1. Chronic Periodontitis
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Chronic Periodontitis
Algonquin College

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.

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

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

5. Clinical Characteristics
Gingiva moderately swollen
Deep red to bluish- red tissues
Blunted and rolled gingival margin
Cratered papilla
Bleeding and/or suppuration

6. Clinical Characteristics
Plaque/calculus deposits
Variable pocket depths
Loss of periodontal attachment
Horizontal/vertical bone loss
Tooth mobility

7. CLASSIFICATION 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 
Advanced
> 7 mm
 5 mm
Mod-severe
vertical

9. DISEASE DISTRIBUTION : It is a site-specific disease
CLINICAL SIGNS -
- Inflammation ,pocket formation ,attacment 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 –FACIALsurface of same tooth
may be without disease.

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

12. Periodontal Pathogens Contn.
Pathogens include:
Nonmotile rods:
Facultative:
Actinobacillus a. E.c.
Anaerobic:
P. g., P. i., B.f., F.n.
Motile rods:
C.r.
Spirochetes:
Anaerobic, motile:
Treponema denticola

13. Pathogenesis – Pocket Formation
Bacterial challenge initiates initial lesion of gingivitis
With disease progression & change in microorganisms  development of periodontitis

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

15. Pocket Formation
Continued extension of JE requires healthy epithelial cells!
Necrotic JE slows down pocket formation
Pocket base degeneration less severe than lateral

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

17. Development of Periodontal Pocket

18. Continuous Cycle!
Plaque  gingival inflammation  pocket formation  more plaque

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

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.

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

22. Clinical & Histopathologic Features
Pocket wall bluish-red
Smooth, shiny surface
Pitting on pressure
Histopathology:
Vasodilation & vasostagnation
Epithelial proliferation, edema
Edema & degeneration of epithelium

23. Clinical & Histopathologic Features Contn…
Pocket wall may be pink & firm
Bleeding with probing
Pain with instrumentation
Histopathology:
Fibrotic changes dominate
 blood flow, degenerated, thin epithelium
Ulceration of pocket epithelium

24. Clinical & Histopathologic Features Contn…
Exudate
Flaccid tissues
Histopathology:
Accumulation of inflammatory products
Destruction of gingival fibers

25. Stages of Periodontal Disease

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

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

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

29. Inflammatory Pathway Interproximal:
Loose CT  periodontal ligament  bone  infrabony pockets & vertical bone loss  transseptal fibers transverse in oblique direction

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

31. Inflammatory Pathway Facial & Lingual:
Loose CT  periodontal ligament  destruction of periodontal ligament fibers  infrabony pockets & vertical or angular bone loss

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

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

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 O D I F Y N G A C T R S

36. Host status and defences
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
Quality & Quantity of periodontopathic bacteria
InflammationPlaque accumulation
Inflammation
Connective tissue destruction.
bacteria
Plaque accumulation
Maturation of Plaque
Quality & Quantity of periodontopathic bacteria
Inflammation
connective tissue destruction.
Host status and defences

37. MANAGEMENT The treatment consists of – Non-surgical procedures
Scaling
Root planing
Curettage
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

39. Prognosis of Individual Teeth
Dependent on:
Attachment levels, bone height
Status of adjacent teeth
Type of pockets: suprabony, infrabony
Furcation involvement
Root resorption