Chronic Periodontitis

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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 lt30 of sites affected
• Generalized gt 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 bluish-red 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 Peri
odontitis is considered localized when lt30 of
the sites assessed in mouth demonstrate
attachment loss and bone loss. Generalized Perio
dontitis is considered generalized when gt30 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 gt 7 mm ? 5 mm Mod-severe 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.

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SYMPTOMS

• 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

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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
• Pocket wall bluish-red
• Smooth, shiny surface
• Pitting on pressure

• Histopathology
• Vasodilation vasostagnation
• Epithelial proliferation, edema
• Edema degeneration of epithelium

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Clinical Histopathologic FeaturesContn

• Clinical
• Pocket wall may be pink firm
• Bleeding with probing
• Pain with instrumentation

• Histopathology
• Fibrotic changes dominate
• ? blood flow, degenerated, thin epithelium
• Ulceration of pocket epithelium

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Clinical Histopathologic FeaturesContn

• Histopathology
• Accumulation of inflammatory products
• Destruction of gingival fibers

• Clinical
• Exudate
• Flaccid tissues

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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 in prevalence
  severity with age.
• Affect both the sexes equally.
• It is an age-associated, not age related disease.

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• 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

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

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MANAGEMENT

• The treatment consists of
• Non-surgical procedures
• Scaling
• Root planing
• Curettage
• Surgical procedure
• Pocket reduction surgery
• Resective
• Regenerative
• Correction of morphological / anatomic defects

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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.