenuation
patterns emanating from the tooth are electronically recorded].
Values are calculated as:
-8 to +9: Clinically firm teeth
10 to 19: Palpable mobility
20 to 29: Visible mobility
30 to 50: mobility in response to lip and tongue pressure
Periodontal pulse
The three-dimensional physiological tooth movement synchronized with the heartbeat is
called periodontal pulsation (Diemer, 1963, 1966; Krber, 1971a,b; Igarashi et al., 1981). It
is produced by changes in the calibre of periodontal vessels due to cardiac pulsation. It has
been suggested that the degree of periodontal pulsation reflects the condition of the
microcirculation and the pathophysiological properties of the periodontal tissues (Hofmann
and Diemer, 1966; Krber, 1971a). The measuring device consisted of a small magnet
attached to the tooth and an amorphous sensor that was used to detect displacement of
the tooth without actually contacting it.
Wassermans index (1973)
1: Normal
2: Slight mobility less than 1mm of buccolingual movement
3: Moderate upto 2 mm of buccolingual movement
4: Severe mobility more than 2 mm movement

Glickmans index (1972)

Normal mobility
Pathologic mobility
Grade I: Slightly more than normal
Grade II: moderately more than normal
Grade III: severe mobility with vertical displacement

The clinical importance of increased tooth mobility is frequently overestimated. It has clearly been shown
in animal experiments that, if plaque-induced inflammation is controlled, increased tooth mobility has no
effect on the level of the connective tissue attachment (Ericson and Lindhe, 1977). Hypermobility of tooth
does not necessarily mean that it has a poor prognosis, and the mobility frequently persists after
successful periodontal treatment (Lindhe and Nyman, 1975, 1984). Nevertheless, increasing tooth mobility
over time should alert the clinician to a possible deterioration of periodontal support, and such teeth
require careful evaluation for loss of clinical attachment.
 All teeth have a slight degree of physiologic mobility, which varies for different teeth
and at different times of the day. Mobility is greatest on arising in the morning and
progressively decreases. During the waking hours, mobility is reduced by chewing
and swallowing forces, which intrude the teeth in the sockets.
Single-rooted teeth have more mobility than multi-rooted teeth; incisors have the
most mobility. Mobility is principally in a horizontal direction.
Tooth mobility occurs in the following two stages:-
1) In the initial stage the tooth moves within the confines of the periodontal ligament
(PDL). This is associated with viscoelastic distortion of the PDL and redistribution of
the periodontal fluids, interbundle content, and fiberes. This initial movement occurs
with forces of about 100g and is about 0.05 to 0.10mm (50-100m).
2) The secondary stage occurs gradually and entails elastic deformation of the
alveolar bone in response to increased horizontal forces.
When a force such as that applied to teeth in occlusion is discontinued, the teeth
return to their original position.
Furcation involvement
Definition: Furcation involvement is the invasion of bifurcation and trifurcation of teeth by
periodontal disease.
Method to check for furcation involvement: A curved probe called Nabers probe is used.
Classification:
Based on horizontal measurement of bone loss, Glickmans classification, 1953
Grade I: Incipient involvement which is felt as a catch with the probe.
Grade II: There is partial loss of bone. Here the probe penetrates partially but does not pass
through and through. There maybe involvement from both sides but these are not connected
since some amount of bone is still remaining. This is called cul de sac which means dead
end.
Grade III: The bone loss is through and through.
Grade IV: Along with through and through bone loss there is gingival recession leading to the
furcation area becoming clinically visible.

Based on vertical measurement of bone loss, Tarnow and Fletcher, 1984

Subclass A: Bone loss is 0 3mm
Subclass B: Bone loss is 4 7mm
Subclass C: Bone loss is greater >7mm
 According to hamp et al 1975
Degree1-horizontal loss of periodontal support not exceeding
1/3rd of the width of the tooth
Degree2 horizontal loss of periodontal support exceeding1/3rd
of the width of the tooth
Degree3- horizontal through and through destruction of
periodontal tissue in the furcation area.
Predisposing factors for furcation involvement are:
1. Short root trunk: Less attachment loss is required for furcation to be involved.
2. Trauma from occlusion: In multi-rooted teeth the axis of rotation is located in
the bone between the roots. Therefore, the bone loss in relation to increased
forces on these teeth would be in the furcation region.
3. Cervical enamel projections: These are flat ectopic extensions of enamel that
extend beyond the normal contours of the cementoenamel junction.
Development: During root formation the Hertwigs epithelial root sheath
disintegrates to allow the dental follicle cells to come in contact with the root
dentin and lay down cementum. In areas where the root sheath has failed to
disintegrate the dental follicular cells are unable to come in contact with the
dentin. The root sheath cells, which are basically the reduced enamel
epithelium, lay down enamel.
Significance: The Sharpeys fibers of the periodontal ligament insert to
cementum on one side and to bone on the other. Therefore, in areas of cervical
enamel projections there is no attachment of the periodontal ligament fibers
thereby allowing easy spread of periodontal disease into the furcation area.
Classification by Masters and Hoskins, 1964:
Grade I: CEP extends towards the furcation entrance
Grade II: CEP approaches the furcation entrance
Grade III: CEP extends into the furcation

