Case History and its relevance in periodontics

Introduction:
Critical procedures in the practice of periodontics are the examination
of the patient and the logical, orderly recording of patient data. A concise,
well-coordinated and well-designed examination paves the way for a logical
planning of treatment.
The objective of the case history are directed towards forming a
tentative diagnosis and determining any systemic factors that might affect the
diagnosis or influence the treatment plan. The findings of a case history must
be priced together so that they provide ‘a meaningful explanation of the
patient’s periodontal problem’.
Little and King in 1971 have presented reasons for evaluation of general
health in the dental office.
1. To identify patients with undetected systemic disease.
2. To identify patients who are taking drugs or indications that could
adversely interact with drugs prescribed or complicate dental treatment.
3. To provide information for the dentist to modify the treatment plan for
the patient in light of any systemic disease or potential drug
interactions.
4. To enable dentist to select and communicate with physician.
5. To help establish good patient-doctor relationship.
Thus a well-conceived evaluation of patient includes.
1. Case history
2. Recording appropriated findings on physical examination.
3. When indicated, ordering and interpreting necessary lab studies.
4. Initiating medical consultation when needed.

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Various stages in patient evaluation
History –
a) Chief complaint – is a description by the patient in his own words of
the symptoms related to the disease for which treatment is being sought.
From the standpoint of periodontal disease, it does not usually relate to
a symptom, except in the presence of ANUG or periodontal abscess.
This is because periodontal disease is so insidious that it may lack signs
and symptoms in early and moderately advanced stages.
The most commonly reported ‘chief complaint’ as an indicator of
periodontal disease includes
1. Bleeding gums.
2. Loose teeth.
3. Spreading of the teeth with the appearance of spaces where none
existed before.
4. Foul taste in the mouth.
5. Itchy feelings in the gums, relieved by digging with a tooth pick.
6. Vague feeling of discomfort or teeth that feel sore in the morning.
7. Pus discharge.
8. Complain of pain of varied type and duration.
9. Sensitivity when chewing.
10. Sensitivity to heat and cold.
11. Burning sensation in the gums.
12. Extreme sensitivity to inhaled air.
13. Receded gums.

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 When the patient complains of extreme symptoms, the process of taking
and recording history is dropped momentarily to deal with the acute lesion.
The chief complaint for most patients consists of low-grade physical
symptoms with possible evidence of a long-standing periodontal disease.

History of Present illness: is a chronological account of the problem

indicated by the chief complaint. In relation to chief complaint, previous
diagnosis and treatment rendered, as well as the effectiveness of those
treatments should be noted here.
Example: If the chief complaint is of bleeding gums then
History of Present illness will include
Example- The site of bleeding.
1. When first noted.
2. Whether it occurs spontaneously.
3. On Brushing / eating.
4. At night or with regular periodicity
5. Whether associated with menustrual period or other specific factors.
6. The duration of bleeding.
7. The manner in which it is stopped.
8. Any other aggravating / relieving factor.

Dental history
The patient as a natural part of periodontal examination accepts questions
relating to previous dental experiences.
It should include the following
1. A list of visits to the dentist should be supplied, including frequency,
date of the most recent visit, nature of the treatment etc.

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 2. Oral hygiene regimen of the patient should be noted – Tooth brushing
frequency, time of the day, method, type of brush and dentifrice,
interval at which brushes are replaced.
Other methods of mouth care-include
a) Use of mouthwashes
b) Finger massage
c) Interdental stimulation
d) Water irrigation & dental floss.
3. Any orthodontic, prosthodontic or restorative treatment undertaken.
4. A bad taste in the mouth, & are as of food impaction can be recorded.
5. Any tooth mobility can be recorded.
6. Past response to local & general anesthesia to be recorded.
7. History of previous periodontal problems including nature of the
condition & if previously treated, the type of treatment received &
approximate period of termination of previous treatment. Clinicians
favor different methods of conducting a dental history.
1) Questionnaire form
2) Face to Face interview.

Medical History- The health history can be obtained verbally by questioning

the patient & recording his/her responses on a blank piece of paper or by
means of a printed questionnaire

Can be relevant in 3 ways

1) The possible role that some systemic diseases, conditions or behavioral
factors may play in the cause of periodontal disease.

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 2) Oral infection may have a powerful influence on the occurrences &
severity of a variety of systemic diseases & conditions.
3) It may influence the therapist’s choice of treatment.
The medical history aids the clinician in the diagnosis of oral manifestation
of systemic disease & in the detection of systemic conditions that may be
affecting the periodontal tissue response to local factors or that which require
special precautions/ modifications in treatment procedures.
Fortunately, in most cares of systemic disease, there are no essential
contraindications to periodontal therapy (surgery). It should include the
following.
1) Is the patient under the care of a physician and if so, what is the nature
and duration of the problem and therapy. The name, address and
telephone number of physician should be recorded since direct
communication with him/her may be necessary.
2) Details on hospitalization and operations, including diagnosis, kind of
operation and events such as anesthetic, hemorrhagic or infectious
complications should be provided.
3) A list should be supplied of all medications being taken and whether
they were prescribed or obtained over the counter. The effects of these
medications should be carefully analyzed to determine effect on oral
tissues and also to avoid administering medications that would interact
adversely with them.
4) History of all medical problems taken.
5) Any possibility of occupational disease noted.

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 6) Abnormal bleeding tendencies such as nose bleed, prolonged bleeding
from minor cuts, spontaneous echymoses, tendency towards extensive
bleeding and excessive menustrual bleeding noted.
7) History of allergy including high fever, asthma, sensitivity to foods or
drugs like aspirin codeine, barbiturates, sulphanomides, antibiotics
procaine and also to dental materials such as eugenol or acrylic resins.
8) Information regarding onset of puberty and for females- menopause
menustral disorders hysterectomy, pregnancy & miscarriage noted.

Family history- is taken to determine if there is a familial predisposition to

disease or if there are diseases in which inheritance is an important factor. e.g.
Diabetes mellitus. A patient with a strong family history of Diabetes mellitus
& no apparent signs or symptoms should be evaluated periodically since
clinical features may appear later in life.
Other diseases include – Cancer, heart diseases, (hypertension) mental
disorders, seizure disorders may be familial.

Personal & Social history-

May assist in determining the patient’s response to the demands &
conflicts of modern society. It explains the untoward incidence of patients to
health problems & to therapeutic recommendations.
It includes
1) Patients occupations- Hazards associated with it.
2) Marital status
3) Diet
4) Use of alcohol, tobacco/ drugs or pan.

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 5) Possible exposure to various infectious disorders (Hepatitis B, herpes
or AIDS determined).
Thus, it is important in assessing whether the patient is in high-risk group
for conditions such as alcoholism, drug addiction or contagious diseases.
The personal interview allows the practioner to evaluate the patients
mental status in a non threatening atmosphere.
A questionnaire can be used in conjunction with a dialogue history to
obtain a more complete medical history.
Questionnaire-
1) May help a patient recall frequently used medications and
various symptoms that indicate diseases.
2) Assist dentist in determining which areas to emphasize and
further explore when conducting dialogue.
3) Also alleviate embarrassment regarding habits/ addictions,
venereal desire etc.

Examination of the patient- includes

1) Observation of patients general health and appearance .
2) Extraoral Examination.
3) Intraoral Examination.

1. Observation of patient’s general health and appearance.

➢ Commences when the patient enters the dental office.
➢ Body weight (Recent weight loss may indicate serious
underlying pathology). Eg: Cancer.
(Excessive weight may suggest risk of heart attack or stroke, Type
2 diabetes mellitus).

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 ➢ Breathlessness after minor exertion. (may indicate cardiac or
lung disease)
➢ Awkward gait (Degenerative joint disease, a nervous system
disorder such as multiple sclerosis or a muscle problem.)
➢ Complexion (pallor with anaemia and yellow with jaundice)
➢ Facial scarring (previous surgery, trauma and fights)

2. Extraoral Examination
is carried out using the principles of inspection, palpation and
probing examining, to the extent necessary oral and paraoral structures of
professional concern to the dentist.
Thus it includes,
1) Head, face and neck
2) Eyes, nose
3) Skin
4) Lips
5) Lymph nodes
6) TMJ
7) Salivary glands
8) Nails
9) Masticatory muscles.

1. Look for obvious lumps, defects, skin blemishes, moles and gross facial
asymmetry.
- Facial asymmetry seen in presence of regional
lymphadenopathy, periodontal and alveolar abscess, neoplasia
etc.

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 - Neck should be relaxed to examine the parotid glands (by visual
inspection and palpation)
Example: Unilateral swelling of parotid salivary glands suggests
a) Obstruction of the duct
b) Tumour
c) Abscess
d) Retrograde infection of the gland.
Bilateral swelling seen in
a) Viral infection. Example: mumps.
b) Degenerative changes. Example: Sialoris.

