A case history is the blueprint of the treatment plan. It helps in establishing early diagnosis and enables prompt treatment plan.

1. CASE HISTORY
-Dr.Shraddha Kode

2. IMPORTANCE OF CASE
HISTORY
First & most important step
Correct diagnosis leads to correct treatment
plan
Proper clinical and radiographical examination
is must
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3. 3
NAME
Helps to develop bond with the patient
Communication
Records
AGE
Aggressive periodontitis – common in young;
chronic periodontitis – common in old
Wasting diseases like attrition and abrasion –
common in elderly

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GENDER
Localised aggressive periodontitis with
circumpubertal onset – common in females
Osteoporosis – postmenopausal women –
decreased bone density due to decreased
estrogen levels
SOCIAL STATUS
Economically sound and socially well-placed –
less dental problems
Not well-placed – poor oral hygiene due to
ignorance and fewer visits to the dentist

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OCCUPATION
Occupational stress – attrition, dental and
periodontal problems
People working in chemical factories – erosion +
dentinal sensitivity
Healthcare workers- transmissible diseases (HIV,
Hepatitis)
ADDRESS
Comunication
Records
Geographical distribution of diseases – ex.
Dental fluorosis

6. CHIEF
COMPLAINT
Patient’s own words
Chronological order
As descriptive as possible
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7. HISTORY OF PRESENT ILLNESS
Onset – When did it start?
Location – Endo – sharp and easy to locate pain; perio – dull
and gnawing and cannot usually localise
Duration – For how long?
Character – Sharp pain – endo; dull pain - perio
Aggravating factors – Factors which increase the pain
Relieving factors – Factors which relieve the pain
Timing & Severity –For how long does it last? Perio pain
usually stays for a variable duration without any stimulus and
dull in nature 7

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PAST DENTAL HISTORY
Patient’s attitude towards past dental treatment
Frequency of past dental visits
Previous treatment
Reasons for loss of teeth
Untoward complications if any

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MEDICAL HISTORY
Systemic condition for which the patient is under
treatment and medications
Major illness – h/o hospitalisation
Injuries to the orofacial region ex. Injury to the chin
– temporomandibular joint problem, trauma to the teeth
– devitalization
Medications – drug interactions, drug induced gingival
enlargement (anticonvulsants, calcium channel blockers
and immunosuppresants)
Allergy
Immunization and blood transfusions – high risk of
transmission of diseases

10. Family history
Systemic diseases like diabetes have
genetic factors involved
So, inquiry into presence of disease
states in the family is essential

11. “
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Personal history
Dietary habits & adverse habits
Oral hygiene measures – which
toothbrush, toothbrushing
technique, toothpaste, interdental
aids, tongue cleaning, how
frequently toothbrush is replaced?

12. HARD TISSUE EXAMINATION
Number of teeth present
Carious/decayed – examine with explorer and mention class
Missing
Filled – mention type of restoration
Stains and deposits
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WASTING DISEASES
Grippo 2004:
Attrition – The loss of tooth structure due to tooth to tooth
contact during normal or parafunctional masticatory activity
Abrasion – The pathological wear of tooth substance due to
biomechanical frictional processes ex. Toothbrushing

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Erosion - The loss of tooth substance due to dissolution by
acids of intrinsic or extrinsic origin ex. Gastric acid or
dietary acids

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Abfraction – The pathological loss of tooth substance
caused by biomechanical loading forces due to tooth flexure
leading to fatigue of enamel and dentin at a location away
from point of loading. Types – hairline cracks, striations,
saucer shaped, semilunar shaped and cusp tip invagination

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OCCLUSION
Angle’s classification of malocclusion
Food lodgement – passive accmulation of food
Food impaction – forceful wedging of food into
the periodontium.
2 types: vertical food impaction – due to open
contacts and irregular marginal ridges &
horizontal (lateral) food impaction – gingival
inflammation causes enlarged gingival embrasures
and lateral pressure from lips, cheeks and tongue
causes food impaction

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Plunger cusps – cusps that tend to forcibly
wedge food into the periodontium

18. PROXIMAL TOOTH CONTACTS
Normal proximal contacts do not allow any food
impaction in between the teeth
Open contact areas are usually associated with
food impaction and gingival inflammation
Open contact areas can be found commonly in
malaligned teeth or in proximal caries where
contact has been lost due to tooth decay
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PATHOLOGICAL TOOTH MIGRATION
Tooth displacement that results when the balance
among factors that maintain physiologic tooth position is
disturbed by periodontal disease
Presents as facial flaring, extrusion, rotation,
diastema, drifting of affected teeth
Most common – facial flaring and diastema