4. Enamel pearls: These are large, round deposits of enamel that

can be located anywhere on the root. They are plaque retentive
areas which when present near the furcation area can predispose
the tooth to furcation involvement
5. Accessory pulpal canals: May extend the pulpal inflammation to
the furcation.
 EXAMINATION OF RESIDUAL RIDGE

Seiberts Classification:

Class I: loss of facio- lingual width, with normal apico- coronal height

Class II: loss of ridge height with normal width

Class III: loss of both height & width

STUDY MODELS

Visual aids in discussions

To study occlusion
Position of the gingival margins
Proximal contact relationships
Splinting
Preparation of acrylic plates
Treatment planning
Clinical photograph
Color photographs are useful for recording the appearance of the tissue
before and after treatment.
Photographs cannot always be relied on for comparing subtle color
changes in the gingiva, but they do depict gingival morphologic changes.
With the advent of digital clinical photography, record keeping for
mucogingival problems has become important (e.g. areas of gingival
recession, frenum involvement, papilla loss).
RADIOGRAPHIC EXAMINATION

Root length, root form, root proximity

Estimates of remaining alveolar bone
Osseous defects
PDL space
Lamina dura
Periapical area
Restorations, calculus
Type and density of alveolar bone
Anatomical landmarks
RADIOGRAPHIC CHANGES IN
PERIODONTITIS

Fuzziness or break in lamina dura

Wedge shaped radioluscent areas
on crest
Widening of periodontal ligament
space
Reduction in height of interdental
septum
Interdental craters - areas of
reduced opacity

112
 Furcation -
radiographs at different
angles
Reduced radiodensity in Furcation
furcation involvment
Marked bone loss adjacent to
single molar root
Periodontal abscess
Radiolucency along lateral
aspect of tooth

Periodontal
113 abscess
Intraoral radiographic survey
It requires full mouth intra-oral radiographic series 14 periapical films; 4 bite wings.

Panoramic radiographs are a simple and convenient view of the dental arch and
surrounding structures. They are helpful in detecting developmental anomalies,
pathologic lesion of teeth and jaws, fractures and dental screening examination of large
groups.

They provide information of overall radiographic picture of the distribution and

severity of bone destruction in periodontal disease but a complete intraoral series in
required for periodontal disease diagnosis and treatment planning.

RADIOGRAPHIC EXAMINATION:
The use of radiographic imaging as an aid in diagnosis and treatment of periodontal
disease is widely accepted.

The information supplied by radiographs includes:

Root length, root form, root proximity
Estimates of remaining alveolar bone
Osseous defects
PDL space
Lamina dura
Periapical area
Restorations, calculus
Type and density of alveolar bone
Types of imaging:
I] Conventional:
A] Intra-oral radiographs
Periapical
Bitewing
Occlusal
Technique: Bisecting angle/ Paralleleing cone

B] Extra-oral radiographs
Orthopantomogram and other extraoral views

II] Digital:

Specialized techniques:
Digital subtraction radiography (DSR)
When two images of same object are registered and the image intensities of corresponding
pixels are subtracted, a uniform difference image will be obtained. If a change of follow-up
image has occurred, it will show up as a brighter area when the change represents the gain and
as a darker area when the change represents loss. Subtraction images allow detection of
mineral changes of as little as 5 %.
Tuned aperture computed tomography (TACT)
TACT is built on basic principles of tomosynthesis by shifting and combining a set of basis
projections, arbitrary slices through the object can be brought into focus. Each radiograph is
taken from different angle relative to the object and the receptor. It is shown to improve the
ability of observers to detect osseous defects around implants.
Computed Tomography (CT)
CT provides exquisite 3-D views, however, its ability to show very small details remains limited.
The application of CT imaging for periodontal diagnosis appears to have an unfavorable cost-
benefit ratio.
Computer-assisted densitometric image analysis (CADIA)
Video camera measures the light transmitted through a radiograph, and the signals from the
camera are converted into gray-scale images. The camera is interfaced with an image
processor and a computer that allows storage and mathematical manipulation of the images
 LABORATORY INVESTIGATIONS
Haemoglobin: Differentiate WBC count
Males:14-18gm/dl
Females:12-16gm/dl polymorphs: 55 70%
RBC count: (adult)
Males: 4.6-6.2 49 65% (children)
millions/cumm lymphocytes: 29 40%
Females: 4.2-5.4 (adult)
millions/cumm
30 60% (children)
WBC count: Eosnophil: 1 6%
6000-11000 /cumm
Platelet Count: Monocytes 2 10%
1,50,000-4,00,000/cumm Basophils 0 1%
ESR
men: 4 -10 mm/hr Glucose levels
Women: 8 20 mm/hr Fasting levels: 60-100
mg/dl
Post prandial: <140
 Test Description Normal values Disease with
increased values

Bleeding Time Dukes method and Ivys method. < 8 minutes Purpura, von Willebrand
Dukes: Puncture finger tip/ ear lobe and Disease
measure the time until the bleeding stops.

