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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 chronic adult periodontitis.
- Occur as a result of extension of
inflammation from the gingiva into
deeper periodontal tissue.

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

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

Clinical Characteristics

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

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

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

Involved

Advanced

> 7 mm

5 mm

Modsevere
horizontal
vertical

Involved

DISEASE DISTRIBUTION : It is a site-specific

disease

CLINICAL SIGNS - Inflammation ,pocket formation ,attachment 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.
- E.g..-proximal surface with plaque may have C.A.L.
- And plaque free surface FACIAL surface of same
tooth
may be without disease.

SYMPTOMS
1.
2.
3.
4.
5.
6.
7.
8.

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-- dulldeep radiating in the jaw
Area of food impaction can cause more discomfort
May be gingival tenderness or itchiness found

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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Periodontal Pathogens
Contn

Pathogens include:
Nonmotile rods:
Facultative:
Actinobacillus a. E.c
Anaerobic:
P. g., P. i., T.f., F.n.

Motile rods:
Facultative:
C.r.

Spirochetes:
Anaerobic, motile:
Treponema denticola

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Pathogenesis Pocket
Formation

Bacterial challenge
initiates initial
lesion of gingivitis
With disease
progression &
change in
microorganisms
development of
periodontitis

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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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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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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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Development of Periodontal
Pocket

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Continuous Cycle!

Plaque gingival inflammation

pocket formation more plaque

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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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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.

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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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Clinical & Histopathologic

Features
Clinical :
1. Pocket wall bluishred
2. Smooth, shiny
surface
3. Pitting on pressure

Histopathology:
1. Vasodilation &
vasostagnation
2. Epithelial
proliferation, edema
3. Edema &
degeneration of
epithelium

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Clinical & Histopathologic

Features

Contn
Clinical:

Histopathology:
Pocket wall may be
1. Fibrotic changes
pink & firm
dominate
2. Bleeding with probing blood flow,
degenerated, thin
3. Pain with
epithelium
instrumentation
3. Ulceration of pocket
epithelium
1.

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Clinical & Histopathologic

Features

Contn
Histopathology:

Clinical :
Exudate
2. Flaccid tissues
1.

Accumulation of
inflammatory products
2. Destruction of gingival
fibers
1.

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Stages of Periodontal
Disease

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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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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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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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Inflammatory Pathway
Contn

Interproximal:
Loose CT periodontal ligament bone

infrabony pockets & vertical bone loss

transseptal fibers transverse in oblique
direction

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Inflammatory Pathway
Contn

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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Inflammatory Pathway
Contn

Facial & Lingual:

Loose CT periodontal ligament

destruction of periodontal ligament fibers

infrabony pockets & vertical or angular bone
loss

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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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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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Prevalence:

Chronic
Periodontitis
increases
prevalence & severity with age.

in

Affect both the sexes equally.

It is an age-associated, not age related

disease.

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 defenses
Subgingival Restoration
Environment
Calculus, smoking

Connective Tissue destruction

Genetic influence
Inflammation
Periodontopathic bacteria
Smoking, Calculus

Loss of Attachment

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

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.

MANAGEMENT

1.

The treatment consists of

Non-surgical procedures

Scaling
Root planing
Curettage

2.

Surgical procedure
Pocket reduction surgery

Resective
Regenerative

Correction of morphological / anatomic defects

Overall Prognosis

Dependent on:
Client compliance
Systemic involvement
Severity of condition
# of remaining teeth

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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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MCQs on Chronic
Periodontitis

1.Bacteria considered to be pathogenic

in chronic periodontitis is/are:

a) P. gingivalis
b) P. intermedia
c) A. actinomycetemcomitans
d) Both (a) and (b)

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MCQs on Chronic
Periodontitis

2. The clinical attachment loss in

Moderate periodontitis is

a) 1 to 2 mm
b) 2 to 3 mm
c) 3 to 4 mm
d) 5 mm or more

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MCQs on Chronic
Periodontitis
3.Following histopathological changes occur in
periodontium while pocket formation
except:
a)

Cellular & fluid inflammatory exudate

degenerates connective tissue.
b) Apical migration of junctional epithelium
along root.
c) Apical portion of JE detaches.
d) None of the above.
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MCQs on Chronic
Periodontitis

4. Risk factors for chronic periodontitis

include:

1. Prior history of periodontitis.

2. Plaque accumulation on tooth and
gingival surfaces.
3. Type 2 diabetes.
4. All of the above.

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MCQs on Chronic
Periodontitis

5.The treatment possibilities of chronic

periodontitis include

a) Nonsurgical periodontal therapy.

b) Pocket reduction surgery.
c) Correction of morphological /
anatomic defects.
d) All of the above.

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