2. Eyes
Blinking rate decrease may indicate a psychological problem or
Parkinson’s disease. Increase may indicate anxiety or dryness of eyes.
Example: Sjogren’s syndrome.
Limitation of ocular movement - fracture of Zygoma
Unilateral Exophthalmos - tumors of orbit or cavernus sinus
thrombosis.
Bilateral - Hyperthyroidism, Graves Diseases
Ulceration of conjunctiva- Behcets disease, Mucous membrane
pempigoid
Conjunctival pallor - anaemia
Blue Sclera - Rarely osteogenesis imperfecta
Yellow - Jaundice
Corneal scarring - Mucous membrane pemphigoid
Dry eyes - Sjogren’s syndrome.
3. Nose - By visual inspection in conjunction with questions regarding nasal

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obstruction and associated mouth breathing.
Eg., Gingivitis associated with mouth breathing.

4.Skin - May reflect manifestation of systemic disease but most helpful in

differential diagnosis of dermatological lesions that appear simultaneously in
the oral cavity.
Lichen Planus
Pemphigus Vulgaris
Pemphigoid
Lupus Erythamatosis
Erythema Multiformae
Dermatitis Herpetiformis Linear

5.Lips - By visual examination

- Note muscle tone {Drooping of the commissure and inability to
pursue the lips with Bell’s palsy}
- Any change in color or texture
- Ulceration {Erythema Multiformae)
- Patches
- Herpetic lesions
- Angular chelities
- Also note lip competency/ incompetency
-
6.Lymph Nodes – Examined by extraoral, bimanual palpation from behind
the patient.
Do not extend neck since sternomastoid must be relaxed.

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 Use pulp of fingertips and try to roll the gland against adjacent
harder structures.
Submental - Tip head forward and try to roll the node against inner aspect of
mandible.
Submandibular - Same but with patient’s head tipped to the side being
examined.
Jugulodigastric - Move the ant border of sternomastoid back.
Jugulo-omohyoid – Move post border of sternomastoid forward
If node palpable, record
Site, size, texture
Rubbery hard {Hodgkins}
Stony hard {secondary carcinoma}
Tenderness to palpation {infection}
Fixation to surrounding tissues {Metastasis cancer}
Coalescent {TB}
Number of nodes {Multiple - Glandular fever and leukemia}
If more than 1 node palpable - examination of body for generalized
lymphadenopathy and blood tests.

Palpable Node characteristics

Acute infection - Large, soft, painful, mobile, discrete, rapid, onset
Chronic infection {TB or Leprosy} – Large, firm, less tender, mobile
Lymphoma - Rubbery hard, matted, painless and multiple
Metastatic cancer - stony hard, painless, fixed to underlying tissues
Inflammatory Node - Enlarged, palpable, tender and fairly immobile

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7.Salivary glands
1. Parotid – Palpate for enlargement or tenderness. {Gland is usually located
distal to the ascending ramus of the mandible}
Diagnosis is - lower part of the ear lobe may be turned outward if glands
are swollen.

2. Submandibular S.G. -> Use index and middle finger of hand intraorally
and the same fingers of the other hand extraorally.
Palpate the gland above and below mylohyoid and do not neglect to
examine the ducts of the gland for calculi

8.TMJ -> Investigate for

1) Range of movement -> Measure maximum pain – free jaw opening at
central incisor tips { Female - 35 mm, Male - 40 mm]
Identify whether limitation is caused by
1} Pain
2} Physical obstruction
3} Lateral deviation
- Lateral deviation on openings usually towards the affected size.
- Lower limit for normal lateral excursion is 8mm
- If left TMJ painful, then right lateral excursion is decreased
Mandibular movement may be limited by
1. Infections {pericoronitis, space infections, tonsillitis,
mumps,osteomylitis}
2. Trauma
3. TMJ disorders

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 4. CNS disorders {tetanus, meningitis, Parkinson’s disease}
5. Medication eg., phenothiazine group of drugs
6. Neoplasm
7. Psychological

2) Tenderness -> By bimanual palpation by pressing over lateral aspect

of joint. Follow this intra-auricular palpation by placing the little finger
into external auditory meatus and pressing forwards.
3) TMJ sounds ->
Click -> caused by sudden movement of disc relative to condyle.
Crepitus is a prolonged, continuous, grating or crackling nose. Eg., occurs
with degenerative diseases and acute inflammation {eg., after trauma}
TMJ locking -> Due to malposition and distortion of the disc, which allows
the condyle to rotate but not translate. Rarely jaw may open but fail to close
easily.
Dislocation -> Condyle displaced over articular eminence. This may be
caused by trauma or yawning.

9.Muscles of mastication
Examine for tenderness
Muscles should be tested where they attach to bone (body of muscle is not
usually tender)
a) Masseter -> Origin – From anterior 2/3 of Zygomatic arch
Insertion - Outer aspect of angle of mandible
Use bimanual palpation with finger of one hand intraorally, index and
midfinger of other hand on the cheek

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 b)Temporalis - Origin - From superior and inferior temporal lines above the
ear.
-Insertion -Coronoid process and anterior border of
ascending ramus.
Palpate origin extraorally and insertion intraorally

c) Lateral Pterygoid -Origin - Lateral surface of lateral pterygoid plate

-Insertion - Anterior border of condyle and disk
Not accessible to palpation.
.
d ) Medial Pterygoid - Origin - Between Medial and lateral pterygoid plates
-Insertion - Medial surface of angle of mandible.
{Not accessible to comfortable palpation}

Intraoral examination: should include

- General appraisal of patient’s oral hygiene.
- Soft tissues like
Labial / buccal Mucosa
Palate
Floor of the mouth
Tongue
Saliva

Palate – Depress tongue using a tongue spatula. Visually examine and palpate
hard palate. Visually examine and palpate soft palate
Floor of the mouth – Viewed with tip of tongue raised to touch palate.

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Tongue – Dorsum (Inspect at rest and protruded). Lateral border (use gauze
to hold tip of tongue and move it to one side).

Saliva – Adhesion of mirror to buccal mucosa may indicate decreased salivary

production. Bubbles of air in saliva - decreased salivary production. Note
quality of saliva (sticky, tenacious saliva).

Examination of Dentition
The examination of the teeth includes an assessment of the number,
position, contact relations, missing (congenital, unerupted or impacted)
decayed and filled teeth. Also, an assessment of developmental defects,
anomalies of tooth form, hypersensitivity and wasting diseases of the teeth are
done
Proximal contact provides principle defense against food impaction invasion
with subsequent damage to apical tissues.
In the presence of increased mobility, plunger cusps and inadequate marginal
ridges -> food impaction in posterior teeth is a distinct possibility where there
are only light contacts.
1. Poor or faulty contact -> Teeth with facial or lingual inclination- Here
gingival papillae may have inadequate protection and adjacent marginal
ridges deflect the thrust of bolus and direct food onto occlusal table and fossae
of teeth.
They may cause distal movement of distal molars and increased mobility
associated with occlusal trauma or periodontal diseases.
2.Inconsistent Marginal ridges -> Refers to adjacent marginal ridges at
differing occlusal levels.This contact cannot protect underlying structures
from trauma, food impaction or retention

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3.Malposed and tilted teeth-
o Tooth in buccal version -> presence of inadequate buccal bony plate is
a strong qualifying factor in flap reflection and in location of vertical
releasing incisor.
o Rotated lower canine -> because of long overall cross section of tooth
and drifting of lateral incisor against it, root proximity is found.
o Deep pocket in mesial aspect of second molar tilted into space of
unreplaced missing first molar.

4.Extrusions and Intrusions -> Tooth can be a point of premature contact

and trigger destructive parafunctional habits.
Its implication in construction of FPD and RPD is important. The tooth may
draw its alveolar housing with it, upsetting the configuration of crestal bone
between over–erupted tooth and its neighbors and creating unfavourable
crown / root ratio.

5.Food impaction and retention -> Due to uneven / irregular occlusal plane
-> food forced into and retained in sulcul region.

Contact relations – are significant because

o Slight open contacts permit food impaction.
o Abnormal contact relationships like crowding, malposition and rotation
may initiate occlusal changes such as a shift in the median line between
central incisors, labial version of maxillary canine, buccal or lingual
displacement of posterior teeth and an uneven relationship of the
marginal ridges.

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 o The tightness of contacts checked with a dental floss /or by clinical
observation & patients history of food being wedged between teeth.

Assessment of decayed, missing & filled teeth

➢ Often is correlated with dental history.
➢ Gives an account of patient’s motivation, awareness & oral
hygiene status.
➢ The number of teeth affected by affected by caries is assessed.

Hypersensitivity- Usually root surface exposed by gingival recession may be

sensitive to thermal changes or tactile stimulation.
Patients often direct the operator to sensitive areas and may be located
by gentle exploration with a probe or cold air.