Clotting Time Wrights capillary tube method and Lee and <10 minutes Deficiency of any
Whites method. Wrights: Puncture finger tip procoagulant factor
and collect blood in a capillary tube. At
intervals break the tube and check for a
thread joining the two ends, this is the clot.

Prothrombin Deficiencies of extrinsic and common < 16 seconds Deficiency of factors I,

Time pathway can be detected II, V, VII, and X

Activated Partial Measures efficiency of intrinsic and common < 40 seconds Deficiency of factors III,
Thromboplastin pathways IX, and XI
Time
Laboratory diagnosis
When the dentist detects unusual gingival or periodontal problems that cannot be explained by local causes, the possibility of contributing systemic factors must be explored.
The signs and symptoms of oral manifestations of systemic disease must be clearly understood ad analyzed and discussed with the patients physician.
LABORATORY INVESTIGATIONS
Haemoglobin
Males: 14-18gm/dl; Females: 12-16gm/dl
Significance: if reduced, hampers healing; risk of syncope
RBC count:
Males: 4.6-6.2 millions/cumm
Females: 4.2-5.4 millions/cumm

Decreased: anemia, dietary def., pregnancy, bone marrow failure, hodgkins disease, multiple myeloma, hemoglobinopathies, renal dis., collagen vascular dis.
Increased: COPD, CHD, polycythemia vera
WBC count:
6000-11000 /cumm
Decreased in: reduced defence
Increased in: infections, leukaemia

Platelet Count:
1,50,000-4,00,000/cumm
If less than 1 lakh/cumm: surgery cannot be done

Bleeding time:
Dukes method: < 5 mins
Prolonged: thrombocytopenia, leukaemia, liver disease, drugs(NSAIDs,warfarin, streptokinase, anticoagulants), DIC, collagen vascular dis., connective tissue dis.

Clotting time:
Capillary tube method: 1-7 min
Kruse and Moses method: 2.5-5 mins
Lee and White method: 5-10 mins
Prolonged: Hemophilia, fibrinogen deficiency

Prothrombin time (PT):

Quick Method: 10-20 s
Deficiency of factor II, V, X
Prolonged: Liver disease, fibrinogen deficiency, vit K def., DIC, massive transfusion

Activated partial thromboplastin time (APTT):

30-40 s
Deficiency of factor II, V, VIII, IX, X, XI, XII
Prolonged: cirrhosis, DIC, coumarin, heparin, vit K def., clotting factor deficiency

International Normalised Ratio (INR):

It is used only to assess the control of oral anticoagulant treatment. It is the ratio of patients PT to a normal control based on an international reference thromboplastin which
ensures standardization of anticoagulation between different centers. INR should generally be less than 2.0. For simple surgical procedures, INR less than 2.5 is generally safe.

Glucose levels
Fasting levels: 60-100 mg/dl
Post prandial: <140 mg/dl
Increased in Diabetes
Significance: nutrient for bacterial growth, reduced healing

Glycated hemoglobin (HbA1c)

4-6%: Normal
<7%: good diabetic control
7-8%: moderate diabetic control
>8%: poor diabetic control (poor response to surgery)
BIOPSY
It is the removal of tissue from the living organism for the purposes of microscopic examination & diagnosis.
TYPES:
Excisional biopsy(total excision of lesion)
Incisional biopsy (removal of small section of lesion)
Needle aspiration (fine[FNAC]/thick bore)
Exfoliative cytology(desquamative gingivitis, pemphigus, mucous membrane pemphigoid, lichen planus)
PUNCH BIOPSY
5mm disposable punches
Cutting core of 3-4mm in depth
INCISIONAL BIOPSY
No. 15 blade
BRUSH BIOPSY
Special bristled instrument to retrieve cells from the spinous layer of epithelium when firmly rotated over the mucosal lesion.
Technique
Tissue should be perpendicularly incised with a scalpel
Removed tissue should be handled carefully
Lesion less than 1 cm-excisional biopsy
Larger than 1 cm, suspicious-incisional biopsy
In clinically most suspected area
Part of lesion and part of clinically healthy mucosa should be included in the biopsy
In gingival biopsies, marginal and attached gingiva (effect of local irritants less likely to be present) should be included
Gingival biopsy and leukemia
The existence of leukemia is sometimes revealed by a gingival biopsy to clarify the nature of a troublesome gingival condition and may
indicate the extent of leukemic infiltration. However, they are not sufficient to warrant routine gingival biopsy in such patients.
SUPPLEMENTAL DIAGNOSTIC TESTS
Supplemental diagnostic tests can be used to perform two basic tasks. The first is screening, i.e., to separate diseased from non-
diseased patients. The second is to detect sites or patients undergoing the progression of periodontitis. The second task is more
demanding than the first. It is also of greater importance since the clinician can easily separate healthy from periodontitis patients
based on customary clinical criteria.
 MICROBIOLOGICAL
INVESTIGATION
Bacterial culturing Immunodiagnostic
Direct microscopy methods
Darkfield or Phase- Indirect immunofluorescent
contrast microscopy assay (IFA)
Enzymatic methods Direct immunofluorescent
BANA test assay (DIFA)
DNA probes Membrane
immunoassay(Evalusite)
Restriction Flow cytometry /
endonuclease Cytofluorography
analysis ELISA
Polymerase chain Latex agglutination
reaction (PCR)
Presence of subgingival biofilms and high levels of specific periopathogens subgingivally:
The sole etiologic factor for periodontal disease is the microbial challenge, and a prerequisite for development of the diseased pocket and an active lesion is the presence
of subgingival periopathogens. Most of the subgingival microflora is attached to the root surface as plaque (biofilm), but the depths of the pocket also harbor many non-
attaching, motile species, particularly various sizes and forms of spirochetes.

