This document discusses periodontal disease and bone loss. It states that changes in bacteria from healthy to diseased states are associated with progression from gingivitis to periodontitis. Periodontitis is characterized by inflammatory changes in the gingiva and connective tissue caused by bacteria, leading to destruction of collagen fibers and bone loss. The rate of bone loss without treatment is approximately 0.2mm per year on facial surfaces and 0.3mm per year on proximal surfaces. Bone loss occurs episodically with periods of activity and inactivity.
4. Changes in gingiva from normal to pathologic pocket are associated with different proportions of bacterial cells in dental plaqueHealthy - coccoid cells and straigt rodsDisease - spirochetes and motile rods
5. POCKET FORMATIONBacteria causes inflammatory change in connective tissue wall of the gingival sulcus.Degeneration of surrounding connective tissue, including gingival fibersDestruction of collagen fibers just apical to the junctional epithelium, this area becomes infiltrated with inflammatory cells and edemaImmediately apical to this is a zone of partial destruction and then an area of normal attachment
6. POCKET FORMATIONBacteria causes inflammatory change in connective tissue wall of the gingival sulcus.Degeneration of surrounding connective tissue, including gingival fibersDestruction of collagen fibers just apical to the junctional epithelium, this area becomes infiltrated with inflammatory cells and edemaImmediately apical to this is a zone of partial destruction and then an area of normal attachment
12. Bone LossExtension Of Gingival Inflamation In to The Supporting Periodontal Tissue
13. Rate Of Lone LossLoe : A: 0.2 mm Facial Surface B: 0.3mm Proximal Surface If Disease Untreated
14. LOE et al:1.Approximately 8% Had Rapid Progression characterized By Alveolar Loss Of Attachment Of 0.1 to 1mm2.A proximately 81 % had moderate progression with a yearly loss of attachment of 0.05 to 0.53. 11% had minimal or no progression of destructive disease (0.05 to 0.09 mm yealy)
15. Period of destructionDestruction occurs in an episodic Intermitant fashion with period of inactivity
17. Burst of desturctive activity are Associated with subgingival ulceration And an acut inflammatory reaction , Resulting in rapid loss of alveolar Bone
18. * Burst of destruction activity Coincide with the conversion of a Predominance tlymphocyte lesion to One with a predominance of b Iymphocyte plasma cell infiltrate
19. Period of exacerbation are associated With an Increased of the loss– unattached Motile gram– negative , unaerobic pocket flora And period of remission coincidewith the Formation of adense unattached non motile Gram positive flora with a tendency to Mineralized .
20. Tissue Invasion by one or Several bacterial species is Followed by advanced Local host defense that Controls the attack .Factors Determinig Bone Morphology In Periodontal DiseaseNormal Variation:A : The Thickness , Width And crestalAngulation Of The Inter Dental Septa B : The Thickness Of The Facial And Lingual Alveolar Plates C : The Presence Of Fenestration , Dehiscences Or Both D : The Alignment Of The Teeth E : Root And Root Trunk Anatomy F : Root Position within The Alverlar Process G : Proximity With Another Tooth Surface
35. Osseous craters1/3 Of all defect 2/3 Of all mandibular defect Twice in posterior as anterior segment
36. Reasons for high frequency of cratersA . The inter dental area collects plaque and is difficult to clean B . The normal flat or even concave faciolingualshape of the inter dental septum in lower molars may favor crater formation C . Vascular paterns from the gingiva to the center of the crest may provide a pathway for inflammation
37. Bulbuas bone contoursExostosesButtresing bone formation More common in maxilla than in the mandibule
38. Reversed architectureLoss of inter dental septum without Loss of lingual and buccal plates More common in maxilla