1. Periodontitis
    1. Chronic bacterial infection that affects the gums & bone supporting the teeth
    2. Pathogenesis of periodontitis
      1. Osteoprotegrin ( OPG) Stimulate osteoblast
        1. Bone formation
      2. Receptor Activator of Nuclear factor Kaffa ( RANK) Stimulate Osteoclast
        1. Bone resorption
      3. Ratio of RANK/ OPG = more than 1
        1. Leads to Bone resorption
    3. Chronic periodontitis
      1. Painless
      2. Both M/ F are affected
      3. Age associated disease but not age related
      4. Classification
        1. Mild: 1-2 mm of attachment loss
        2. Moderate: 3-4 mm of attachment loss
        3. Severe: >5 mm of attachment loss
      5. Genetic variant
        1. IL 1 increases chances of periodontitis by 4.4 times
        2. IL 1 + smoker - by 7.7 times
    4. Aggressive periodontitis
      1. AP refers to multifactorial, severe, & rapidly progressive form of periodontitis, which primarily but not exclusively affects younger patients
      2. Gottlieb - ‘diffuse atrophy of alv. Bone’ ‘ Cementopathea’ ‘ Disease of eruption’
      3. Two types
        1. Localised aggresive periodontitis
          1. - Circumferential Bone loss around Incisors & 1 st molars quadrant—>3 Arch—> 6 Mouth—> 12 - strong antibody response - Deep dull radiating pain - A.A. Comitans are responsible
        2. Generalised aggressive periodontitis
          1. - Circumferential bone loss on 3 or more teeth quadrant—> 6 Arch—>12 Mouth—>24 - poor antibody response - PAT: P. Gingivalis A.A comitans Tanorellia forsythia
      4. Pathogenesis of Aggressive Periodontitis
        1. 1. Increased HLA A9 & HLA B15: cause increased chances of Agressive periodontitis
        2. 2. Decreased HLA A2 : Increases chances of agressive periodontitis
        3. 3. Hyperresponse of Monocytes: Cause Increased level of PGE2 & further causes Bone loss
        4. 4. Increased HLADR4
        5. 5. IgG2 - increases bone loss
    5. Refractory Periodontitis
      1. Condition that repeats itself, even after t/t DOC: Metronidazole 2 nd DOC: Clindamycin
  2. Periodontal Therapy in female pt’s
    1. Progesterone Increases
      1. Stimulate PGE2 & Increase Gingival Inflammation
      2. Increase Permeability Increase folate metabolism Altered Immune Response Altered rate of collagen production in gingiva
    2. PMN chemotaxis
      1. Increase by progesterone decrease by estradiol No effect by Testosterone
    3. Pregnancy gingivitis
      1. Pinard recognised
      2. Characterized by Erythema, Edema, Hyperplasia & increased bleeding
      3. Ant> post more in interproximal region
      4. Mostly occur in third trimester
    4. Periodontal disease in a pregnant lady
      1. Increase the risk of preterm baby & the low birth weight baby
      2. Mothers with low birth weight baby has following bacteria ( PAT2)
        1. P. Gingivalis
        2. AA comitens
        3. Tannerella forsythia
        4. Treponema Denticola
    5. Estrogen Increases
      1. Keratinization decreases
    6. Estrogen & Progestrone Increases
      1. Perimylolysis, Erosion of enamel & dentin ( mainly on lingual surface of maxillary ant. Teeth)
  3. Periodontal Pocket
    1. Pathological deepening of gingival sulcus
    2. Microtopography of Pocket wall
      1. 1. Area of Relative Quisence
      2. 2. Area of bacterial accumulation
      3. 3. Area of emergence of Leukocyte
      4. 4. Area of leukocyte & Bacterial interaction
      5. 5. Area of Epithelial desquamation
      6. 6. Area of ulceration
      7. 7. Area of Hemorrhage
    3. Pathophysiology
      1. 1. Leukocyte increases more than 60%
      2. 2. Activates MMP (matrix metalloproteases): Most destructive extra cellular enzyme
      3. 3. Destroy collagen fibre
      4. 4. Degrade JE & also proliferate it
    4. Surface Morphology of tooth wall in periodontal pocket
      1. 1. Cementum covered by calculus
      2. 2. Attached plaque
      3. 3. Unattached plaque
        1. Plaque free zone
      4. 4. Zone of attachment of JE to tooth 500 micrometer: Normally 100 micrometer: P. Pocket
        1. Plaque free zone
      5. 5. Semi destroyed Connective tissue
        1. Plaque free zone
      6. 6. Intact connective tissue
    5. CAL & Periodontal pocket
      1. Clinical attachment level Distance from CEJ to base of sulcus
      2. Periodontal pocket From crest of marginal gingiva to Base of sulcus
        1. Classification
          1. 1. According to involved tooth surfaces
          2. 1. Simple pocket : Involve one surface
          3. 2. Compound pocket : Involve more than one surface
          4. 3. Complex or spiral pocket: Originating on one tooth surface & twisting around the tooth to involve one or more additional surfaces
          5. 2. Based on location
          6. A. Gingival pocket (Pseudopocket): Formed by gingival enlargement without destruction of the underlying tissues. The sulcus is deepened because of increased bulk of the gingiva
          7. B. Periodontal pockets: occurs with destruction of supporting periodontium. Is of two types
          8. 1. Supra bony & Infrabony pocket
          9. Given by Goldman & Cohen
          10. 1. Suprabony pocket
          11. 2. Infrabony pocket
          12. 1. One walled defect : Only one bony wall is present
          13. 2. Two walled defect : Two bony walls are present
          14. 3. Three walled defect: Three bony walls are present
          15. 4. Combined defect: e.g Three walls in apical half & two walls in occlusal half are involved
      3. Severity of attachment loss is not always corelated with depth of pocket as periodontal pocket of same depth may be associated with different degree of attachment loss or vice versa
    6. Important points to remember
      1. Distance b/w apical extent of calculus & Alveolar crest is always : 1.97 mm
      2. Distance b/w apical edge of calculus & Bottom of pocket : 0.2-1mm
      3. Range of effectiveness or radius of action: 1.5-2.5 within bacterial plaque. Larger bone defect >2.5mm from tooth surface maybe caused by presence of bacteria in tissue
      4. Epithelial attached plaque is a reason for CAL in a periodontal disease
  4. Inter- Radicular Defects/ Furcation defects
    1. A. Glickman classification
      1. Grade I : Pocket formation into the flute, but intact interradicular bone
      2. Grade II : Loss of interradicular bone & pocket formation, but not extending through to the opposite side
      3. Grade III: Through and through lesion
      4. Grade IV : through & through lesion with gingival recession, leading to a clearly visible furcation area
    2. B. Goldman
      1. Grade I : Incipient
      2. Grade II : cul-de-sac
      3. Grade III: Through & through
    3. C. Tarnow & Fletcher : sub classification based on degree of vertical involvement
      1. Subclass A. 0-3mm vertical bony loss in furcation
      2. Subclass B. 4-6mm vertical bone loss in furcation
      3. Subclass C. > 7 mm vertical bony loss in furcation