In the biofilms, the microorganisms live in a well-organized symbiosis, supplied with nutrients via microchannels through the plaque matrix and inaccessible to
phagocytozing leukocytes, chemical plaque control agents, and antibiotics.

At 1996 World Workshop in Periodontics, it was concluded that human periodontitis is caused mainly by Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis
(exogenous, transmissible pathogens) and Bacteroides forsythus (endogenous, opportunistic pathogen). Recently, Machtei et al (1997) showed that, in deep periodontal
pockets, high levels of B forsythus increase the risk for further loss of periodontal attachment seven-fold. Other species of opportunistic endogenous periopathogens are
Prevotella intermedia and Treponema denticola. The presence and levels of subgingival periopathogens can be evaluated by subgingival sampling, with a sterile curette or
paper point, and DNA probe analyses, conventional anaerobic culture techniques, or chairside tests.

Bacterial culturing
It has been frequently used as the reference method when determining the performance of a new detection method. It is the only current method capable of determining
the invitro antimicrobial susceptibility of periodontal pathogens. It can also provide a quantitative measurement of all major viable microorganisms in the specimen. It
identifies only live microorganisms, therefore strict sampling and transport conditions are essential. Some of the putative pathogens are fastidious and difficult to culture.
The sensitivity of culture methods is rather low. It requires sophisticated equipment, experienced personnel and is relatively time-consuming and expensive.

Direct microscopy
Darkfield or Phase-contrast microscopy has been suggested as an alternative to culture methods on the basis of its ability to directly and rapidly assess the
morphology and motility of bacteria in the sample. However, most of the putative periodontal pathogens (Aa, Pg, Bf, Ec) are nonmotile and therefore cannot be identified.

Immunodiagnostic methods
Immunodiagnostic methods employ antibodies that recognize specific bacterial antigens to detect target microorganism.
Advantages:
Do not require viable bacteria
Less susceptible to variation in sample processing
Less time consuming
Easier to perform (than culture)
Disdvantages:
Accuracy of immunodiagnostic tests depends greatly on the quality of the reagents used
Generally show poorer detection limits than DNA probe and PCR
Expensive

Indirect immunofluorescent assay (IFA):

It employs a secondary fluorescein-conjugated antibody that reacts with the primary antigen-antibody complex.

Direct immunofluorescent assay (DIFA):

It employs monoclonal and polyclonal antibodies conjugated to fluorescien marker that binds with bacterial antigen to form a fluorescent immunocomplex
detectable under a microscope.

Membrane immunoassay(Evalusite):
It is a commercially developed, antibody-based sandwich enzyme-linked immunosorbent assay fro detection of Aa, Pg, P intermedia. It involves linkage
between the antigen and membrane-bound antibody to form an immunocomplex that is later revealed through a colorimetric reaction. The sample wells are
first coated with antibodies against antigens specific for the target bacterial species. Antibody-antigen reactions are then detected by adding enzyme-linked
antigen-specific antibodies to the sample wells, followed by the addition of enzyme substrate.

Flow cytometry/Cytofluorography:
It is for rapid identification of oral bacteria and involves labeling bacterial cells from a patient plaque sample with both species-specific antibody and a second
fluorecscein conjugated antibody. The suspension is then introduced into the flow cytometer, which separates the bacterial cells into an almost single-cell
suspension by means of a laminar flow through a narrow tube. The sophistication and cost involved in this procedure precludes its wide usage.

ELISA:
It is similar to other radioimmunoassay in principle, but an enzymatically derived color reaction is substituted as the label in place of radioisotope. The intensity
of colour depends on the concentration of the antigen and is usually read photometrically for optimal quantification. It has been used to detect
periodontopathogens.