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Posterior bite collapse – one of the reasons
for pathological tooth migration
Increased occlusal load and reduced
periodontal support in case of secondary
trauma from occlusion – forces from tongue,
lips and cheeks put forces on teeth –
sufficient to cause pathologic tooth migration

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FREMITUS TEST
Abnormal forces from opposing teeth may lead to
slight discomfort to severe pain
Occlusal disharmony is due to traumatic occlusion/
trauma from occlusion
Fremitus test is used to detect trauma from occlusion
Vibratory pattern of teeth is observed when they are
brought into contact
A dampened index finger is placed over the buccal and
labial surface of the maxillary teeth. Patient is asked
to tap teeth together in maximum intercuspal position
and grind systematically in lateral, protrusive
contacting positions

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Class
I
Mild vibrations or
movements are detected
Class
II
Easily palpable vibrations
but no visible movements
Class
III
Movements visible with
naked eye

23. SOFT TISSUE EXAMINATION
Examine the labial and buccal mucosa,
tongue, soft and hard palate, floor of
the mouth, vestibular depth and frenum
attachment
Examination of gingiva:
Colour – coral or pale pink. Pigmentation
may be present
Chronic periodontitis – reddish pink /
bluish in colour
Acute periodontitis – bright red in colour
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Contour – healthy – scalloped with knife edged gingival
margins that adapt closely around the tooth
Papilla is pointed and pyramidal, fills interproximal areas
In case of space between two teeth – saddle or flat-
shaped
Pre of inflammation – rounded gingival margins due to
edematous and fibrotic changes; papilla is bulbous,
flattened and blunted

25. Consistency – healthy gingiva is firm and
resilient. Can be checked by palpating with side
of a blunt instrument
Gingival inflammation – soft edematous (spongy)
gingiva dents readily when gently pressed
Chronic inflammation due to fibrotic changes
(gingiva is pink and stippled but bleeding on
probing present) – firm and hard
Marginal gingiva easily displaced from the tooth
surface with a light air blast – indicates
destruction of gingival fibres that support
gingival margin
25

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Surface texture – stippled
appearance
“orange peel appearance”
Microscopic elevations and
depressions due to connective tissue
projections within the tissue
Dry the gingiva with cotton and view
it under broad daylight (light from all
directions required to see it clearly)
Stippling is absent in infancy,
appears in about 5 years of age,
increases until adulthood and
frequently begins to disappear in old

27. Size– check for normal size; enlarged in
case of gingival enlargement or reduced in
gingival recession
Position – Normally present at CEJ
Apical migration from CEJ is termed as
gingival recession; coronal position – gingival
enlargement
Gingival exudate – discharge from gingival
sulcus indicates disease activity
Put slight pressure on the lateral surface of
the gingiva – white purulent material oozing
from gingival sulcus indicates presence of
exudate 27

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Bleeding on probing – spontaneous, immediate or delayed
indicator of tissue inflammatory response to bacteria
First sign of gingivitis
Chronic inflammation – gingiva may appear fibrotic but
inflammation may be actively present in the gingival
sulcus and junctional epithelium
Smokers – reduced BOP due to effects of nicotine
Acute – bleeding may occur even after slight provocation
like short burst of compressed air

29. Embrasures – present cervical to the
interproximal contact area
NORDLAND & TARNOW CLASSIFICATION
OF INTERDENTAL PAPILLARY HEIGHT
(1998)
29
Normal The interdental papilla occupies the entire embrasure space
apical to the interdental contact point
Class I Tip of interdental papilla is located between the interdental
contact point and the level of CEJ on the proximal surface
of the tooth
Class II Tip of interdental papilla is located at or apical to the level
of CEJ on the proximal surface of the tooth but coronal to
the level of CEJ mid-buccally
Class III Tip of interdental papilla is located at or apical to the level
of CEJ mid-buccally

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Based on three anatomic landmarks :
Interdental contact point
Coronal extent of proximal CEJ
Apical extent of facial CEJ

31. McCall’s festoons – life preserver-shaped rolled
margins of the gingiva where the gingiva shows
fibrotic properties
Stillman’s clefts – First sign of recession – formation
of small groove in the gingiva; this term for the cleft
like recession
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Examination of the periodontium:
Done in a systematic way, examining all the
surfaces of every tooth and record the findings in
the periodontal chart
Pocket depth – The distance between the gingival
margin and the base of the pocket
Clinical attachment level – The distance between
the CEJ and base of the pocket
CLINICAL ATTACHMENT
LEVEL
POCKET DEPTH
CE
J GINGIVAL
MARGIN

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TOOTH MOBILITY
The movement of tooth in the socket resulting
from an applied force
Physiologic tooth mobility present normally
Apply firm pressure with either one metal
instrument and a gloved finger or two metal
instruments