Etiology or factors contributing include

A. Exposure of cementum and dentin
1. Gingival recession
a. Pathologic Eg. Inflammation that may
initiate proliferation of junctional epithelium
along root surface.
b. Traumatic-Eg. Toothbrush with an abrasive
dentifrice.
2. Periodontal procedure for pocket elimination.
B. Anatomy of CEJ
A zone of dentin occurs in enamel & cementum in
approximately 10% of teeth .

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 C. Loss of cementum
Through abrasion, erosion, dental caries, SRP polishing with an
abrasive agent or air abrasive instrument. The dentin is uncovered
and dentinal tubules are exposed.
D. Loss of enamel
The dietary erosion, fracture, toothbrush abrasion, occlusal wear
and parafunctional habits. When enamel erosion results from
repeated induced vomiting of bulimia, the teeth may be sensitive.

Patients should be explained

1. Appears as a result of exposure of dentin, which is inevitable if plaque
and calculus buried in the root, are to be removed.
2. It slowly disappears over a few weeks.
3. Plaque control is important for decrease in Hypersensitivity.
4. De-sensitising agents can be used but do not produce immediate relief
and should be used for several days or weeks.

Mechanism of Action→ 1] Closure of dentinal tubules.

a) Formation of smear layer produced by burnishing exposed
surface- coating.
b) Formation of insoluble protein precipitates with in dentinal
tubules→ coagulation.
c) Impregnation of dentinal tubules with calcific barrier.
d) Sealing of dentinal tubules
2] Formation of Secondary dentin- Irritation and stimulation from
external agents over time results in build up of Secondary dentin.

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Wasting disease of teeth → defined as any gradual loss of tooth substance
characterized by formation of smooth, polished surface with out regard to
possible mechanism of the loss.

1) Attrition- Occlusal wear resulting from functional contact with opposing

teeth.
- A certain amountt of physiological attrition is common.
Etiology:
1) Bruxism (1988- Seligman)
2) Age (1990- Salonen).

Accelerated attrition usually results in formation of a facet.

A wear facet is a worn and flattened area on a tooth surface that occurs
as a result of attrition, bruxism or malocclusion .
❖ When active tooth grashing occurs→ enamel rods fracture, which is
highly reflective to light → Thus shiny, smooth and curvilinear facets
formed.
❖ Vary in size and location depending on whether produced by
physiologic or abnormal wear.
❖ Not sensitive to thermal or tactile sensation.
❖ Angle of facet to tooth surface is significant.
Horizontal → Direct forces in the vertical exist to which
periodontium can adapt effectively.
Angular→Direct occlusal forces laterally and increase risk of
periodontal consequences.

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 ❖ Excessive wear → flat or cuneiform occlusal surface and obliteration
of cusps.
Reversal of occlusal plane of premolar in advanced stages of wear.

2) Abrasion→ Refers to loss of tooth substance indicated by mechanical wear

other than mastication.
- Saucer shaped or wedge shaped indentations with a smooth shiny
surface.
- On exposed cementum than enamel or dentin.
Etiology-
1) Tooth brushing with on abrasive dentifrice (continued exposure with
decalcification of enamel by locally formed acids→ result in loss of
enamel followed by loss of dentin).
2) Action of clasps.
3) Habits such as holding objects (Bobby pin or tacks) in teeth → abrasion
of incisal edges.

3) Erosion- (Cuniform defect)

• Sharply defined wedge shaped depression
• Affects group of teeth generally
• In early stages confined to enamel, then extends to involve dentin
and cementum.

Etiology- 1) Decalcification by acid beverages, cirtrus fruits along with

combined effect of acid salivary secretion and friction. Sugannes 1977→

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referred dentoalveolar ablations and attributes them to forceful frictional
actions between oral soft tissue and adjacent hard tissues.

Sensitivity to percussion
• Feature of acute inflammation of the periodontal ligament.
• Gentle percussion at different angles to long axis aids in localizing site
of inflammatory involvement.

Examination of Occlusion-
• Can detect conditions such as irregularly aligned teeth, supraerupted or
extruded teeth, overbite, open bite, cross bite, improper proximal
contacts and plunger cusp ( associated with areas food impaction )
• Dentitions that appear normal when jaws are closed may present
marked functional abnormalities.
1. Overbite and overjet → in anterior region may cause
impingement of teeth on gingiva and food impaction followed by
gingival inflammation, gingival enlargement and pocket
formation.
(Alexander 1970)→ stated this effect is controversial.
2. Open bite→ Here abnormal vertical spaces exist between
maxillary and mandibular teeth .
- Most often anteriorally than posteriorly
- Decreased mechanical cleansing by passage of food may lead to
accumulation of debris, calculus formation and even extrusion .

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 3. Cross- bite →
1. Trauma from occlusion
2. Food impaction
3. Spreading of mandible teeth
4. Associated gingival & periodontal disturbances

4. Food impaction / Plunger cusps→ is forceful wedgign of food into

periodontium by occlusal forces.
➢ Maintained by integrity and location of proximal contacts along
with contour of marginal rides and developmental groove.
➢ As teeth wear down the original convex proximal surfaces become
flattened and wedging effect of opposing cusp is exaggerated
➢ Cusps that tend to forcibly wedge food into interproximal
embrasures- plunger cusps
➢ Also observed when missing teeth not replaced and relation between
proximal contact of adjacent teeth is altered.
Factors leading to the food impaction
1. Uneven occlusal wear.
2. Opening of contact point as a result of loss of proximal
support
3. Extrusion
4. Congenital morphologic abnormalities
5. Improperly constructed restorations.
In addition to collecting standard data on static occlusal relationship, a
functional evaluation of occlusion is done which includes
1) Identification of Intercuspal zones of contact

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 3. By placing mylar strips between teeth and ask patient to close
and hold
4. By occlusal indicator wax or marking ribbon
5. Presence or absence of contact registered.
2) Excursive movement -> The quality of tooth contact patterns during
mandibular movement out of Intercuspal zones of contact recorded by
asking patient to move into protrusion and laterotrusion (left and right)

Pathologic tooth Migration – Refers to tooth displacement that results when

the balance among the factors that maintain physiologic tooth position is
disturbed by periodontal diseases.
Most frequently occurs in anterior region, teeth can move in any direction, but
usually accompanied by mobility and rotation.

Pathogenesis – Alteration in any of the following leads to pathologic

migration
1. Tooth morphologic features.
2. Cuspal inclination.
3. Presence of full complement of teeth.
4. Physiologic tendency towards mesial migration.
5. Contact point relation.
6. Axial inclination of teeth.
7. Attrition.

Thus weakened periodontal support leads to

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 ▪ Inablity to maintain its normal position in the arch and moves
away from the opposing force unless restrained by proximal
contact.
▪ Forces acceptable to an intact periodontium become injurious
when periodontal support decreases.
Example: Tooth with abnormal proximal contact.
Here anterior component of force becomes a wedging force
and moves tooth occlusally..

Changes in force exerted to teeth

1. Unreplaced missing teeth occur in mesial direction with tilting or
extrusion.
2. Failure to replace first molar
-Second or third molar tilt -> decrease in vertical dimension.
-Premolars move distally and mandiblur incisors drift lingually
-Anterior Overbite increased.
-Maxillary incisors pushed labially and laterally
-Anterior teeth extrude
-Diastema.
3. Trauma from occlusion
4. Pressure from tongue
5. Pressure from granulation tissue of periodontal pockets.

Trauma from occlusion

• Refers to tissue injury, when occlusal forces exceed the adaptive
capacity of tissues.

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 6. Periodontal findings that suggest the presence of Trauma from
occlusion include
a) Excessive tooth mobility
b) Evidence of widened periodontal space.(R/G)
c) Vertical or angular bone destruction
d) Infrabony pockets.
e) Pathologic migration (especially of anterior teeth)

7. Usually examination of Trauma from occlusionis by Fremitus test.

Fremitus (functional mobility) is measurement of vibratory patterns of the
teeth when the teeth are placed in contacting positions or movement.Can often
be detected earlier than bidigital tooth mobility and has been associated with
presence of inflammation and increased bone and attachment loss, when
compared to teeth without fremitus ( Pihlstrom 1980).

Method – The index finger is placed on the labial surface of maxillary teeth
and patient is asked to grind in the lateral and protrusive movements. Any
movement seen or felt is considered fremitus.
Class I -> Mild vibration or movement detected.
Class II -> Easily palpable vibration but no visible movement.
Class III -> Movement visible with naked eyes.
Fremitus differs from tooth mobility in that Fremitus is tooth
displacement created by patient’s own occlusal form.
Therefore amount of force varies greatly from individual to individual.
For posterior teeth, it can be used but with minimal confirmatory
authenticity.

