This document discusses chronic periodontitis, including its characteristics, pathogenesis, clinical presentation, histopathology, and classification. Key points include:
- Chronic periodontitis can be localized or generalized. It typically has an onset in adulthood and is initiated by plaque, with calculus and poor oral hygiene contributing. Progression can be slow or have periods of rapid change, and is modified by local/systemic factors and smoking.
- The extent and severity are classified based on the percentage of sites affected and amount of clinical attachment level (CAL) loss/bone loss. Pockets form from bacterial challenge causing gingival inflammation and destruction of connective tissue fibers.
- Histopathology shows
2. 2
Learning Outcomes
1. Describe the development of a
periodontal pocket.
2. Relate clinical characteristics to the
histopathologic changes for chronic
periodontitis.
3. Compare the gingival pocket with the
periodontal pocket.
4. Determine the severity of PD activity
using clinical data.
3. 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. 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. 5
Clinical Characteristics
Deep red to
bluish-red tissues
Thickened
marginal gingiva
Blunted/cratered
papilla
Bleeding and/or
suppuration
Plaque/calculus
deposits
7. 7
Pathogenesis – Pocket
Formation
Bacterial
challenge initiates
initial lesion of
gingivitis
With disease
progression &
change in
microorganisms
development of
periodontitis
8. 8
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
9. 9
Pocket Formation
Continued
extension of JE
requires healthy
epithelial cells!
Necrotic JE slows
down pocket
formation
Pocket base
degeneration less
severe than lateral
10. 10
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
13. 13
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
14. 14
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
19. 19
Root Surface Wall
Necrotic areas of cementum form;
clinically soft
Act as reservoir for bacteria
Root planing may remove necrotic
areas firmer surface
20. 20
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
22. 22
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
23. 23
Inflammatory Pathway
Interproximal:
– Loose CT periodontal ligament
bone infrabony pockets & vertical
bone loss transseptal fibers
transverse in oblique direction
24. 24
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
25. 25
Inflammatory Pathway
Facial & Lingual:
– Loose CT periodontal ligament
destruction of periodontal ligament
fibers infrabony pockets & vertical or
angular bone loss
29. 29
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, exudate
– May last days, weeks, months
30. 30
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
32. 32
Prognosis of Individual Teeth
Dependent on:
– Attachment levels, bone height
– Status of adjacent teeth
– Type of pockets: suprabony, infrabony
– Furcation involvement
– Root resorption
33. 33
Subclassification of Chronic
Periodontitis
Severity Pocket
Depths
CAL Bone
Loss
Tooth
Mobility
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