Chronic periodontitis is a slowly progressive infectious disease that results in inflammation of the gums and bone destruction around the teeth. It is caused by a subgingival biofilm of bacteria that spreads below the gumline. Common symptoms include bleeding gums, deepening pockets between teeth, and loose or mobile teeth. Treatment involves nonsurgical procedures like scaling and root planing to remove plaque and tartar, as well as surgery in some cases to regenerate lost bone and reduce pocket depths. Prognosis depends on factors like patient compliance, systemic health issues, disease severity, and tooth-specific characteristics such as attachment levels and furcation involvement.
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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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 ,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--
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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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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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
ConnectiveTissue:
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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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
ConnectiveTissue destruction
Genetic influence
Inflammation
Periodontopathic bacteria
Smoking, Calculus
Loss of Attachment
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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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