describes the clinical features & Management of Chronic Periodontitis

1. Chronic
Periodontitis
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2. Definition
Chronic Periodontitis can be defined as “an infectious disease resulting
in inflammation within the supporting tissues of the teeth, progressive
attachment loss, and bone loss.”
- Previously known as adult periodontitis or slowly progressive
periodontitis.
- Occur as a result of extension of inflammation from the gingiva into
deeper periodontal tissue.
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3. Common Characteristics
Onset - any age; most common in adults
Plaque initiates condition
Subgingival calculus common finding
Slow-mod progression; periods of rapid progression possible
Modified by local factors/systemic factors/stress/smoking
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4. Extent & Severity
Extent:
◦ Localized: <30% of sites affected
◦ Generalized: > 30% of sites affected
Severity: entire dentition or individual teeth/site
◦ Slight = 1-2 mm CAL
◦ Moderate = 3-4 mm CAL
◦ Severe =  5 mm CAL
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5. Clinical Characteristics
Gingiva moderately
swollen
Deep red to bluish-red
tissues
Blunted and rolled
gingival margin
Cratered papilla
Bleeding and/or
suppuration
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6. Clinical Characteristics
Plaque/calculus deposits
Variable pocket depths
Loss of periodontal
attachment
Horizontal/vertical bone
loss
Tooth mobility
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7. CLASSIFICATION
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A) Based on Disease Distribution:
Localized:
Periodontitis is considered localized when <30% of
the sites assessed in mouth demonstrate attachment
loss and bone loss.
Generalized:
Periodontitis is considered generalized when >30% of
the sites assessed demonstrate attachment loss and
bone loss.
The pattern of bone loss in chronic periodontitis can
be vertical or horizontal.

8. Sub classification of Chronic
Periodontitis
Severity Pocket
Depths
CAL Bone
Loss
Furcation
Early 4-5 mm 1-2 mm Slight
horizontal
Moderate 5-7 mm 3-4 mm Sl – mod
horizontal
 
Advanced > 7 mm  5 mm Mod-
severe
horizontal
vertical
 
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9. DISEASE DISTRIBUTION : It is a site-specific disease
CLINICAL SIGNS -
- Inflammation ,pocket formation ,attachment loss ,bone loss - All
caused by site specific effects of a sub-gingival plaque
accumulation
- That is why the effect are on one side only –other surface may
maintain normal attachment level.
- Eg.-proximal surface with plaque may have C.A.L.
- And plaque free surface –FACIAL surface of same tooth
may be without disease.

10. SYMPTOMS
Patient notices--
1. gum bleed
2. space appear between teeth due to tooth movement
3. May be painless (sleeping disease )goes unnoticed
4. Some time pain due to caries , root hypersensitivity
5. To cold /hot or both
6. PAIN-may be-- dull—deep radiating in the jaw
7. Area of food impaction can cause more discomfort
8. May be gingival tenderness or itchiness found