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Suppuration -> Presence of an abundant number of neutrophils in gingival
fluid transforms it into a purulent exudate.
Formed in inner pocket wall.
Diagnosis is by placing the ball of the index finger along lateral aspect of
marginal gingiva and applying pressure in a rolling motion towards the crown.

Habits - A good searching record of oral habits practiced by the patient

should be included in the history.
A habit can be defined as the tendency towards an act that has
become a repetitive performance, relatively fixed, consistent and easy to
perform by the individual.

Classification
1) William James -
1.Useful habits
2.Harmful habits
2) Empty habits
Meaningful habits
3) Pressure habits
Non-pressure habits
Biting habits
4) Simm’s and Finn –
a) Compulsive habits
b) Non compulsive habits
Primary
- Thumb sucking
- Tongue thrusting

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 b) Secondary
- Along with primary habits.

Bruxism - is the clenching or grinding of teeth when the individual is not

chewing or swallowing
▪ is defined as diurnal or nocturnal parafunctional activity including
clenching, bracing, gnashing & grinding of teeth.
▪ Occur as brief, rhythmic strong contractions of the jaw muscles during
eccentric lateral jaw movements. (When this occurs in maximum
intercuspation- clenching).
▪ 5% of individual’s brux to an unusually active extent at any one time
(Rugh 1988).
▪ Occurs equally in children and adults.
▪ May lead to tooth wea,r fracture of the teeth or dental restorations , or
uncosmetic muscle hypertrophy.
Etiology : Etiology unknown, but believed to be a CNS instability that occurs
idiopathically.
➢ Most people are not aware of their bruxism habit unless it is
audible or brought to their attention.
➢ Thus considered as a mutifactorial, psychosomatic phenomenon,
with individuals displaying aggressive, controlling, precise
energetic personality types on one hand and anxious tense types
on the other. These psychological characteristics fall with in the
normal limits of personality structure.
Olkinuora in 1974 divided bruxers into 2 categories-
1) Stress bruxists ( Bruxism associated with stressful events)
2) Non-stress bruxists ( Bruxism with no such association)

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 3) Hereditary bruxism falls under (2).

Diagnosis – History and clinical examination

1) Wear from bruxism, usually seen as facet patterns.
2) Confirmed by observing excessive tooth wear, fracture of teeth and
restorations.
3) History of sore or stiff jaws and muscle pain in the morning and TMJ
pain and discomfort.
4) Roommate/ spouse may relieve sounds of nocturnal grinding.
5) Electromyographic examination to check for hyperactivity of muscles.
-Bruxism can occur at any stage of sleep usually (stageII) i.e. transition from
a deeper stage of sleep to a lighter stage (Harada and Satoh – in 1971).

Treatment – Nightguard appliances and maxillary stabilisation appliances are

most effective in managing bruxists.
There is no association between bruxism and gingival inflammation
(Clark 1981).

Tongue thrust- defined as a condition in which the tongue makes contact

with any teeth anterior to the molars during swallowing.
Etiology- as stated by Fletcher.
1. Genetic factors like anatomic or neuromuscular variations in the
orofacial region. Eg: Hypertonic orbicularis oris activity.
2. Learned behaviour -> Pre-disposing factors
- Improper bottle feeding
- Prolonged thumb sucking

28
 - Prolonged tonsillar and urinary tract infections
- Prolonged duration of tenderness of gum / teeth -> resulting in
change in swallowing pattern to avoid pressure on tender zone.
3. Maturational – Retention of infantile swallow.
4. Mechanical restrictions -> Macroglossia, constricted dental archs and
enlarged adenoids.
5. Neurological disturbance -> Hyposensitive palate and moderate motor
disability.
6. Psycogenic factors -> Result of forced discontinuation of other habits
like thumb sucking.

Classification of tongue thrust (Braner and Holt)

Type I – Non – deforming tongue thrust.
Type II - Deforming tongue thrust
Subgroup 1 – Anterior open bite
2 – Anterior proclination
3 – Posterior cross bite

Type III - Deforming lateral tongue thrust

Subgroup 1 – Posterior open bite
2 – Posterior cross bite
3 – Deep overbite

Type IV – Deforming anterior and lateral tongue thrust

Subgroup 1 – Anterior and Posterior open bite
2 – Proclination of anterior teeth
3 – Posterior Cross bite

29
Non – deforming ->implies that interdigitation of teeth and profile are with in
normal range.
Deforming -> Always associated with a dento – alveolar defect.

Simple Complex
1- Normal tooth contact during 1– Teeth apart swallow
swallowing
2- Presence of anterior open bite 2- Anterior open bite can be diffuse
or absent
3- Tongue is thrust to help 3- Contraction of circum - oral
establish anterior lip seal muscles during swallowing.

Clinical features in diagnosis - Proclination of Anterior teeth

Anterior open bite
Bimaxillary. Protrusion
Posterior cross bite
Posterior open bite in case of lateral tongue thrust
Management – Habit interception followed by correction of malocclusion.

Mouth breathing: can result in altered jaw and tongue posture which alters
oro– facial equilibrium, leading to malocclusion.

Classification: Obstructive
Habitual

30
 Anatomic

Etiology : Obstructive -> Complete or partial obstruction of nasal passage.

1. Deviated nasal septum
2. Nasal polyps
3. Chronic inflammation of nasal mucosa
4. Localized benign tumors
5. Congenital enlargement of nasal turbinates
6. Allergic reaction of nasal mucosa
7. Obstructive adenoids.
Habitual - Here, it is a deep-rooted habit that is performed unconsciously.
Anatomic – Lip Morphology: example: Short upper lip.
Pathophysiology – During mouth breathing
- Lowering of the mandible.
- Positioning of tongue downwards and forwards.
- Tipping back of head.
Lowering of tongue and mandible upsets oro– facial equilibrium and there is
unrestricted buccinators activity which influences position of teeth and growth
of jaws.

Clinical features–
1. Long and narrow face
2. Narrow nose
3. Short and flaccid upper lip
4. Contracted upper arch with posterior cross bite
5. Increased over jet due to flaring of incisors
6. Anterior marginal gingivitis -> due to drying of gingiva

31
 7. Dryness of mouth leading to caries
8. Anterior open bite can occur.

Diagnosis –
1) History
2) Clinical examination – by various tests and clinical examination.
1. Mirror test -> Double ended mirror is held between nose and
mouth. Fogging on nasal side indicates nasal breathing.
2. Water test -> Fill mouth with water and retain for 2-3 minutes.
3. Cotton test -> A butterfly shaped piece of cotton is placed over
the upper lip below the nostrils. Fluttering downwards indicates
nasal breath.

Treatment –
1. Removal of nasal obstruction
2. Interception of habit -> Vertibular screen
3. Rapid maxillary expansion -> increased nasal airflow and decreased
nasal resistance.

Mouth odors -> Halitosis also termed as fetor exore, fetor oris and oral
malodor.
❑ Is foul or offensive odor emanating from the oral cavity.
❑ May be of diagnostic significance
❑ Caused primarily by Volatile sulphur compounds, specifically,
hydrogen sulphide and methyl mercaptan, which result from bacterial
putrefaction of proteins containing sulphur amino acids. Thus these

32
 could be involved in the transition from health to gingivitis to
periodontitis.

Intraoral -> Local

Extraoral -> Systemic

Local causes
1) Tongue and gingival sulcus
2) Retention of odoriferous food particles on and between the teeth
3) Necrotizing Ulcerative Gingivitis
4) Dehydration states
5) Caries
6) Artificial Dentures
7) Smokers breath
8) Healing surgical or extraction sockets.

Systemic causes
1) Infections or lesions of respiratory tract (bronchitis, pneumonia and
bronchiectasis)
2) Alcoholic breath
3) Acetone breath of diabetes mellitus
4) Uremic breath of kidney dysfunction
5) Odors that are excreted through lungs from aromatic substances in
blood stream

Diagnosis

33
 1) History mainly complaint of the patient regarding foul odor is the first
recognition of halitosis.
2) Organoleptic scoring scale -> or use of one’s nose to smell and rank the
intensity of odors emanating from the mouth. This is the Gold Standard
for measurement of oral malodor.
1. Absence of odor
2. Questionable to slight odor- Odor is deemed to exceed the
threshold of malodor detection.
3. Moderate Malodor - odor definitely detected
4. Strong Malodor - Malodor objectionable but examiner can
tolerate
5. Severe Malodor - Overwhelming malodor
These scores vary from 0-5 point scale.
Disadvantage: Uncomfortable procedure.