Latex agglutination:
It is a very simple immunological assay based on the binding of protein to latex. Latex beads are coated with species-specific antibody, and when these beads
come in contact with the microbial cell surface antigens or antigen extracts, cross-linking occurs; its agglutination or clumping is visible usually in 2-5 mins.
Because of their simplicity and rapidity, these assay have great potential for chairside detection or periodontopathogens.

.
Enzymatic methods
BANA test
B forsythus, Pg, Treponema denticola and capnocytophaga species share a common enzymatic profile, since all have in common trypsin-like enzyme. The
activity of this enztme can be measured with the hydrolysis of the colour substrate N-bezoyl-dl-arginine-2-naphthylamide (BANA). When the hydrolysis takes
place, it releases the chromophore, -naphthylamide, which turns orange red when a drop of fast granet is added to the solution.
Diagnostic kits have been developed using this reaction (e.g. Perioscan).
BANA test can serve as a marker of disease activity. Loesche et al showed that shallow pockets exhibited only 10% positive BANA reactions, while deep
pockets (>7mm) exhibited 80-90% positive BANA tests. Beck et al used BANA as a risk indicator for periodontal attachment loss.
However, it detects a very limited number of pathogens.

DNA probes:
DNA probes entail segments of single-stranded nucleic acid, labeled with an enzyme or radioisotope that can locate and bind to their complementary nucleic
acid sequences with low cross-reactivity to target organisms. The assay can rapidly test for multiple bacteria, including Aa, Pg, B intermedius, C rectus, E
corrodens, F nucleatum, and T denticola.

Restriction endonuclease analysis

Restriction endonucleases recognize and cleave double-stranded DNA at specific base pair sequences. The DNA fragments are separated by electrophoresis,
stained with ethidium bromide and visualized with UV light. These DNA fragment patterns constitute a specific fingerprint to characterize each strain.

Polymerase chain reaction (PCR)

PCR involves a reiterate (repeated) amplification of a region of DNA flanked by a selected primer pair specific for target species. The presence of specific
amplification product indicates the presence of the target microorganism.
Advantages:
Best detection limits among nucleic acid based assays
No cross-reactivity under amplification conditions
Easy to perform
Disadvantages:
Most PCR assays use relatively small quantity of sample for the amplification process. If this quantity does not contain the targeted microorganisms, the
assay will not detect it.
Subgingival plaque mat contain enzymes which may alter the amplification process.
PCR has the potential for being an ideal detection method of periodontal pathogens
 Recent increase in PD and CAL
Recent increases in PD and CAL are highly indicative of diseased pockets, active lesions, and further attachment loss. Periodontal disease is characterized by periods of quiescence and
exacerbation. This was demonstrated by Goodson et al (1982); in untreated subjects with existing periodontal pockets, PAL was measured every month for 1 year. During this period, 83% of sites
did not change significantly, 6% exhibited significant further LOA, and 11% exhibited loss of attachment.
In individuals who are more susceptible to periodontal disease (smokers, those with genetic IL-1 polymorphism, and type 1 diabetes) more attachment loss may be seen.

Loss of compact bone from the alveolar crest
Loss of compact bone from alveolar crest and diffused lamina dura indicates active bone resorption. It can be evaluated by periodic radiographs.

BOP
The absence of BOP is a reliable parameter of periodontal stability, provided that the assessment procedure is standardized (Lang et al, 1990). Numerous studies have shown that a 30%
probability for future attachment loss may be predicted for sites that repeatedly exhibit BOP (Claffey et al, 1990; Lang et al, 1986).
Lang et al (1991) showed an almost linear relationship between probing force and the percentage of bleeding sites. At probing forces of greater than 0.25N (0.25g), bleeding is the result of tissue
trauma, rather than a sign of inflammation.
Because the absence of BOP at 0.25N indicates periodontal stability, with a negative predictive value of 98-99% (Lang et al, 1990), this is the most reliable clinical variable for monitoring patients
progress in daily practice.

Increase in periodontal pocket temperature
One of the cardinal signs of inflammation includes calor (increase in temperature) which is related to vascular changes. Regeneration of most human periopathogens is retarded at increased
temperature. Fever is one of the nonspecific host response to local and general infections. Because body temperature has long been used to evaluate the occurrence and severity of infectious
diseases, it seems logical to include measurement of the subgingival temperature in the evaluation of periodontal pockets. This was the rationale underlying the innovation of a digital
microthermometer, combined with a flat, thin periodontal probe, to identify diseased periodontal pockets (Axelsson, 1982). Commercial devices have been introduced in recent years (e.g.
PerioTemp System).

The PerioTemp System has been described by Kung et al (1990). The device is about the size and shape of a periodontal probe and uses a small thermistor bead to determine temperature. The
probe tip housed in a casing with low thermal conductivity so that the probe itself does not alter the ambient temperature. The probe is sensitive to 0.1C and assesses the temperature rapidly so
that the entire mouth (6 sites per tooth, 168 sites for 28 teeth) can be evaluated quickly. The device is linked to a computer. Advanced disease is associated with a mean increase of 0.65C at a
site.