11. Periodontal Pathogens
•Gram negative organism dominate
•P.g., P.i., A.a. may infiltrate:
• - Intercellular spaces of the epithelium
• - Between deeper epithelial cells
• - Basement lamina
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12. Periodontal Pathogens Contn.
Pathogens include:
 Nonmotile rods:
 Facultative:
 Actinobacillus a. E.c.
 Anaerobic:
 P. g., P. i., B.f., F.n.
 Motile rods:
 Facultative:
 C.r.
 Spirochetes:
 Anaerobic, motile:
 Treponema denticola
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13. Pathogenesis – Pocket Formation
Bacterial challenge
initiates initial lesion of
gingivitis
With disease
progression & change in
microorganisms 
development of
periodontitis
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14. Pocket Formation
Cellular & fluid inflammatory exudate  degenerates CT
Gingival fibers destroyed
Collagen fibers apical to JE destroyed  infiltration of inflammatory
cells & edema
Apical migration of junctional epithelium along root
Coronal portion of JE detaches
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15. Pocket Formation
Continued extension of
JE requires healthy
epithelial cells!
Necrotic JE slows down
pocket formation
Pocket base
degeneration less severe
than lateral
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16. Pocket Formation
Continue inflammation:
◦ Coronal extension of gingival margin
◦ JE migrates apically & separates from root
◦ Lateral pocket wall proliferates & extends into CT
◦ Leukocytes & edema
◦ Infiltrate lining epithelium
◦ Varying degrees of degeneration & necrosis
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17. Development of Periodontal
Pocket
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18. Continuous Cycle!
Plaque  gingival inflammation  pocket formation  more plaque
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19. Classification of Pockets
Gingival:
◦ Coronal migration of gingival margin
Periodontal:
◦ Apical migration of epithelial attachment
◦ Suprabony:
◦ Base of pocket coronal to height of alveolar crest
◦ Infrabony:
◦ Base of pocket apical to height of alveolar crest
◦ Characterized by angular bony defects
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20. Histopathology
Connective Tissue:
◦ Edematous
◦ Dense infiltrate:
◦ Plasma cells (80%)
◦ Lymphocytes, PMNs
◦ Blood vessels proliferate, dilate & are engorged.
◦ Varying degrees of degeneration in addition to newly
formed capillaries, fibroblasts, collagen fibers in some
areas.
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21. Histopathology
Periodontal pocket:
◦ Lateral wall shows most severe degeneration
◦ Epithelial proliferation & degeneration
◦ Rete pegs protrude deep within CT
◦ Dense infiltrate of leukocytes & fluid found in rete pegs & epithelium
◦ Degeneration & necrosis of epithelium leads to ulceration of lateral wall,
exposure of CT, suppuration
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22. Clinical & Histopathologic Features
Clinical :
1. Pocket wall bluish-red
2. Smooth, shiny surface
3. Pitting on pressure
Histopathology:
1. Vasodilation & vasostagnation
2. Epithelial proliferation, edema
3. Edema & degeneration of
epithelium
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23. Clinical & Histopathologic
Features Contn…
Clinical:
1. Pocket wall may be pink & firm
2. Bleeding with probing
3. Pain with instrumentation
Histopathology:
1. Fibrotic changes dominate
2.  blood flow, degenerated, thin
epithelium
3. Ulceration of pocket epithelium
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24. Clinical & Histopathologic
Features Contn…
Clinical :
1. Exudate
2. Flaccid tissues
Histopathology:
1. Accumulation of inflammatory
products
2. Destruction of gingival fibers
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25. Stages of Periodontal Disease
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26. Root Surface Wall
Periodontal disease affects root surface:
◦ Perpetuates disease
◦ Decay, sensitivity
◦ Complicates treatment
Embedded collagen fibers degenerate  cementum exposed to
environment
Bacteria penetrate unprotected root
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27. Root Surface Wall Contn…
Necrotic areas of cementum form; clinically soft
Act as reservoir for bacteria
Root planing may remove necrotic areas  firmer surface
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28. Inflammatory Pathway
Stages I-III – inflammation degrades gingival fibers
◦ Spreads via blood vessels:
Interproximal:
 Loose CT  transseptal fibers  marrow spaces of cancellous bone
 periodontal ligament  suprabony pockets & horizontal bone loss
transseptal fibers transverse horizontally
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29. Inflammatory Pathway
Interproximal:
◦ Loose CT  periodontal ligament  bone  infrabony pockets &
vertical bone loss  transseptal fibers transverse in oblique direction
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30. Inflammatory Pathway
Facial & Lingual:
◦ Loose CT  along periosteum  marrow spaces of cancellous bone 
supporting bone destroyed first  alvoelar bone proper  periodontal
ligament  suprabony pocket & horizontal bone loss
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31. Inflammatory Pathway
Facial & Lingual:
◦ Loose CT  periodontal ligament  destruction of periodontal ligament
fibers  infrabony pockets & vertical or angular bone loss
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32. Periodontal Disease Activity
Bursts of activity followed by periods of quiescence
characterized by:
◦ Reduced inflammatory response
◦ Little to no bone loss & CT loss
Accumulation of Gram negative organisms leads to:
◦ Bone & attachment loss
◦ Bleeding, exudates
◦ May last days, weeks, months
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33. Periodontal Disease Activity
Period of activity followed by period of remission:
◦ Accumulation of Gram positive bacteria
◦ Condition somewhat stabilized
Periodontal destruction is site specific
PD affects few teeth at one time, or some surfaces of given teeth
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34. Prevalence:
Chronic Periodontitis increases in prevalence &
severity with age.
Affect both the sexes equally.
It is an age-associated, not age related disease.

35. RISK FACTORS FOR DISEASE:
1) PRIOR HISTORY OF PERIODONTITIS—predictor-more risk for developing damage
to periodontium.
2) LOCAL FACTORS:
Plaque Accumulation
Oral Hygiene
Tooth Malposition
Restoration
Preserve & Quantity of certain bacteria
Host defences
Subgingival Restoration
Environment
Calculus, smoking
Connective Tissue destruction
Genetic influence
Inflammation
Periodontopathic bacteria
Smoking, Calculus
Loss of Attachment
M
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36. 3) SYSTEMIC FACTORS:
Type II or Non – Insulin dependent Diabetes Mellitus (NIIDDM)
4) ENVIRONMENTAL & BEHAVIORAL FACTORS:
◦ Smoking
◦ Emotional Stress
5) GENETIC FACTORS:
◦ Frequent among family members and across different generations.
GENERAL CONCEPT FOR ETIOLOGY OF CHRONIC PERIODONTITIS
Plaque accumulation
Maturation of Plaque
Quality & Quantity of periodontopathic Plaque accumulation
Maturation of Plaque
Quality & Quantity of periodontopathic bacteria
InflammationPlaque accumulation
Maturation of Plaque
Quality & Quantity of periodontopathic bacteria
Inflammation
Connective tissue destruction.
Connective tissue destruction.
bacteria
Inflammation
Connective tissue destruction.
Host
status and
defences
Plaque accumulation
Maturation of Plaque
Quality & Quantity of
periodontopathic bacteria
Inflammation

37. MANAGEMENT
The treatment consists of –
1. Non-surgical procedures
◦ Scaling
◦ Root planing
◦ Curettage
2. Surgical procedure
◦ Pocket reduction surgery
◦ Resective
◦ Regenerative
◦ Correction of morphological / anatomic defects

38. Overall Prognosis
Dependent on:
◦ Client compliance
◦ Systemic involvement
◦ Severity of condition
◦ # of remaining teeth
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39. Prognosis of Individual Teeth
Dependent on:
◦ Attachment levels, bone height
◦ Status of adjacent teeth
◦ Type of pockets: suprabony, infrabony
◦ Furcation involvement
◦ Root resorption
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40. Thank You
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