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

1. 1
Chronic Periodontitis
Localized
Generalized

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

6. 6
Clinical Characteristics
 Variable pocket
depths
 Horizontal/vertical
bone loss
 Tooth mobility

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

11. 11
Development of Periodontal
Pocket

12. 12
Continuous Cycle!
Plaque  gingival inflammation 
pocket formation  more plaque

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

15. 15
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

16. 16
Clinical & Histopathologic
Features
 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

17. 17
Clinical & Histopathologic
Features
 Clinical :
1. Exudate
2. Flaccid tissues
 Histopathology:
1. Accumulation of
inflammatory
products
2. Destruction of
gingival fibers

18. 18
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

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

21. 21
Periodontal Pocket
 Suprabony pocket

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

26. 26
Stages of Periodontal Disease

27. 27
Periodontal Pathogens
Gram negative organisms dominate
P.g., P.i., A.a. may infiltrate:
– Intercellular spaces of the epithelium
– Between deeper epithelial cells
– Basement lamina

28. 28
Periodontal Pathogens
 Pathogens include:
– Nonmotile rods:
• Facultative:
– A.a., E.c.
• Anaerobic:
– P. g., P. i., B.f., F.n.
– Motile rods:
• Facultative:
– C.r.
– Spirochetes:
• Anaerobic, motile:
– Treponema denticola

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

31. 31
Overall Prognosis
Dependent on:
– Client compliance
– Systemic involvement
– Severity of condition
– # of remaining 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
 