Periodontitis Lec 6 PDF

PERIODONTITIS Prof. Dr Rasha Wagih Contents Definition Clinical features Changes in the nomenclature of case definition of Periodontitis Chronic Periodontitis Aggressive Periodontitis The most recent Case definition of Periodontitis abscess Necrotizing disease Diagnosis and pro...

PERIODONTITIS Prof. Dr Rasha Wagih Contents Definition Clinical features Changes in the nomenclature of case definition of Periodontitis Chronic Periodontitis Aggressive Periodontitis The most recent Case definition of Periodontitis abscess Necrotizing disease Diagnosis and prognosis Periodontitis is a chronic multifactorial inflammatory disease associated with dysbiotic plaque biofilms and characterised by the progressive destruction of the tooth-supporting apparatus. is characterized by three factors: 1. The loss of periodontal-tissue support, manifested through clinical attachment loss (CAL) and radiographically assessed alveolar bone loss 2. The presence of periodontal pocketing 3. Gingival bleeding. Signs and symptoms of periodontitis can include: Swollen or puffy gums Bright red, dusky red or purplish gums Gums that feel tender when touched Gums that bleed easily Pink-tinged toothbrush after brushing Spitting out blood when brushing or flossing your teeth Bad breath Pus between your teeth and gums Armitage 1999The classification to define Periodontitis used for the longest period was by American Academy of Periodontology (AAP) 1999 Chronic Periodontitis A. Localized B. Generalized (> 30% of sites are involved) Aggressive Periodontitis (A. Localized B. Generalized (> 30% of sites are involved) Periodontitis as a Manifestation of Systemic Diseases A. Associated with hematological disorders B. Associated with genetic disorders C. Not otherwise specified Necrotizing Periodontal Diseases A. Necrotizing ulcerative gingivitis B. Necrotizing ulcerative periodontitis Periodontitis Associated With Endodontic Lesions A. Combined periodontic-endodontic lesions 1999 (AAP) classification  Chronic periodontitis has been defined as "an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss.” Site-specific disease Slight (mild) periodontitis: No more than 1 to 2 mm of clinical attachment loss Moderate periodontitis: 3 to 4 mm of clinical attachment loss Severe periodontitis: 5 mm or more of clinical attachment loss  Clinical Diagnosis Detection of chronic inflammatory changes in the marginal gingiva Presence of periodontal pockets Loss of clinical attachment It is diagnosed radio graphically by: Localized or generalized loss of alveolar supporting bone, horizontal or vertical 8. Localized periodontitis: less than 30% of the sites demonstrate attachment loss and bone loss 9. Generalized periodontitis: less than 30% or more of the sites demonstrate attachment loss and bone loss  Clinical diagnosis of periodontitis Clinical attachment loss Gingival inflammation Pain: Localized or deep pain in the jaw. Tooth mobility, Diastema and tooth migration may be present. Tooth mobility: Reversible: due to spread of inflammation Irreversible: due to loss of attachment and bone  Bacterial invasion There is bacterial invasion of the apical and lateral aspects of the pocket wall.(Gram – ve organisms: Filaments, rods and coccoids). There are periods of activation and remission in the inflammatory process as a result of bacteria- host interaction. The bacterial-leukocytes interaction leads to : *Intense epithelial desquamation, *Ulceration, *Hemorrhage, *Cementum fragmentation and necrosis *Prevent attachment of gingival fibroblasts  Mechanism of collagen destruction Collagen fibers are destroyed by collagenases and enzymes secreted by the host cells (fibroblasts, PNMs, macrophages) Phagocytosis of collagen by fibroblasts. Collagen loss → proliferation of apical cells of junctional epithelium along the root surface → detachment of the coronal portion of the junctional epithelium from the root → more deepening of the pocket. Histologically: Pocket epithelium is thin and ulcerated Inflammatory cell infiltration (PMNs, plasma cells) Clinical features Histopathologic features The gingival wall of the due to circulatory stagnation. periodontal pocket is bluish red due to destruction of gingival fibers in color. due to atrophy of epithelium Its surface is flaccid(soft), due to edema and degeneration smooth, shiny and pitting on pressure. The gingival wall may be firm and The fibrotic changes are predominant pink Bleeding on gentle probing Due to increased vascularity, atrophy and degeneration of epithelium and proximity of the elongated vessels to the inner aspect of the pocket wall Pain by exploration of the inner Due to ulceration of the inner aspect of the wall aspect of the wall Pus on digital pressure Due to suppuration and inflammation Diagnosis By probing the gingival margin along each tooth surface. Pockets presence or depth is not detected by radiographic examination because the periodontal pocket is soft tissue loss whereas radiographs detect areas of bone loss where pockets are suspected. Localized aggressive periodontitis Localised aggressive periodontitis A striking feature is lack of clinical inflammation despite the presence of deep periodontal pockets and advanced bone loss. The plaque that is present forms a thin biofilm on the teeth and rarely mineralizes to form calculus. Rate of bone loss about three to four times faster than in chronic periodontitis. Localised aggressive periodontitis clinical features Distolabial migration of the maxillary incisors with concomitant diastema formation. Increasing mobility of the first molars. Sensitivity of denuded root surfaces to thermal and tactile stimuli, and Deep, dull, radiating pain during mastication, probably because of irritation of the supporting structures. Localized Aggressive Periodontitis radiographic features Vertical loss of alveolar bone around the first molars and incisors, beginning around puberty in otherwise healthy teenagers. Radiographic findings may include an “arc-shaped loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar”. Etiology The possible reasons for the limitation (localization) of periodontal destruction to certain teeth: 1. After initial colonization of the first molars and incisors by Actinobacillus actinomycetemcomitans and the destruction of the periodontal tissues, adequate immune defenses are stimulated to produce a strong antibody response to enhance neutralization and phagocytosis of bacteria. 2. Bacteria antagonistic to A. actinomvcetemcomitans may colonize the periodontal tissues and inhibit A actinomycetemcomitans from further colonization of periodontal sites in the mouth. 3. Actinobacillus actinomycetemcomitans may lose its leukotoxin- producing ability for unknown reasons thus arresting the progression of the disease. 4. A defect in cementum formation may be responsible for the localization of the lesions.  Radiographic Findings i. Vertical loss of alveolar bone around the first molars and incisors. ii. “arc-shaped” loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar. iii. The alveolar bone loss patterns are usually bilateral and similar on both sides and has been referred to as being a ‘mirror-image’ pattern iv. usually horizontal bone pattern of bone loss at the interproximal surface of the incisors as the bone is thinner than at the interproximal surface of the molars. Generalized aggressive periodontitis Generalized aggressive periodontitis Usually affects individuals