The reference temperature used is the sublingual temperature which is generally higher than the subgingival temperature. The temperature increases in deeper pockets (34.6 C in 4 mm pockets
to 35.8 C in 6 mm pockets). In a study by Fedi and Killoy (1992), the temperature of the pockets more than 5 mm deep with BOP was 1-1.8 C higher than that of pockets less than 3 mm without
bleeding. Normal temperature is indicated by emission of a green light, slightly elevated temperature by a yellow light, and marked elevation of temperature by a red light. When the device was
used to predict risk of future PAL (Haffajee et al, 1992), the most obvious difference was observed for shallow sites (less than 4 mm). It was found that 8.9% of sites with BOP and markedly
elevated temperature lost 2.0 mm of PAL, compared to only 1.4% of sites that did not bleed and were in the normal temperature range.

A study of the relationship of temperature to subgingival microflora revealed that elevated subgingival temperature was associated with the presence of some putative pathogens like Prevotella
intermedia and Peptostreptococcus micros (Haffajee et al, 1992).

Increase in volume of GCF
There is strong statistical association between the volume of GCF and the extent of gingival inflammation which has led to the widespread use of measurements of GCF as an objective assessment
of gingival inflammation in clinical research studies.

Presence of purulent exudate
Conceptually, purulent exudate can be regarded as a PMNL-rich variant of GCF. Clinically, suppuration is an important sign of ongoing infection. A strong association with the risk of disease
progression was reported by Armitage et al (1994). In subjects with untreated periodontitis, the sites with suppuration at baseline (25% of total sites) were at three-fold higher risk of further bone
loss during the following 6 months.

Increase in levels of makers of periodontal disease activity: PGE2, MMPs, IL-1 in GCF
Curtis (1991) clearly differentiated disease markers as
Indicators of current disease
Predictors of future disease progression, and
Predictors of future disease at currently healthy sites.
GCF has the potential to reflect both host systemic responses and local modulation of those responses arising from interaction with the
bacterial burden. The GCF is regarded as a serum transudate because most serum proteins are present in concentrations similar to those
in serum itself (Cimasoni, 1983); it thus broadly reflects the systemic immunoglobulin and complement status of the host. However, GCF
is modified by the local environment associated with the periodontal crevice or pocket.

As the GCF migrates from the host microcirculation, through inflamed tissues, and into periodontal pocket, it acquires mediators involved
in the destructive host response and by-products of local tissue metabolism as well as PMNLs, microorganisms, and their products from
the periodontal pocket. The following four mediators in GCF have been investigated extensively for their potential application in
diagnosis of active periodontal disease and prediction of further loss of periodontal support:
Prostaglandin E2 (PGE2)
-glucouronidase (G)
Neutrophil elastase (NE)
Aspartate aminotransferase (AST)

Prostaglandin E2 (PGE2)
It is a proinflammatory metabolite of arachidonic acid.
Released from: macrophages, PMNLs, fibroblasts
Effects:
Vasodilation/increased vascular permeability
Enhanced responsiveness of receptors to painful stimuli
Release of collagenase by inflammatory cells
Activation of osteoclasts
Recruitment of inflammatory cells
Studies:
In a study by Offenbacher et al (1986), crevicualr fluid levels of PGE2 were three times more in subjects with aggressive periodontitis
(who experience rapid disease progression) than those with chronic periodontitis.
In another study by Offenbacher et al (1986), GCF from sites with active periodontal disease contained a mean PGE2 concentration of
305.6g/ml, while inactive sites contained about 65.7g/ml of PGE2.

genetic IL-1 polymorphism compared to patients without genetic polymorphism.

 -glucouronidase (G) & neutrophil elastase
-glucouronidase (G) and neutrophil elastase (serine endopeptidase) two enzymes released from the lysosomes of phagocytozing PMNLs.
Actions of G and NE:
Generation of reactive oxygen metabolites (Cell damage, inactivation of protease inhibitors)
Degradation of the connective tissue ground substance (Collagenase, elastase)

G has been correlated with the number of PMNLs in the crevice (which increase in no. during periodontal disease).

Harper et al (1989) observed that the total G activity in GCF was significantly correlated with the occurrence of subgingival periodontal
pathogens associated with the occurrence of subgingival periodontal pathogens, associated with more severe periodontal disease.

Lamster et al (1988) found that the total amounts of G level in GCF were related to the CAL over time. In another study it was found that the
in previously treated patients, persistently elevated levels of G in GCF were associated with an increase of 6-14 times in the risk PAL during
the monitoring period [Lamster et al (1995)].

NE activity is higher in patients with periodontitis than those with gingivitis; NE increases with development of experimental gingivitis
(Listgarten and Levin, 1981); and periodontal therapy tends to reduce NE activity in the fluid (Listgarten, 1992).

Aspartate aminotransferase (AST)
It is a cytoplasmic enzyme present in many body tissues. Its extracellular release is associated with cellular damage and cellular death.