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Norm
al
Physiologic tooth mobility
Class
I
Mobility less than 1mm in
horizontal direction
Class
II
Mobility more than 1mm in
horizontal direction
Class
III
Mobility more than 1mm in
horizontal & vertical
direction
TOOTH MOBILITY
CLASSIFICATION (MILLER 1985)

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Grad
e I
Slightly more than normal
Grad
e II
Moderately more than
normal
Grad
e
III
Severe tooth mobility
faciolingually or
mesiodistally with vertical
displacement
TOOTH MOBILITY GRADING
(GLICKMAN 1972)

37. FURCATION INVOLVEMENT
The extension of inflammatory periodontal disease
into the interradicular area of the multirooted teeth
is known as furcation involvement.
Diagnosis is based on clinical and radiographic
findings.
Clinical detection – Nabers probe
Mandibular molar furcation easy to detect since 2
roots
Maxillary molar furcation – mesial furcation– go for
palatal direction (mesial furcation is located palatal
to the midpoint on mesial surface); distal furcation – 37

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GLICKMAN’S CLASSIFICATION (1953) –
FOR HORIZONTAL COMPONENT
Grade I Incipient or early stage of furcation involvement. Suprabony
pocket and primarily affects soft tissues. No radiographic
changes
Grade II Cul-de-sac with a definite horizontal component.
Radiographs may or may not depict furcation involvement.
Grade III Bone is not attached to the dome of the furcation.
Difficulty in passing the probe through the furcation because
of the interference with the bifurcational ridges or
facial/lingual bony margins. Radiographically, radiolucent
area in the crotch of the tooth.
Grade IV Interdental bone is destroyed and the soft tissues have
receded apically so that the furcation opening is clinically

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TARNOW & FLETCHER’S CLASSIFICATION (1984) – FOR
VERTICAL COMPONENT (Depending on the distance from the
base of the defect to the roof of the furcation)
Subgroup
A
Vertical destruction of bone upto 1/3rd of
the inter-radicular height (1-3mm)
Subgroup
B
Vertical destruction of bone upto 2/3rd of
the inter-radicular height (4-6mm)
Subgroup
C
Vertical destruction beyond the apical
third(7mm or more)

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GINGIVAL RECESSION
The apical migration of the gingival margin from
the normal position at the CEJ is known as
gingival recession
SULLIVAN & ATKIN’S
CLASSIFICATION
(1968)
Shallow-
narrow
Shallow-wide
Deep-narrow
Deep-wide

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MILLER’S CLASSIFICATION OF GINGIVAL RECESSION
(1985)
Class I Marginal tissue recession not extending to the
mucogingival junction. No loss of interdental bone
or soft tissue
Class II Marginal tissue recession extends to or beyond
mucogingival junction. No loss of interdental bone
or soft tissue.
Class III Marginal tissue recession extends to or beyond
the mucogingival junction. Loss of interdental bone
or soft tissue or teeth malpositioning.
Class IV Marginal tissue recession extends beyond
mucogingival junction. Loss of interdental bone and
soft tissue loss interdentally and/or severe tooth
malpositioning

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44. WIDTH OF ATTACHED
GINGIVA
Identify 2 landmarks – sulcus/pocket depth and
mucogingival junction
For mucogingival junction identification –
TENSION TEST – Stretch the lip/cheek
outwards. Identify the junction of immovable
attached gingiva and movable alveolar mucosa
ROLL TEST – Roll the alveolar mucosa over the
attached gingiva with a blunt instrument. Here,
the movable alveolar mucosa accumulates ahead of
the instrument till the mucogingival junction when
pushed coronally 44

45. Measurement approach – Measure the
sulcus/pocket depth. Measure the distance from
the gingival margin to the mucogingival junction.
Subtract the two measurements = width of
attached gingiva
45

46. Histochemical method – Schiller’s potassium or
Lugol’s iodine is painted on the gingiva and oral
mucosa. Due to glycogen content of alveolar mucosa –
brown colour. Attached gingiva – glycogen free –
unstained. Now, measure the total width of unstained
gingiva and subtract the sulcus/pocket depth = width
of attached gingiva
Greatest in the incisor region (3.5-4.5mm in
maxilla, 3.3-3.9mm in mandible) and less in the first
premolar areas (1.9mm in maxilla and 1.8mm in
mandible) 46

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DEPTH OF VESTIBULE
Related to the width of attached gingiva
If the width is normal. The vestibular depth is
adequate
If the width of attached gingiva is minimal –
shallow vestibule – vestibular depth inadequate

