Chronic periodontitis is a slowly progressive infectious disease that results in inflammation of the supporting tissues of the teeth and bone loss. It is caused by an extension of gingival inflammation into deeper periodontal tissues due to plaque accumulation. Key characteristics include a localized or generalized onset at any age, usually in adults, with periods of rapid progression possible. Treatment involves non-surgical procedures like scaling, root planing, and curettage as well as surgical procedures like pocket reduction surgery to correct anatomical defects. Prognosis depends on factors like patient compliance, systemic involvement, disease severity, and status of remaining teeth.

1. CHRONIC
PERIODONTITIS
Dr.D.Navya, MDS
1

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.
2

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
3

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
4

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

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

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
8

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. Bleeding gums
2. spaces 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
11

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
12

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
14

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
 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
21

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
22

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
23

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
31

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
32

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
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

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:
 Patient compliance
 Systemic involvement
 Severity of condition
 status of remaining teeth
38

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. conclusion