Crevicular AST levels are correlated with disease severity. In a 2-year study by Persson et al (1990), sites with loss of CAL by 2mm or more
exhibited significantly elevated levels of AST in GCF.

IL-1
Gamonal et al (2000) showed that the amount of crevicular IL-1, IL-8 and IL-10 was associated with periodontal status. Engebretson et al
(1999) showed that the amount of IL-1 was 2.5 times higher in GCF and 3.5 times higher in gingival tissues before periodontal treatment in
patients with
DIAGNOSIS OF VARIOUS PERIODONTAL
CONDITIONS
 Classification of periodontal disease and condition (1999
international workshop for a classification of periodontal
disease and conditions)
The new classification (1999) is as follows:
1.GINGIVAL DISEASES
a) Dental plaque induced gingival disease.
(Can occur without attachment loss or on a periodontium with
attachment loss that is not progressing)
1.Gingivitis associated with dental plaque only:
a) Without other local contributing factors
b) With local contributing factors (See VIII A)

 2.Gingival diseases modified by systemic factors
a) Associated with the endocrine system
1. Puberty assoicated gingivitis
2. Menstrual cycle associated gigivitis
3. Pregnancy assoicated
a) gingivitis
b) pyogenic granuloma
1. Diabetes mellitus assoicated gingivitis
c) assoicated with blood dyscrasias
1. leukemia assoicated gingivitis
2. Other
3. Gingival diseases modified by medications
d) drug influenced gingival diseases
1. drug influenced gingival enlargements
2. drug influenced gingivitis
a) oral contraceptive assoicated gingivitis
b) other
4.Gingival diseases modified by malnutrition
a) ascorbic acid deficiency gingivitis
b) other
B. Nonplaque induced Gingival lesions
1. Gingival disease of specific bacterial origin
a. Nesseria gonorrhea assoicated lesions
b. Treponema pallidum associated lesions
c. Streptococcal species assoicated lesions
d. Others
2. Gingival disease of viral origin
a) herpes virus infection
3. primary herpetic gingivostomatitis
4. recurrent oral herpes
5. varicella zoster infections
 b. other
1. Gingival disease of fungal origin
a) candida species infections
1. generalized gingival candidiasis
b. linear gingival erythema
c. histoplasmosis
d. other
4. Gingival lesions of genetic origin
a. hereditary gingival fibromatosis
b. other
5. Gingival manifestations of systemic conditions
a. mucocutaneous disorders
1. lichen planus
2. pemphigoid
3. pemphigus vulgaris
4. erythema multiforme
5) Lupus erythematosus
6) Drug-induced
7) Other
 b. Allergic reactions
1) Dental restorative materials
a) Mercury
b) Nickel,
c) Acrylic
d) Other
2) Reactions attributable to
a) Toothpastes /dentifrices
b) Mouth rinses / mouth washes
c) Chewing gum additives
d) Foods and additives
3) Other
 6) Traumatic lesions (factitious, iatrogenic, accidental)
a) Chemical injury
b) Physical injury
c) Thermal injury
7) Foreign body reactions
8) Not otherwise specified (NOS)

 . Chronic Periodontitis
a) Localized
b) Generalized
III. Aggressive Periodontitis
a) Localized
b) Generalized
IV. Periodontitis as a manifestation of systemic diseases.
A) Associated with hematological. disorders.
1) Acquired neutropenia
2) Leukemias
3) Other
 B) Associated with genetic disorders
1. Familial and cyclic Neutropenia
2. Down syndrome
3. Leukocyte adhesion deficiency syndromes
4. Papillon - Lefevre syndrome
5. Chediak Higashi syndrome
6. Histiocytosis syndrome
7. Glycogen storage disease
8. Infantile genetic agranulocytosis
9. Cohen syndrome
10. Ehlers Danlos syndrome (Types IV and VIII)
11. Hypophosphatasia
12. Other
 V. Necrotising Periodontal Diseases
a) Necrotising ulcerative gingivitis
b) Necrotising ulcerative periodontitis
VI. Abscesses of the periodontium
a) Gingival abscess
b) Periodontal abscess
c) Periocoronal abscess
VII Periodontitis assoicated with endodontic lesions
A. Combined periodontal endodontic lesions
VIII. Developmental or Acquired Deformities and conditions
A. Localized tooth related factors that modify or predispose to plaque induced gingival disease / periodontitis
1. Tooth anatomic factors
2. Dental restorations / appliances
3. Root fractures
4. Cervical root resorption and cemental tears
 B. Mucogingival deformities and conditions around teeth
1. gingival / soft tissue recession
a. facial or lingual surfaces
b. interproximal (papillary)
2. lack of keratinized gingiva
3. decreased vestibular depth
4. aberrant frenum / muscle position
5. gingival excess
a. pseudopocket
b. inconsistent gingival margin
c. excessive gingival display
d. gingival enlargement (see section I, parts A3 and B4)
abnormal color
 C. Mucogingival deformities and conditions on edentulous ridges
1. vertictal and / or horizontal ridge deficiency
2. lack of gingiva / keratinized tissue
3. gingiva / soft tissue enlargement
4. aberrant frenum / muscle position
5. decreased vestibular depth
6. abnormal color

