Transcript Chronic Periodontitis

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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.

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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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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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Clinical Characteristics
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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

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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.
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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
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
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-- dull—deep 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
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
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
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

1.
2.
3.
Clinical :
Pocket wall bluishred
Smooth, shiny
surface
Pitting on pressure

1.
2.
3.
Histopathology:
Vasodilation &
vasostagnation
Epithelial
proliferation, edema
Edema &
degeneration of
epithelium
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Clinical & Histopathologic Features
Contn…

1.
2.
3.
Clinical:
Pocket wall may be
pink & firm
Bleeding with probing
Pain with
instrumentation

1.
2.
3.
Histopathology:
Fibrotic changes
dominate
 blood flow,
degenerated, thin
epithelium
Ulceration of pocket
epithelium
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Clinical & Histopathologic Features
Contn…

1.
2.
Clinical :
Exudate
Flaccid tissues

1.
2.
Histopathology:
Accumulation of
inflammatory products
Destruction of gingival
fibers
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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.
 Affect
 It
in
both the sexes equally.
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



2.
Scaling
Root planing
Curettage
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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