3) Measurement of Volatile Sulphur compounds

Lab–base -> discovered by Joseph Tonzetich in 1970’s, used a gas
chromatograph equipped with a selective flame detector to demonstrate
Volatile Sulphur compounds.
Chair – side -> In 1990 by Rosenberg
- Measure Volatile Sulphur compounds in exhaled air. This
Portable instrument is referred to as Halimeter.
- Significantly correlates with organoleptic score

Disadvantage

34
 1. Can never be validated by gas chromatography in regard to
specificity of sulphur compounds detected.
2. Volatile Sulphur compounds detected by halimeter accounts for
only 18- 41% of organoleptic scores indicating that other important
odorants such as volatile fatty acids and cadaverine are not detected
by halimeter.
3. Sensors for Volatile Sulphur compounds have been integrated into
periodontal probes and paddles, which can be placed directly into
pocket or tongue ( Diamond probe) again correlating with
organoleptic scores.
4. A volatile sulphur compound moniter, used a zinc oxide thin film
semiconductor sensor correlated with organoleptic scores (useful
substitute for nose).

Treatment
1. Remove etiology
2. If oral malodor is originating from tongue then 1) tongue brushing
Otherwise
1) Tooth brushing
2) Use of mouthrinses containing essential oils, Chlorhexidine,
Zinc chloride, cetylpyridinium chloride, chlorine dioxide.

Examination of the periodontium

The periodontal examination should be systematic, starting in the molar
region in either the maxilla or mandible and proceeding around the arch.
Charts to record the periodontal and associated findings provide a guide
and also help in evaluating the response to treatment and for comparison at

35
recall visits. Computerized dental examination systems using high resolution
graphics and voice activated technology permit easy retrival and comparison
of data {Baum Gartner 1988 }

1) Plaque and Calculus

1. Supragingival Calculus -> can be directly observed and amount
measured with a calibrated probe.
2. Subgingival Calculus -> Each tooth surface is carefully
checked to level of gingival attachment with a sharp No. 17or
3A explorer. Warm air can be used to deflect gingiva and aid in
visualization of calculus.
2) Gingiva - {1} Must be dried before accurate observations can be
made.
- Light reflection from moist gingiva obscures details
- Visual Examination and Exploration with instrument and gentle
palpation for detecting pathologic alterations in normal features
performed.
Gingival features include - 1. Color 2. Size 3. Contour
4. Consistency 5. Surface texture 6. Position

Color - Defined as coral pink and produced by tissues vascularity,

epithelial keratinisation and physiologic pigmentation of the individual
In Chronic inflammation -> Red or bluish red color is because of vascular
proliferation and decrease of keratinisation due to epithelial compression by
inflamed tissue.
Venous stasis -> contributes to bluish hue.

36
In acute inflammation -> Color change could be marginal, diffuse or patch
like depending on underlying acute condition.
In ANUG → Marginal
In AHGS→ Diffuse
In acute reaction to chemical irritation→ patch like or diffuse.
- Vary with intensity of inflammation In severe acute
inflammation red color gradually becomes dull whitish gray.

Metallic pigmentation-
Heavy metals (Bismuth, arsenic, Mercury, Lead, Silver) produce a
black or bluish line in the gingival margin.
Also as isolated black blotches involving interdental, marginal and
attached gingiva.

Color changes associated with systemic factors

Endogenous oral pigmentation due to melanin, bilirubin or iron.
Melanin → Increased in Addison’s disease, Peutz-Jeghers syndrome
And Albrights syndrome

Bilirubin→ Increased in jaundice ( Yellowish)

Iron→ Increase in hemochromatosis (blue- gray oral mucosa)

Endocrine and Metabolic disturbances

-Diabetes mellitus and pregnancy, Blood dyscrasias such as
Anaemia, Polycythemia and Leukemia.
Exogenous factors include-

37
 Atmospheric irritants like coal & metal dust, coloring agents in food
and lozenges.
Localized bluish-black areas of pigment – Amalgam tattoo.

Size → Sum total of cellular and inter cellular elements and their vascular
supply.
In inflammatory conditions→ diffuse edema with puffiness.

Contour → is related to teeth, underlying bone and presence or absence of

disease.
` Normal gingiva- Tissue fills interdental space and gingival margin ends
in a knife like edge coronal to CEJ and Interdental papilla are tucked behind
contact points.
This depends on factors like
1. Adjacent teeth
2. Facial lingual position
3. Mesial distal position
4. Spacing of teeth
5. Carious lesions
6. Proximal contact.

Consistency- Normal –Firm and resilient produced by collagenous nature of

lamina propria, gingival fibers and its contiguity with mucoperiosteum of
alveolar bone.
In chronic gingivitis depending on destructive (edematous) and
reparative changes (fibrotic) consistency varies.

38
Surface texture → Normally stippled with orange peel appearance.
- Evaluated by drying the gingiva.
In chronic inflammation → smooth shiny or firm and nodular depending on
whether the changes are exudative or fibrotic.
In atrophic gingivitis → epithelial atrophy is seen.
In Desquamative gingivitis → peeing of surface
In Drug induced gingival overgrowth → Nodular surface and leathery texture.

Position-
Recession→ Exposure of root surface by on apical shift in position of gingiva.
Actual → Level of epithelial attachment on tooth.
Apparent→ Level of crest of marginal gingiva.
Visible→ clinically observable
Hidden → covered by gingiva and measured only by inserting probe to
level of epithelial attachment.

Etiology→ Result of cumulative effect of minor pathologic involvement/

repeated minor direct trauma to gingiva.
1. Faulty toothbrushing technique
2. Tooth malposition
3. Friction from soft tissues.
4. Gingival inflammation
5. Abnormal frenal attachment.

Susceptibility is increased by

39
 1. Position of teeth in arch
2. Root bone angle
3. Mesiodistal curvature of tooth surface
4. Fenestrations and Dehiscence’s.

Clinical significance –
1. Increased susceptibility to caries
2. Increased sensitivity due to abrasion/crown exposed by retention.
3. Hyperemia of pulp and associated symptoms.
4. Oral hygiene problems and plaque accumulation.
5. Can create open embrasures and expose radicular flutings.

Presurgical examination and correlation of recession using classification

proposed by Miller (1982).
Class I – Marginal tissue recession that does not extend to mucogingival
junction. No loss of bone or soft tissue interdentally. (Narrow or wide).
Class II- Extends to or beyond the Mucogingival junction (Wide and Narrow).
Class III- Marginal tissue recession extends to or beyond Mucogingival
junction. There is bone/soft tissue loss interdentally or there is malpositioning
of teeth.
Class IV- With serve bone/soft tissue loss interdentally and severe
malpositioning of teeth.

Sullivan and Atkins in 1968

Stage I – Shallow Narrow
Stage II – Shallow Wide
Stage III – Deep Narrow

40
Stage IV – Deep Wide.

Assessment of Tooth Mobility-

All teeth have slight degree of physiologic mobility which varies at
different times of day and also for different teeth ( O’ Leary 1963).
• Greatest on arising in morning and progressively decreases. The increase
is due to slight extrusion of tooth because of limited occlusal contact
during sleep. During waking hours mobility is decreased by chewing and
swallowing forces which intrude teeth into the sockets.
• Single tooth have more mobility.
• Principally in a horizontal direction although some axial mobility do occur.

Occurs in 2 stages
1) Initial or intrasocket stage- where tooth moves with in the confines
of the periodontal ligament. Associated with viscoelastic distortion
of ligament and redistribution of periodontal fluids, inter bundle
content and fibers ( Kurashima 1965). Initial movement with forces
of 100 lb and is in order of 0.05 – 0.10mm.
2) Secondary stage –Occurs gradually and entails elastic deformation
of alveolar bone in response to increased horizontal forces (
Muhleman 1965).
Forces of 500lb → 100 to 2000 microns- Incisors
50 to 90 microns- Canines
8 to 10 microns- Incisors
40 to 80 microns- Molars
When the force is discontinued the teeth return to original position in 2 stages.

41
 1) First is immediate spring like elastic coil.
2) Second is slow, asymptomatic recovery movement. The recovery
movement is pulsating which is associated with normal pulsation of
periodontal vessel.

Etiology-
1. Loss of tooth support (bone loss) Amount of mobility depends on
severity and distribution of bone loss at individual root surface , length
and shape of roots and root size compared to crown.
Because bone loss results from a combination of factors, severity of tooth
mobility not necessarily correspond to amount of bone loss.
2. Trauma from occlusion → Injury produced by
a) Excessive occlusal forces
b) Occlusal habits E.g. Bruxism and clenching. Mobility produced
by Trauma from occlusion occurs initially as resorption of
cortical layer of bone, leading to decrease fiber support and later
as on adaptation phenomenon in a widened periodontal space.
3. Extension of inflammation form gingiva or from periapex into
periodontium.
4. Periodontal surgery (Temporarily)
5. Increased in pregnancy and associated with menstrual cycle or use of
hormonal contraceptives (due to physico chemical changes in
periodontal tissues).
6. Pathologic procedures of jaws that destroy alveolar bone/roots of teeth
e.g. Osteomylitis and Jaw tumors
7. Higher proportion of Campylobacter rectus, Peptostreptococcus Micros
→ This is a hypothesis ( Grant 1995).

