Transcript Chronic Periodontitis

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
slowly progressive periodontitis.
- Occur as a result of extension of inflammation
from the gingiva into deeper periodontal tissue.
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Common Characteristics
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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
 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.
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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
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Advanced
> 7 mm
 5 mm
Modsevere
horizontal
vertical
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
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 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.
SYMPTOMS
Patient notices-1.
2.
3.
4.
5.
6.
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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., B.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 
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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:
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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:
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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
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Clinical :
1. Pocket wall bluish-red
2. Smooth, shiny surface
3. Pitting on pressure
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Histopathology:
1. Vasodilation &
vasostagnation
2. Epithelial
proliferation, edema
3. Edema &
degeneration of
epithelium
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Clinical & Histopathologic
Features
Contn…
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Clinical:
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1. Pocket wall may be
1.
pink & firm
2. Bleeding with probing 2.
3. Pain with
instrumentation
3.
Histopathology:
Fibrotic changes
dominate
 blood flow,
degenerated, thin
epithelium
Ulceration of pocket
epithelium
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Clinical & Histopathologic
Features
Contn…

Clinical :
1. Exudate
2. Flaccid tissues
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Histopathology:
1. Accumulation of
inflammatory
products
2. 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
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Stages I-III – inflammation degrades gingival
fibers
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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
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Interproximal:
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Loose CT  periodontal ligament  bone 
infrabony pockets & vertical bone loss 
transseptal fibers transverse in oblique direction
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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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Inflammatory Pathway
 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 in prevalence &
severity with age.
 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 defences
Subgingival Restoration
Environment
Calculus, smoking
Connective Tissue destruction
Genetic influence
Inflammation
Periodontopathic bacteria
Smoking, Calculus
Loss of Attachment
M
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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
Plaque accumulation
Connective
tissue destruction. of Plaque
Maturation
bacteria
Inflammation
Quality & Quantity of
Connective tissue destruction.
periodontopathic bacteria
Connective tissue destruction.
Host
status and
defences
Inflammation
MANAGEMENT
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The treatment consists of –
1. Non-surgical procedures
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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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