D. Occlusal trauma
1. Primary occlusal trauma
2. Secondary occlusal trauma
 Clinically healthy gingiva

Pale pink
Stippled
Thin margins
Firm and resilient
 DIAGNOSIS OF GINGIVITIS

Clinical signs
Redness
Swelling (due to increased vascular permeability; Lindhe
& Rylander, 1975)
Bleeding on probing (objective sign)
Exudate
Severity of gingivitis
Le & Silness Gingival index (1963)
 GINGIVITIS

CLINICAL PRESENTATION
Most common form of periodontal disease
PD: 1-3 mm
Clinical signs of inflammation
Plaque usually present; calculus often seen
Precedes periodontitis but does not always lead to
periodontitis
Reversible
RADIOGRAPHIC PRESENTATION
No bone loss seen
DIAGNOSIS OF PERIODONTITIS

Local factors
Age of onset
Family history
Clinical attachment loss
Rate/Duration of destruction/symptoms
Radiographic evidence of destruction
Nature and composition of microbial flora
Alteration in host immune response
 CHRONIC PERIODONTITIS

CLINICAL PRESENTATION:
Pocket depth >3mm
BOP, suppuration, other signs of active disease
Fremitus/tooth mobility
Furcation invasion
RADIOGRAPHIC PRESENTATION:
Horizontal to angular bone loss
RADIOGRAPHIC PRESENTATION:
Bone loss localized to the distal of the deciduous first
molar
Localized form <30% of sites involved
Generalized form >30% of sites involved

Slight 1-2 mm of attachment loss

Moderate 3-4 mm of attachment loss
Severe 5 mm of attachment loss
LOCALIZED AGGRESSIVE PERIODONTITIS
[PREPUBERTAL PERIODONTITIS]

CLINICAL PRESENTATION:
Little or no inflammation of gingiva
Usually amenable to standard periodontal therapy with
appropriate antibiotics
Seen after eruption of primary teeth

RADIOGRAPHIC PRESENTATION:
Bone loss localized to the distal of the deciduous first
molar
GENERALIZED AGGRESSIVE PERIODONTITIS
[PREPUBERTAL PERIODONTITIS]

CLINICAL PRESENTATION:
Extreme gingival inflammation
Rapid bony destruction
Often accompanied by sever functional defects of
neutrophils and monocytes
Otitis media and URTI also found
In some cases more sever lesions are refractory to
antibiotics

RADIOGRAPHIC PRESENTATION:
Generalized bone loss
ABSCESSES OF THE PERIODONTIUM

GINGIVAL ABSCESS
Is a localized purulent infection that involves marginal gingiva or interdental
papilla.
Confined to marginal tissues
Previously non-diseased site
Impaction of foreign material
Short history of onset

PERICORONAL ABSCESS
Localized purulent infection within the tissues surrounding a partially erupted
tooth.

PERIODONTAL ABSCESS
A periodontal abscess is a localized accumulation of pus within the gingival
wall of a periodontal pocket.
History of onset, progression, previous periodontal therapy
Continuity with gingival margin
Vitality of tooth
Presence/ absence of caries
Radiographic examination
Necrotizing Ulcerative Periodontitis (NUP)

CLINICAL PRESENTATION:
Usually observed in individuals with HIV;
immunosuppression; or severe malnutrition
Generalized or localized rapid soft and hard tissue
destruction
Bone sequestration, denudation
Teeth may become mobile
Spontaneous, usually nocturnal, gingival bleeding
Fetid breath
Intense, deep-seated pain
May be preceded by necrotizing ulcerative gingivitis
Periodontitis associated with endodontic lesions

A- Primary endodontic lesion

B- Primary endodontic lesion with secondary
periodontal lesion
C- Primary periodontal lesion
D- Primary periodontal lesion with secondary
endodontic lesion
E- True combined lesions
Periodontitis associated with endodontic lesions

A- Primary endodontic lesion

B- Primary endodontic lesion with secondary
periodontal lesion
C- Primary periodontal lesion
D- Primary periodontal lesion with secondary
endodontic lesion
E- True combined lesions
 Good prognosis: Control of etiologic factors and adequate peri-
odontal support ensure the tooth will be easy to maintain by
the patient and clinician.
Fair prognosis: Approximately 25% attachment loss and/or
Class I furcation involvement (location and depth allow proper
maintenance with good patient compliance).
Poor prognosis: 50% attachment loss, Class II furcation
involvement (location and depth make maintenance possible
but difficult).
Questionable prognosis: >50% attachment loss, poor crown-to
root ratio, poor root form, Class II furcations (location and
depth make access difficult) or Class III furcation
involvements; >2+ mobility; root proximity.
Hopeless prognosis: Inadequate attachment to maintain
health,comfort, and function