42
Evaluation of Tooth Mobility
Mobility is graded clinically as follows – The tooth is held firmly
between the handles of 2 metallic instruments or with metallic instrument and
1 finger and an effort is made to move it in all directions and it is graded as
follows.
Miller’s Mobility index –1950
Mobility1 – First distinguishable sign of movement. greater than normal.
Mobility2 – Movement of 1 mm from normal position in any direction.
Mobility 3 – Greater than 1mm and Rotation or depression.
Fleszar etal –1980 used a modification of Miller’s scale.
Class O – Physiologic mobility
Class I – Slightly increased mobility
ClassII – Definite to considerable increase in mobility, but no impairment of
function.
Class III – Extreme mobility faciolingually/ mesiodistally combined with
vertical displacement.

Miller’s modified scale of Mobility Index-

0- Physiological mobility
1- < Than 1mm in faciolingual direction
2- > Than 1mm faciolingual direction
3- > Than 2 mm faciolingual direction. and mesiodistal and
also compressible in the socket.

43
Many attempts have been made to develop mechanical or electronic device
for precise measurement of tooth mobility.
1. Macroperiodontometer (Muhleman 1954)
-Application limited to anterior teeth and Premolar
2. Microperiodontometer ( O’ Leary and Rudd 1963)
- Application to all teeth.
3 . Periotest – The instrument is compact resembling a dental handpiece
and has an electomagnetically retracting tapping head. The tapping head has
a preset constant speed of 0.2 meters per sec and contact time with tooth varies
from 0.3-0.2 millisecond. Contact time upon impact is less- Then more
support (less mobile).
(Shulte et al 1992 and Teerlinck et al 1991)

Periodontal probing and assessment of periodontal pockets-

Pocket probing is mainly aimed at detecting pockets.
Two different pocket depths
1) Biologic or Histologic depth
2) Clinical or probing depth.

1. Is distance between gingival margin and base of the pocket

(coronal end of Junctional epithelium)
Measured only in carefully prepared and adequately oriented
histologic sections (1.8mm) with variations from 0-6mm.
2. Is distance to which an adhoc instrument (probe) penetrates into
the pocket. (2-3mm)

44
 Depth of penetration of probe depends on
1) Size of the probe
2) Force with which it is introduced
3) Direction of penetration
4) Resistance of tissues
5) Convexity of crowns.

Probe penetration can vary depending on the force of introduction shape

and size of probe tip and degree of tissue inflammation.
Errors of measurement in clinical probing will occur because of
1) Excessive probing force
2) Incorrect placement and angulation of probe
3) Failure to systematically probe all areas.
4) Excessibly large probe
5) Indistinct mm marking grooves / bands
6) Incorrectly placed mm markings
7) Needle- tip probes.

Armitage 1977 evaluated probe penetration in beagle dogs with a force of 25

gms and found
❖ In healthy specimens - Probe penetrated to about 2/3 of its length.
❖ In gingivitis- It stopped 0.1mm short of its apical end
❖ In periodontitis- Went past apical length of Junctional epithelium.

45
 ❖ In humans, probe tip penetrates to the most coronal intact fibers of the
connective tissue attachment. Depth of penetration in connective tissue
apical to Junctional epithelium in pocket is about 0.3mm ( Sagli 1975).
This is important in evaluating differences in probing depth before and
after treatment.
-Probing force for manual probes 0.75 N.

Probing technique: Probe should be inserted parallel to vertical axis of the

tooth and walked circumferentially around each surface of each tooth to detect
areas of deepest penetration.
Probing is commenced at most distal molar and carried around the
upper arch tooth by tooth, testing the facial and then lingual surface and vice
versa and then mandibular arch. Probe is moved with in crevice in very short
steps of approximately 1mm from distal to mesial contact area. At contact area
of adjacent teeth, the probe must be angled in which pocket extends apically
just beneath the contact area. Commonly 6 measurements are recorded per
tooth, with each root of molars treated as a single tooth.
6 facial and 6 lingual recording for each mandibular molar.
6 facial and 3 palatal recording for each maxillary molar.

To detect an interdental crater, probe placed obliquely from both facial

and lingual so as to explore the deepest point of pocket depth located beneath
contact point.

Detection of pockets-Careful exploration with periodontal probe.

Examination includes.

46
 1) Presence and distribution on each tooth surface.
2) Pocket depth.
3) Level of attachment on root.
4) Type of pocket.

Signs → Color changes (Bluish-red marginal gingiva or bluish-red vertical

zone extending from gingival margin to attached gingiva).
o Rolled edge
o Enlarged and edematous gingiva.
o Presence of bleeding and suppuration and loose extruded tooth.

Symptoms → Pain can be localized or radiating or sensation of pressure after

eating which gradually diminishes. Foul taste in localized areas.

When to probe –Probing is done at various times for diagnosis, and for
monitering the course of treatment and maintainence
➢ Initial probing of moderate or advanced cases is tempered by abundant
calculus and heavy inflammation.
➢ Purpose of this initial probing, together with clinical examination and
radiograph is done to determine whether tooth can be saved or
extracted.
➢ After adequate plaque control, a more accurate probing can be
performed.
➢ This two time probing is for the purpose of accurately establishing level
of attachment and degree of involvement of roots furcations.
➢ This provides valuable information for treatment decisions.

47
 ➢ During treatment, probings are done to determine changes in probing
depth and to ascertain healing process after different procedures.

Pocket depth → Distance between base of the pocket and gingival margin.
- Changes even in untreated periodontal disease owing to changes
in position of gingival margin, and may be unrelated to existing
attachment of tooth.

Attachment level- Distance between base of the pocket and a fixed point on
the crown eg. CEJ.
Changes in attachment level are a better indication of degree of periodontal
destruction.
Thus shallow pockets attached at apical 2/3 of root connot more severe
destruction than deep pockets attached at coronal 1/3.

Determining level of attachment

When gingival margin located on anatomic crown,
Attachment level = Subtracting from the depth of pocket the distance from
gingival margin to CEJ.
When gingival margin coincide with CEJ, loss of attachment = probing depth

When gingival margin apical to CEJ

Attachment level = Adding the distance between CEJ and gingival margin to
probing depth .

Bleeding on probing: To test for bleeding on probing, probe is introduced

into bottom of the pocket and gently moved laterally along pocket wall.

48
Sometimes, bleeding appears immediately after probe removal or may be
delayed by a few seconds. Recheck for bleeding 30 to 60 seconds after
probing.

Alveolar bone loss→ Probing is helpful for determining.

1) Height and contour of facial and lingual bones obscured on radiograph
by dense roots.
2) Architecture of interdental bone.

Amount of attached gingiva

❖ Width is determined by subtracting the sulcus or pocket depth
from total width of gingiva.
❖ Methods
1. Pushing adjacent mucosa coronal with a dull instrument.
2. Painting mucosa with Schiller’s potassium iodide
solution, which stains keratin.
3. Stretching lip or check to demarcate mucogingival line
line while pocket is being probed.

Assessment of furcation: Furcation is an area of complex anatomic

morphology that may be difficult or impossible to be debrided by routine
periodontal instrumentation.

Etiology
1) Bacterial plaque and its inflammatory consequences.

49
 2) Local anatomic factors such as root trunk length, root morphology and
local developmental anamolies like cervical enamel projections.
3) Factors that complicate oral hygiene producedures and rate of plaque
deposition contributing to development of periodontitis and attachment
loss.

Diagnosis- Clinical examination + careful probing with a No 3 pigtail

explorer or furca-finder or Nabers probe.
Probing to determine presence and extent of furcation involvement, position
of attachment relative to furca, extent and configuration of furcation defect.
Goal of diagnosis:
1. Identify and classify furca.
2. Identify factors that contribute to its development and also affect
treatment outcome.
1) Morphology of affected tooth.
2) Position of tooth relative to adjacent teeth
3) Local anatomy of alveolar bone.
4) Configuration of any bony defects.
5) Presence and extent of caries or pulpal necrosis.

81% have furca orifice < 1mm

58% have furca orifice < 0.75 mm
-So probe of small cross section is required.
Recording furcation involvement is extremely important in developing a
treatment plan and prognosis.
Insert instrument into crevice or pocket, rotate it to inter-radicular depth of
furca, and move it laterally and coronally to determine

50
 1) Catch
2) Instrument slipping out of furca in any or all direction.

