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PERIODONTOLOGY

LECTURE (5) 2017. أستاذ . د. رائد عزيز. PERIODONTOLOGY. Pathogenesis of periodontal disease. Is the biologic and histologic events that occur in the tissues during conversion from a healthy state to diseased state. Periodontal diseases: - (Gingivitis and Periodontitis)

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PERIODONTOLOGY

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  1. LECTURE (5) 2017 أستاذ . د. رائد عزيز PERIODONTOLOGY

  2. Pathogenesis of periodontal disease Is the biologic and histologic events that occur in the tissues during conversion from a healthy statetodiseased state.

  3. Periodontal diseases: - (Gingivitis and Periodontitis) Gingivitis: -Inflammation is confined to gingival tissue No loss of attachment 1- Redness 2- swelling 3- Bleeding

  4. Periodontitis: - inflammation of the supporting with ((apical migration of junctional epithelium with associated loss of attachment.)) Usually progression = ((loss of bone and Periodontal ligament.))

  5. Localised periodontitis Localized gingivitis Generalized gingivitis Generalized periodontitis

  6. Evidence for a primary role of bacteria in the etiology of p.d.disease:- 1- The acute phases of P.d.diseases can be alleviated by antibiotics, clearly indicating that microorganisms are the etiologic agents of this P.d.disease.

  7. Intensive plaque control improves clinical gingivitis • Leaving of P.con. plaque accum. gingivitis. 3-An increase serum antibodies against specific subgingival organisms.

  8. The possible pathogenic mechanisms Bacterial invasion 1- invasive nature of spirochetes in necrotizing ulcerative gingivitis (NUG). 2- Aggretibacteractinomycetemcomitans (Aa):- In localized aggressive Periodontitis (LAP) they invade the connective tissue;

  9. ((Exotoxins)) A.a. (Exotoxin) (leukotoxin) 1- (leukotoxin) its toxic to (PMNs). 2- (Leukotoxin) enable Aa to reduce phagocytosis of (PMNs). ((Cell constituents: (Endotoxin )) • G-ve bacteria form endotoxin, which is a constituent of the cell wall of G-ve bacteria. Endotoxin (also termed lipopolysaccharide)

  10. Endotoxin has the following effects:- 1- Production of leukopenia. 2- Activation of factor XII which affect the clotting system ((Intravascular coagulation.)) 3- Activation of complement system. 4- Toxic effect on cells such as fibroblasts. 5- Induce bone resorption.

  11. Enzymes • Collagenase. Hyaluronidase. Gelatinase. Alkaline and acid phosphatase. ((P.gingivalis and A.a. produce)) Collagenase Degradation of collagen Hyaluronidase: Increasing gingival permeability by widening the intercellular spaces.

  12. Gingival inflammation:- Within 10-20 days of plaque accumulation Clinical signs of gingivitis are established ----------------------------------------------- Gingivitis microscopically appears in 4 stages

  13. 1- Initial lesion: ((2-4 days of plaque accumulation)) The first microscopically changes occur In this stage vascular changes are: • 1- More blood is brought to the area. • 2- Dilation of the blood vessels. • 3- An increase in the vascular permeability results so that fluids and proteins exude into the tissues.

  14. 2- Early lesion:- Occurs after 4-7 days of plaque accumulation. 1- The major characteristic ((formation of a dense lymphocyte infiltrate. Representing predominant inflammatory cells.)) 2- The junctional epithelium begin to from retepegs. *3- The gingiva will begin to show clinical symptoms.

  15. 3- Established lesion:- • Is observed after 2-3 weeks of plaque accumulation. 1- The plasma cell is now the predominant inflammatory cell type. 2- plasma cells produce immunoglobulins(antibodies), primarily of the IgGclass.

  16. 4- Advanced lesion: • In many cases the advanced lesion never appears. • The area of the lesion enlarges. • Crestal alveolar bone resorption occurs, • The plasma cell continues to be the predominant cell type.

  17. THE END

  18. EXAM

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