2. KEY STAGES OF PERIODONTAL DIAGNOSIS
History taking
↓
Examination
↓
Investigations
↓
Diagnosis
↓
Treatment plan
3. History taking
Medical history
Dental history
Family/ social history
Habits
Casts
Clinical photographs
4. Review of initial examination
EMERGENCY TREATMENT
GINGIVAL ABSCESS
SECOND VISIT – In case there is no emergency
treatment
5. Examination
Oral hygiene
Accumulated food debris, plaque and tooth surface
stains.
Disclosing agent will enhance plaque disclosure.
Simplified Oral Hygiene Index – Aids objective
measure
Halitosis – Important in AUG
6. GINGIVAL EXAMINATION
Gingival
features
In
health
Factors
responsible
In disease Factors
responsible
Clinical changes Disease
conditions
Color Coral
pink
Vascular
supply
Thickness/deg
ree of
keratinisation
Pigment
containing
cells
Color change:
marginal,
diffuse, or
patch like
Shades of red,
blue,
Bright red
erythema to
-Shinny slate
gray, -dull
whitish gray
Black line following
margin contour
Bluish red or deep
blue linear
pigmentation
(Burtonian line)
Violet marginal line
Chronic gingivitis
Ch ronic gingivitis
Acute gingivitis
-ANUG
-Herpetic
gingivostomatitis
-Chemical
irritation
Bismuth, arsenic
& Mercury
pigmentation
Silver
pigmentation
Systemic
diseases causing
pigmentation
Vascular
proliferation
↓ Keratinisation
-Venous stasis
-Tissue necrosis
Perivascular
pption of metallic
sulfides in
subepithelial C.T
in areas of
inflammation
7. Contour Marginal: scalloped &
knife edged
Interdental pappila: Ant-
Pyramidal
Post- tent shaped
-Shape of tooth & alignment
in arch
-Proximal contact location &
size
-Facial & lingual gingival
embrassures dimensions
Rolled margin
Punched & crater like
depressions at the crest of
interdental papilla
Irregularly-shaped denuded
appearance
Exagerated scalloping
Apostrophe-shaped
indentation extending into
marginal gingiva
Life saver like enlargement
of marginal gingiva (canine
& Pm facial region)
Chronic gingivitis
ANUG
Chronic
desquamative
gingivitis
Gingival recession
Stillman’s cleft
McCall’s festoon
Inflammatory
changes
Described by
Stillman as a result
of trauma
8. consistency Firm & resilient
(except free
margin)
Collagenous
nature of
lamina propria
& its contiguity
with the
mucoperiosteu
m of alveolar
bone
-Soggy
puffiness that
pits on
pressure
-marked
softness &
Friability
-firm leathery
-Diffuse
puffiness &
softening
-Sloughing:
grayish flake
like particle of
debris
-vessicle
formation
Chronic
gingivitis
Exudative
Fibrotic
Acute gingivitis
-Infiltration by
fluids & cells of
inflammatory
exudate
-C.T &
epithelium
degeneration
Fibrosis &
epithelium
proliferation
Diffuse edema
of acute
inflammatory
origin
Necrosis with
pseudomembr
ane formation
Edema
(Inter/Intracell
ular)
9. Size Normal Sum total of
bulk of cellular
& intercellular
elements &
vascular supply
Increased Gingival
enlargement
↑ fibres & ↓
cells (non-
inflammatory)
↑ cells & ↓
fibres
(Inflammatory )
10. Surface
texture
Stippling
present
Due to attchment of
gingival fibres to
underlying bone
Microscopically by
alternate rouded
protuberance &
depression on gingival
surface
Loss of stippling
-Smooth &
shiny
Firm & nodular
Peeling of
surface
Leathery
texture
Minutely
nodular surface
Gingivitis
Exudative
chronic
Fibrotic
nodular
Chronic
desquamative
Hyperkeratosis
Non
inflammatory
gigngival
hyperplasia
Due to
destruction of
gingival fibres
as a result of
inflammation
11. Position 1mm above
CEJ
Position of
tooth in the
arch
Root bone
angle
Mesiodistal
curvature of
tooth surface
Apically placed
Corronally
placed
Gingival
recession
Pseudopockets
Toothbrush
trauma
Inflammation
High frenum
attachment
Tooth
malposition
Friction from
soft tissue
12. Bleeding on
probing
Intact sulcular
epithelium &
normal
capillaries
Present
Chronic
recurrent,
spontaneous
bleeding or
bleeding on
slight
provocation
Chronic
gingivitis
ANUG
Systemic
diseases
Dilation &
engorgement
of capillaries
& thinnig or
ulceration of
sulcular
epithelium
13. Palpation
Aids in
detecting pathologic alterations in normal
resilience
locating areas of pus formation
locating the origin of radiating pain that the
patient cannot localise
14. Probing
Probing is done at various times for diagnosis and
for monitoring the course of treatment and
maintainance
Inactive lesions may show little or no bleeding on
probing while active lesions bleed more readily on
probing
15. Subgingival temperature
A measure of periodontal inflammation that may
be useful when usual clinical signs are unreliable.
Example of a commercially available system is the
Periotemp probe
16. Advanced diagnostic methods
Bacterial culture –
Relative and absolute counts of the cultured
species can be obtained.
It is the only in vitro method that is able to
assess for antibiotic susceptibility of the
microbes
Culture method can only grow live organisms,
strict sampling and transport conditions are
essential
17. Immunodiagnostic methods
IMMUNOFLUORESCENT ASSAY (IFA)
Direct and Indirect IFAs are able to identify the
pathogen and quantify the percentage of the
pathogen directly using a plaque smear.
IFA has been used mainly to detect A.
aggregatibacter and P. gingivalis
Flow cytometry – sophisticated and expensive.
Not widdely used.
18. ENZYME LINKED IMMUNO-SORBENT
ASSAY (ELISA)
E.g. Evalusite
Evalusite has been designed to detect A.
aggregatibacter, P. gingivalis and P. intermedius
found a detection limit of 105 for A aggregatibacter
and 106 for P. gingivalis
19. Diagnostic assays based on
molecular biology techniques
Nucleic acid probes –
oligonucleotide probes complementary to variable
regions of the 16S rRNA bacterial genes have been
developed
Chekerboard DNA-DNA hybridisation technology
Rapid processing of large numbers of plaque samples
with multiple hybridisation for up to 40 oral species
in a single test.
The probes can detect 104 cells of each species
20. Polymerase chain reaction
16S rRNA-based PCR method has been developed to
determine the prevalence of A. aggregatibacter, T.
forsythia, C. recta, P. gingivalis, P. intermedius, and
T. denticola
PCR has lower detection limit (25-100 cells)
compared with culture
21. Tretament of gingival lesion
Step 1: limited plaque control instruction which
include the correct use of toothbrush.
Step 2: supragingival calculus removal
Step 3: correction of defective restorations and
crowns
22. Step 4: treatment of carious lesion
Step 5: Comprehensive plaque control instruction with
toothbrush, dental floss any other desirable
complimentary method.
Step 6: subgingival root treatment. Root planing to
achieve smooth and regular contours on all surfaces.
Step 7: tissue re-evaluation for assessment of need for
further therapy
23. REVIEW OF PHASE I THERAPY
The effect of the phase I therapy is evaluated about
4 weeeks after completion of the scaling and root
planing. This will allow for both epithelia and
connective tissue healing and allows the patient
enough to practice the oral hygiene skills
SURGICAL THERAPY – Decision based on
outcome of non-surgical therapy