Glickman grading-
Grade I -Incipient lesions –A detectable fluting exists where furcation begins
or where the extent is such that a catch in furca prevents instrument slipping.
Suprabony pocket is present, affects soft tissues. No radiographic changes
observed.
Grade II - Can affect 1 or more furcations of the same tooth. It is a cul-de –
sac with a definite horizontal component. If multiple defects present, then they
do not communicate since a portion of alveolar bone remains attached to
tooth. Definite catch of inserted furca-finder prevents instrument from
slipping out when moved laterally or coronally.
Grade III - Radiolucent area in crotch of the tooth.Bone not attached to dome
of furcation and only filled with soft tissue.
A through and through furcation involvement exists only when probe is
inserted in 1 furca and appears to connect directly with 1 or more furcas.
Grade IV –Interdental bone destroyed and soft tissue receded apically so that
furca opening is clinically visible.A tunnel exists between roots of such an
affected tooth.
Radiographic aids in examination
❖ Valuable aid in diagnosis of periodontal disease,
determination of prognosis and evaluation of outcome of
treatment.
❖ Hence an adjunct to clinical examination and not a
substitute for it.

51
 ❖ Should consist of a minimum of 14 intraoral films and 4
posterior bitewings and a panoramic x-ray.
Advantage of IOPA → IOPA is superior in providing details of individual
tooth and a clear view of the periapical region.
Panoramic → Used for detection of developmental anomalies, pathologic
lesions of teeth and jaws, fractures, and dental screening examination for
larger groups. Also provides information of overal radiographic picture of
distribution and severity of bone destruction in periodontal disease.
Bite wing- Using this both maxillary and mandibular bony crests are visible.
Also caries identification (Interproximally)
The bony crest is usually 1-2 mm apical to CEJ because of attachment of
collagen fibers immediately below enamel.
Slight bone loss not usually seen. Radiograph shows less severe bone loss than
that actually present.

Pattern of bone destruction: In periodontal disease, interdental septa

undergo changes that affect the lamina dura, crest radio density, size and shape
of medullary spaces, height and contour of bone.
If level of interdental bone is decreased, such that crest is horizontal
and perpendicular to long axis of adjacent teeth – Horizontal bone loss.
Vertical defects occur in an oblique direction leaving a hollowed out trough
in the bone along side the root, base of the defect is located apical to
surrounding bone.
Only those occuring interdentally usually seen on radiograph.
Evaluated by drawing a line connecting adjacent CEJ’s across the interdental
space.

52
Horizontal bone loss is indicated when the bone loss interproximally on 2
adjacent teeth is equidistant from CEJ on each tooth.
Vertical bone loss when bone crest is more apical to CEJ adjacent to one tooth
than to the other.

Radiographic changes in periodontitis

1. Fuzziness and break in continuity of lamina dura at mesial/ distal aspect
of crest of interdental septum.
This results from extension of gingival inflammation into bone causing
widening of vessel changes and a decrease in calcified tissue at septal
margin.
2. A wedge shaped radiolucent area at mesial /distal aspect of crest of
alveolar bone.Results from resorptions of bone of lateral aspect of
interdental septum with widening of periodontal space.
2. Destruction process extends across crest of interdental septum and
height decreased. Finger like Radiolucent projections extend from crest
into septum.
Results from deeper extension of inflammation into bone.
3. Height of interdental septum is decreased by extension of
inflammation. and resorption of bone.
Radiographic appearance of Inter dental osseous craters
❖ Seen as irregular areas of decreased radio opacity on alveolar bone
crests.
❖ Not sharply demarcated from rest of bone with which they blend
gradually.

53
Radiographic appearance of furcation
Variations in technique may obscure presence and extent of furcation
involvement.
E.g. A tooth may present marked bifurcation in 1 film but uninvolved in
another.
To assist in detection of furcation, following diagnostic criteria are suggested.
1) Slight change in furcation area investigated clinically, especially if
there is bone loss on adjacent roots.
2) Diminished radiodensity in furcation area in which outlines of busy
trabeculae are visible.
3) When there is marked bone loss in relation to single molar root→
furcation involved.

Radiographic appearance of abscess

• Discrete area of radiolucency along lateral aspect of root.
• Abscesses on facial or lingual surface obscured by radiopacity of root.
Also lesions in soft tissue wall of periodontal pocket less likely to
produce radiographic changes than those deep in supporting tissue.

Radiographic appearance in Localized Aggressive periodontitis

1) Bone loss intially in maxillary and mandibular Incisors, 1st molar
area, usually bilaterally and results in vertical arc like destructive
patterns.
2) Loss of alveolar bone generalized but less pronounced in
premolar areas.

54
Radiographic appearance in Trauma From Occlusion-
❖ Can produce changes in Lamina Dura, morphology of alveolar-crest
width of periodontal space and density of surrounding cancellous bone.
❖ Traumatic lesions manifest clearly in faciolingual aspects, because
mesiodistally, tooth has added stability from contact areas of adjacent
teeth.
❖ Injury phase → Loss of lamina dura noted in apices, furcations and or
marginal areas. This results in widening of periodontal space.
❖ Repair phase → Widening of periodontal space that may be generalized
or localized (an attempt to strengthen the periodontal structures to better
support increased load).
❖ Advanced traumatic lesions → deep angular bone loss which when
combined with marginal inflammation can lead to intrabony pocket. In
terminal lesions, lesions extend around root apex, producing a wide
radiolucent periapical image (Cavernous lesions).

Haematological Examination:
Include evaluations of –I) Complete blood count
a) Haemoglobin
b) RBC count
c) WBC count
d) DLC count

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II) Blood glucose levels – to evaluate glucose metabolism.
III) Blood Urea Nitrogen – Used as a screening test for kidney function.

Screening tests for hemorrhagic disorders-

1) Bleeding time
2) Clotting time
3) Platelt count
4) Prothrombin time
5) Partial thromboplastin time.
Prothrombin time prolonged in anticoagulant therapy with aspirin and
deficiency in factors I, II, V, VII, X as well as liver damages.
Partial thromboplastin time. is prolonged in anticoagulant therapy with
heparin.

Microbiological Examination- include

1) Culture of viable bacteria and assessment of antimicrobial specificity.
2) DNA probes that detect specific bacterial DNA or cell wall
components.
3) Enzymatic detection of bacterial products
Use of clinical casts and photographs
- Are extremely useful adjuncts in the oral examination.
Casts-
• Indicate position of gingival margin, position and inclination of teeth
proximal contact relationship, food impaction areas.
• Also provide a view of lingual –cuspal relationship.
• They are important records of the dentition before it is altered by
treatment.

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 • Serve as visual aids in discussions with the patient and are useful for pre
and post treatment comparisons as well as for reference at check up
visits.

Clinical photographs
Color photographs are useful for recording the appearance of the tissue
before and after treatment.
But cannot be relied for comparing subtle color changes in the gingiva,
but they do depict gingival morphologic changes.

Diagnosis- Once the history ( mainly dental and medical) and clinical
examination of the patient, radiographs and lab analysis are obtained , a
diagnosis can be determined.
Diagnosis is based on the AAP classification of periodontal diseases

Prognosis
Determination of Prognosis
Factors to be considered when determining a prognosis.
1) Overall clinical factors
Age, disease severity, plaque control, patient compliance
2) Systemic /environmental factors
Smoking, systemic disease, genetic factors and stress.
3) Local factors
Plaque/ calculus, sub gingival restorations

Anatomic factors include

➢ Short, tapered roots

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 ➢ Cervical enamel projections
➢ Enamel pearls
➢ Bifurcation ridges
➢ Root concavities
➢ Developmental grooves
➢ Root proximity
➢ Furcation involvment
➢ Tooth mobility
4) Prosthetic/ Restorative factors
Abutment selection
Caries, Non vital and root resorption.

Excellent prognosis → No bone loss, excellent gingival condition, good

patient co-operation, no systemic/ environmental factors.
Good prognosis → One or more of the following- adequate remaining bone
support, adequate possibilities to control etiologic factors and establish a
maintainable dentition, adequate patient co-operation, no systemic/
environmental factors ( if present, well controlled).
Fair prognosis → Less than adequate remaining bone support, some tooth
mobility, grade I furcation , adequate maintainence possible, acceptable
patient co-operation, presence of limited systemic / environmental factors.
Poor prognosis → Moderate to advanced bone loss, tooth mobility, grade II
furcation, difficult to maintain/ doubtful patient co-operation, presence of
systemic/ environmental factors and I.

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Questionable prognosis → Advanced bone loss, grade II and III furcation,
tooth mobility, inaccessible areas, presence of systemic/ environmental
factors
Hopeless prognosis → Advanced bone loss, non maintainable areas,
extraction indicated, presence of uncontrolled systemic / environmental
factors.

Overall tooth prognosis

1. Patient Age – For two patients with comparable levels of remaining

connective tissue attachment and alveolar bone, prognosis better in older of
the two.
For younger patient, prognosis is not so good because of shorter time
frame in which the periodontal destruction has occurred. (Even though his
reparative capacity greater, destruction has occurred.
2. Disease severity- Patients with history of previous periodontal disease-
more susceptible to future breakdown. Following variables should be
recorded for determining past history of periodontal disease.
a. Probing Depth
b. Clinical Attachment Level
c. Degree of bone loss
d. Type of bony defect → Determined by clinical and radiographic
evaluation.

