Lec16: Pathogenesis of Periodontal Disease PDF

# Lec16: Pathogenesis of Periodontal disease ## Dr. Nafhat Almisk Amir Salih # 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)...

# Lec16: Pathogenesis of Periodontal disease ## Dr. Nafhat Almisk Amir Salih # 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) ## Gingivitis: - Inflammation is confined to gingival tissue No loss of attachment 1. Redness 2. Swelling 3. Bleeding # Periodontitis: - Inflammation of the supporting with (apical migration of junctional epithelium with associated loss of attachment). Usually progression = (loss of bone and Periodontal ligament). ## Gingivitis - Inflamed gum ## Periodontitis - Plaque & tartar - Pocket - Bone loss - Crest of alveolar bone - Junctional epithelium # Gingivitis - Localized gingivitis - Generalized gingivitis # Periodontitis - Localized periodontitis - Generalized periodontitis # 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. - Intensive plaque control - Improves clinical gingivitis - Leaving of P.con. - Plaque accum. - Gingivitis. 3. An increase serum antibodies against specific subgingival organisms. # The possible pathogenic mechanisms ## Bacterial invasion 1. Invasive nature of spirochetes in necrotizing ulcerative gingivitis (NUG). 2. *Aggretibacter actinomycetemcomitans* (*Aa*):- - In localized aggressive Periodontitis (LAP) they invade the connective tissue; ## (Exotoxins). - *Aa*. - (Exotoxin) - (leukotoxin) - (Leukotoxin) its toxic to (PMNs). - (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) # 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. # 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. # Gingival inflammation: - Within 10-20 days of plaque accumulation - Clinical signs of gingivitis are established - Gingivitis microscopically appears in 4 stages # 1- Initial lesion: ((2-4 days of plaque accumulation)) - The first microscopically changes occur - In this stage vascular changes are: - More blood is brought to the area. - Dilation of the blood vessels. - An increase in the vascular permeability results so that fluids and proteins exude into the tissues. # 2- Early lesion: - Occurs after 4-7 days of plaque accumulation. - The major characteristic - (formation of a dense lymphocyte infiltrate. Representing predominant inflammatory cells.)) - The junctional epithelium begin to from retepegs. - The gingiva will begin to show clinical symptoms. # 3- Established lesion: - Is observed after 2-3 weeks of plaque accumulation. - The plasma cell is now the predominant inflammatory cell type. - plasma cells produce immunoglobulins (antibodies), primarily of the IgG class. # 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. # THANKS