48. FRENUM ATTACHMENT
TENSION TEST - Lip is moved outwards, upwards
or downwards and sidewards – marginal or interdental
papilla moves away from the tooth surface – positive
tension test
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PLACEK CLASSIFICATION (1974)
Mucosal Frenal fibres are attached upto mucogingival
junction
Gingival Frenal fibres are attached within the attached
gingiva
Papillary Fibres extend into the interdental papilla
Papilla
penetrating
The frenal fibres cross the alveolar process and
extend upto palatine papilla

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50. ABSCESS
Gingival abscess – localised painful swelling affecting
marginal and interdental gingiva; impaction of foreign
objects ex. Fish bone, popcorn kernel
Periodontal abscess – localised purulent inflammation
of periodontal tissues including deep pockets,
furcation, vertical osseous defects (lateral or parietal
abscess)
Pericoronal abscess – localised purulent inflammation
surrounding crown of a partially or fully erupted
tooth
Periapical abscess – localised purulent inflammation
surrounding apex of the tooth 50

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RADIOGRAPHIC FINDINGS
Used to know the extent of periodontal destruction in
the form of bone loss
Periapical radiographs or orthopantomogram
Record the amount of bone remaining, bone density,
continuity of lamina dura, radiolucent areas, pattern of
bone loss

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PROVISIONAL DIAGNOSIS
Initially determined to be the diagnosis
Followed by investigations which help in making
the final diagnosis
Generalised
(>30% of sites
involved) /
Localised
(<30% of sites
involved)
Marginal
Marginal & Papillary
Diffuse (Marginal,
Papillary and
Attached gingiva
involvement)
CHRONIC
Mild (1-2mm)
Moderate (3-4mm)
Severe (>5mm)
(*After recording mean CAL)
1
2
3
4
GINGIVITIS
PERIODONTITIS

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HOW TO RECORD
CAL?
4
2
NORMAL SULCUS
DEPTH = 2-3mm
1
4
2
0
MEAN CAL = 6 + 5
2
= 5.5
SEVERE

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CLASSIFICATION
Gingival Diseases
Plaque induced gingival diseases
Associated with dental plaque only
Gingival diseases modified by systemic factors –
diabetes mellitus, puberty, pregnancy associated
Gingival diseases modified by medications – Drug
induced gingival diseases
Non-plaque induced gingival diseases
Bacterial, viral, fungal, genetic origin
Gingival manifestations of systemic conditions
Allergic reactions, traumatic lesions, foreign body
reactions

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Chronic Periodontitis
Aggressive Periodontitis
Periodontitis as a manifestation of systemic diseases
Necrotising Periodontal Diseases
Abscesses of the periodontium
Periodontitis associated with Endodontic Lesions
Developmental and Acquired Deformities and Conditions
Mucogingival Deformities and conditions
Occlusal trauma

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SPECIAL INVESTIGATIONS
Routine blood examination – complete blood
count, bleeding time, clotting time, haemoglobin
levels
Study casts
Biopsy – in case of gingival overgrowth
Microbiological analysis – culture for isolation
and identification of bacteria

58. FINAL DIAGNOSIS
Complete and accurate diagnosis is important
for an appropriate treatment plan
Final diagnosis should involve all the periodontal
conditions for which the patient requires
treatment
Ex. Generalised marginal chronic gingivitis with
localised severe chronic periodontitis with
periodontal abscess/ pericoronitis/ trauma from
occlusion with respect to ____
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PROGNOSIS
Prediction of the probable course, duration and
outcome of the disease based on the general
knowledge of the pathogenesis of the disease and
the presence of risk factors for the disease
Overall prognosis – patient’s age, systemic
factors, severity of the disease, smoking,
presence of plaque, calculus, patient compliance,
prosthetic possibilities
Individual prognosis –determined after overall
prognosis and affected by it

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PROGNOSIS
Good prognosis Control of etiologic factors and adequate
periodontal support
Fair prognosis Approx 25% attachment loss and/or Class I
furcation involvement
Poor prognosis 50% attachment loss and Class II furcation
involvement
Questionable
prognosis
>50% attachment loss, poor crown-root
ratio, poor root form, Class II or class III
furcation involvement, >Grade II mobility,
root proximity
Hopeless prognosis Inadequate attachment to maintain health,
comfort and function

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TREATMENT PLAN
An accurate and complete
diagnosis helps to formulate an
appropriate treatment plan
Divided into 4 phases:
If the patient is in pain –
elimination of pain or other
emergency treatment
After completion of phase I
therapy – patient is placed on
maintenance phase (phase IV) to
preserve the results obtained and
prevent any further deterioration
and disease recurrence.
Phase I / Etiotropic
phase
Phase II
Phase
III
Phase IV
Preliminary phase

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65. TAKE HOME MESSAGE
Case history is the blueprint of
the treatment plan
Appropriate treatment plan may
prevent unnecessary complications
Case history provides detailed
information regarding risk factors
associated with disease progression

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