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 ➢ A teeth with deep pockets and little attachment and bone loss has better
prognosis when compared to shallow pockets with severe attachment
and bone loss.
➢ Prognosis is adversely affected if base of pocket or attachment level is
close to root apex. Presence of apical disease as a result of endodontic
involvement also worsens prognosis.
➢ Prognosis is related to height of remaining bone. If bone support
minimal then poor prognosis. If bone support is sufficient then fair
prognosis The height of remaining bone, when it is in between then
bone level assessment alone is insufficient for determining overall
prognosis.
➢ Type of defect
Horizontal → Prognosis depends on height of existing bone because if
less bone height then regeneration can be induced by therapy. Vertical
→ if contour of existing bone and number of osseous walls favourable
then regeneration of bone can be induced by therapy.
-When greater bone loss has occurred on one surface, bone height on less
involved surface should be taken into consideration when determining
prognosis. Here centre of rotation will be nearer to crown and result in
favourable distribution of forces to periodontium and less tooth mobility.

3. Plaque control → Primary etiology

4. Patient Compliance / co-operation → Prognosis dependent on patients
attitude, desire to retain natural teeth and willingness and ability to
maintain good oral hygiene.

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 5. Systemic factors
a) Smoking – Direct relationship exists between smoking and
prevalence and incidence of periodontitis. Smoking affects not
only severity, but also the healing potential of periodontal
tissues. Prognosis in patients who smoke and have slight to
moderate periodontitis → Fair to poor and with severe poor
periodontitis →poor to hopeless.
b) Systemic disease / condition – Periodontitis is significantly
higher in patients with type 1 and2 diabetes mellitus and level of
glycemic control also affects periodontitis.
Prognosis depends on patient compliance relative to both
medical and dental status. Well-controlled patients with slight to
moderate periodontitis – good prognosis.
Prognosis questionable → when surgical periodontal treatment
required, but cannot be provided because of patients . health.
Incapacitating conditions like (Parkinson’s disease) also affect
prognosis.
6. Genetic factors→ influence both chronic and aggressive periodontitis.
Cause
1) Genetic polymorphisms in IL-L genes result in increased production
of IL- 1β → increased risk of generalized chronic periodontitis.
2) Genetic factors influence serum IG2 antibody titres and expression of
FC-γRII receptors on neutrophil → increase risk of aggressive
periodontitis.
3) Leukocyte adhesion deficiency type 1 can influence neutrophil function
and increase risk of aggressive periodontitis.

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 4) Familial aggregation.
Thus knowledge of patient IL-1 genotype can aid clinician in assigning
prognosis.
-Detection of genetic variations linked with periodontal disease can
influence prognosis.
1) Early detection → lead to early implementation of preventive and
treatment measures.
2) Identification → during course of treatment can influence treatment
recommendations, such as use of antibiotic therapy or increased
frequency of maintainence visits.
3) Identification of young individuals who have not been evaluated for
periodontitis, but who are recognized as being at risk because of
familial aggregation seen in aggressive periodontitis, can lead to
development of early intervention strategies.
7. Stress → Physical and emotional stress, as well as substance abuse→
may also affect prognosis.
8. Prosthetic/ Restorative factors- Overall prognosis requires general
consideration of bond levels and attachment levels to establish whether
enough teeth can be saved to serve as abutments for useful prosthetic
replacement of the missing teeth.
At this point, overall prognosis and individual prognosis overlapp because
prognosis for key individual teeth may affect overall prognosis for prothetic
rehabilitation.
9.Caries, Non- Vital teeth and root resoption. Caries → feasibility of adequate
restoration and endodontic therapy should be considered before undertaking
periodontal treatment.

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Root resorption (idiopathic or due to ortho) can affect stability of teeth affect
response to periodontal treatment.
Prognosis of treated non vital teeth not different form vital teeth.

Individual prognosis
1) Plaque/ calculus
2) Subgingival resorations and Margins → Increase plaque accumulation
Increase gingival inflammation.
Increase bone loss.
Overhangs can negatively impact the periodontium.
Tooth with discrepancy in subgingival margins has poorer prognosis than a
tooth with well –contoured supragingival margins.
3) Anatomic factors
a) Short tapered roots with larger crown → Poor prognosis
(Because disproportionate Crown to root ratio, and reduced root
surface for periodontal support, periodontium susceptible to injury
by occlusal forces.
b) Cervical enamel projections, enamel pearls and bifurcation
ridges.
The presence of these interferes with attachment apparatus and
may prevent regenerative procedures form achieving maximum
potential causing negative impact in prognosis.
c) Tooth morphology → Root concavities exposed through loss of
attachment can vary from shallow flutings to deep depressions.
They create areas that can be difficult for both dentist and patient
to clear.

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 d) Developmental grooves → create an accessibility problem, and
difficulty for clinician and patient to clear the areas.
4) Furcation involvement → Does not automatically indicate hopeless
prognosis. When lesion reaches the furcation, it creates 2 additional
problems.
1. First, is difficulty of access to area for scaling and root
planing and surgery.
2. Second, inaccessibility of area to plaque removal by
patient.
If both these problems solved, then prognosis is similar to single rooted
teeth with a similar degrees of bone loss. Maxillary first premolar →
usually prognosis is unfavorable when lesion reaches furcation.
5) Location of remaining bone in relation to individual tooth surfaces
(Same as disease severity).
6) Tooth Mobility- stabilization by splinting may have beneficial effect
on prognosis.

Prognosis
1. Gingivitis with dental plaque only → Good provided all local irritants
are removed , local factors contributing to plaque retention eliminated
and adequate patient co-operation.
2. Gingivitis modified by systemic factors → Long term prognosis

depends not only on plaque control but also correction of systemic

factors.
3. Non plaque induced gingivitis.

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 → Bacterial, viral, fungal → Prognosis dependent on elimination of
source of infectious agent.
Periodontitis
Chronic → a) With good oral hygiene and removal of plaque retentive
factors → good prognosis.
b) With furcation involvement increase mobility and non-compliant patients
→ fair to poor.
Aggressive – Can have fair, poor or questionable prognosis depending on
treatment modality and severity of disease.

Treatment plan: is the blue print for case management.

Aim → is co-ordination of all treatment procedures for the purpose of creating
a well functioning dentition in a healthy periodontal environment.

Phases of Treatment plan- The sequence in which the phases of therapy are
performed may vary in response to requirement of the case. However, the
preferred sequence is as follows.
1) Preliminary phase
Treatment of emergencies
-Dental or periapical
-Periodontal
-Other
Extraction of hopeless teeth and provisional replacement if needed.
Removal, retention or interim retention of 1 or more teeth is an important part
of overall treatment plan.
A tooth is extracted if

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 1) So mobile that function becomes painful.
2) Cause acute abscesses during therapy.
3) No use for it in the overall treatment plan.
Can be retained temporally if
1. It acts as posterior stops. It can be removed after treatment where
it can be replaced by prosthesis.
2. It may be functional after implant placement in adjacent areas
when implant is exposed, teeth can be extracted.
3. In anterior esthetic areas a tooth can be retained during
periodontal therapy and removed when treatment is completed
and a permanent restorative procedure can be performed.
2) Etiotropic phase (Phase I Therapy)
-Plaque control and patient education
a) Diet control ( Rampant caries individuals)
b) Removal of plaque/ calculus and root planing.
c) Correction of restorative and prosthetic irritational factors.
d) Excavation of caries and restoration ( temporary or final ) depending
on whether a definitive prognosis for tooth has been arrived at and on
location of caries.
e) Antimicrobial therapy
f) Occlusal therapy and correction of habits.
g) Minor orthodontic treatment.

Provisional splinting and prosthesis

Evaluation of response to etiotrophic phase
Recheck
- Pocket depth and gingival inflammation .

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 - Plaque and calculus, caries
(To preseve results obtained and prevent further deterioration and recurrance
of disease)
While the patient is in maintainence phase he/she enters the surgical and
reparative phases of treatment.
2) Surgical phase (Phase II therapy)
- Periodontal therapy ( including placement of implants)
- Root Canal Therapy
3) Restorative phase (Phase III)
Final restoration
Fixed / Removable prosthodontic appliance.
Evaluation of response to restorative procedures
4) Maintainence phase (Phase IV)
Periodic recall
- Plaque and calculus
- Pockets, inflammation. (gingival condition)
- Occlusion , tooth mobility
- Other pathologic changes.

Conclusion:
Traditional case history recording, clinical examination and laboratory
aids provide a historical evaluation of periodontium on an anatomic basis.
Thus, they aid in diagnosing treating a particular disease with proper adjuncts
used.
Thus, case history is the first step towards any treatment strategy
undertaken.

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