Aggressive Periodontitis OR MIP (1).pptx

Aggressive Periodontitis OR MIP (1).pptx

• 1.
  WHAT IS AGGRESSIVEPERIODONTITIS
• 2.
  PRIMARY FEATURES • NON-CONTRIBUTORYMEDICAL HISTORY • RAPID ATTACHMENT LOSS AND BONE DESTRUCTION • FAMILIAL AGGREGATION
• 3.
  SECONDARY FEATURES • MICROBIALDEPOSITS INCONSISTENT WITH SEVERITY • ELEVATED PROPORTIONS OF AGGREGATIBACTOR ACTINOMYCETEMCOMITANS • PHAGOCYTE ABNORMALITIES • HYPER RESPONSIVE MACROPHAGE • BURN OUT
• 4.
  GINGIVAL RESPONSES 1. SEVERELY, ACUTELY INFLAMED TISSUE. SUPPURATION, ULCERATED AND FIERY RED. 2. PINK, FREE OF INFLAMMATION WITH / WITHOUT STIPPLING.
• 5.
  TYPES • LOCALIZED AGGRESSIVEPERIODONTITIS • GENERALIZED AGGRESSIVE PERIODONTITIS
• 6.
  LOCALIZED AGGRESSIVE PERIODONTITITS •FIRST MOLAR AND INCISORS. TWO TEETH APART FROM THEM • 0.1 TO 0.5% PREVALENCE
• 7.
  CLINICAL FEATURES • CIRCUMPUBERTALONSET • RAPID • LOCALIZED MOLAR/ INCISOR PRESENTATION • ROBUST SERUM ANTIBODY RESPONSE TO INFECTING AGENTS
• 8.
  OTHER FEATURES • DIASTEMAFORMATION • INCREASING MOBILITY • SENSITIVITY • DEEP, DULL RADIATING PAIN DURING MASTICATION
• 9.
  REASONS OF LIMITATIONOF PD DESTRUCTION TO CERTAIN TEETH 1. A A EVADES HOST RESPONSE BY CHEMOTAXIS INHIBITING FACTORS, ENDOTOXINS, COLLEGENASES, LEUKOTOXIN. STRONG ANTIBODY RESPONSE LATER ON. 2. ANTAGONIST BACTERIA TO AA COLONIZE PERIODONTAL TISSUES 3. AA MAY LOOSE ITS LEUKOTOXIN PRODUCING ABILITY 4. DEFECT IN CEMENTUM FORMATION RESPONSIBLE FOR LOCALIZATION
• 10.
  RADIOGRAPHIC FINDING • ARC-SHAPED BONE LOSS FROM DISTAL OF SECOND PREMOLAR TO MESIAL OF SECOND MOLAR
• 11.
  GENERALIZED AGGRESSIVE PERIODONTITIS •0.13 % PREVALENCE • 3 TEETH OR MORE APART FROM MOLARS AND INCISORS. • POOR SERUM ANTIBODY RESPONSE TO INFECTING AGENTS
• 14.
  RADIOGRAPHIC FINDINGS • SEVEREBONE LOSS • 25 TO 60 % BONE LOSS
• 15.
  RISK FACTORS FORAGGRESSIVE PERIO • MICROBIOLOGIC FACTORS • IMMUNOLOGIC FACTORS • GENETIC FACTORS • ENVIRONMENTAL FACTORS
• 16.
  MICROBIOLOGIC FACTORS • NOSIGNIFICANT CLEAR ASSOCIATION WAS FOUND BETWEEN AGGRESSIVE AND AA • BACTERIAL INVASION OF CONNECTIVE TISSUE
• 17.
  IMMUNOLOGIC FACTORS • DISPLAYFUNCTIONAL DEFECTS OF PMN , MONOCYTES OR BOTH • CAN BE DUE TO BACTERIAL INFECTION OR MAY BE GENETIC • HIGH AMOUNT OF IGG2 IN RESPONSE TO AA IN LAP
• 18.
  GENETIC FACTORS • MAJORGENE OR SET OF GENES PLAY A ROLE • AUTOSOMAL DOMINANT PATTERN
• 19.
  ENVIRONMENT FACTORS • SMOKINGHAS MORE OF AN IMPACT ON GENERAL AGGRESSIVE COMPARED TO LOCALIZED AGGRESSIVE
• 20.
  THE END