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.”



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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.”

  • 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.



Onset - any age; most common in adults

  • 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:

  • Extent:

  • Severity: entire dentition or individual teeth/site

    • Slight = 1-2 mm CAL
    • Moderate = 3-4 mm CAL
    • Severe =  5 mm CAL


Gingiva moderately swollen

  • Gingiva moderately swollen

  • Deep red to bluish-red tissues

  • Blunted and rolled gingival margin

  • Cratered papilla

  • Bleeding and/or suppuration



Plaque/calculus deposits

  • Plaque/calculus deposits

  • Variable pocket depths

  • Loss of periodontal attachment

  • Horizontal/vertical bone loss

  • Tooth mobility







DISEASE DISTRIBUTION : It is a site-specific disease

  • 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.



Patient notices--

  • 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



Gram negative organism dominate

  • Gram negative organism dominate

  • P.g., P.i., A.a. may infiltrate:

    • - Intercellular spaces of the epithelium
    • - Between deeper epithelial cells
    • - Basement lamina


Pathogens include:

  • 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


Bacterial challenge initiates initial lesion of gingivitis

  • Bacterial challenge initiates initial lesion of gingivitis

  • With disease progression & change in microorganisms  development of periodontitis



Cellular & fluid inflammatory exudate  degenerates CT

  • 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



Continued extension of JE requires healthy epithelial cells!

  • Continued extension of JE requires healthy epithelial cells!

  • Necrotic JE slows down pocket formation

  • Pocket base degeneration less severe than lateral



Continue inflammation:

  • 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




Plaque  gingival inflammation  pocket formation  more plaque

  • Plaque  gingival inflammation  pocket formation  more plaque



Gingival:

  • 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


Connective Tissue:

  • 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.


Periodontal pocket:

  • 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


Clinical :

  • Clinical :

  • Pocket wall bluish-red

  • Smooth, shiny surface

  • Pitting on pressure



Clinical:

  • Clinical:

  • Pocket wall may be pink & firm

  • Bleeding with probing

  • Pain with instrumentation



Clinical :

  • Clinical :

  • Exudate

  • Flaccid tissues





Periodontal disease affects root surface:

  • Periodontal disease affects root surface:

    • Perpetuates disease
    • Decay, sensitivity
    • Complicates treatment
  • Embedded collagen fibers degenerate  cementum exposed to environment

  • Bacteria penetrate unprotected root



Necrotic areas of cementum form; clinically soft

  • Necrotic areas of cementum form; clinically soft

  • Act as reservoir for bacteria

  • Root planing may remove necrotic areas  firmer surface



Stages I-III – inflammation degrades gingival fibers

  • 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


Interproximal:

  • Interproximal:

    • Loose CT  periodontal ligament  bone  infrabony pockets & vertical bone loss  transseptal fibers transverse in oblique direction


Facial & Lingual:

  • 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


Facial & Lingual:

  • Facial & Lingual:

    • Loose CT  periodontal ligament  destruction of periodontal ligament fibers  infrabony pockets & vertical or angular bone loss


Bursts of activity followed by periods of quiescence characterized by:

  • 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


Period of activity followed by period of remission:

  • 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



Prevalence:

  • 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:

  • 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



3) SYSTEMIC FACTORS:

  • 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.


The treatment consists of –

  • The treatment consists of –

  • Non-surgical procedures

    • Scaling
    • Root planing
    • Curettage
  • Surgical procedure

    • Pocket reduction surgery
      • Resective
      • Regenerative
    • Correction of morphological / anatomic defects


Dependent on:

  • Dependent on:

    • Client compliance
    • Systemic involvement
    • Severity of condition
    • # of remaining teeth


Dependent on:

  • Dependent on:

    • Attachment levels, bone height
    • Status of adjacent teeth
    • Type of pockets: suprabony, infrabony
    • Furcation involvement
    • Root resorption


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