The pathological periodontal pocket

1.The remaining tooth associated epithelium has been transformed to a pocket epithelium which is characterized by proliferations of sc rete peg formations and by an increased permeability for cells and fluid. In some areas the connective tissue is devoid of epithelium and there may be a direct contact between the pocket environment and the connective tissue. Lateral to the pocket epithelium in the connective tissue there is a dense accumulation of immune cells of various types. Plasma cells predominate the immune infiltrates. The collagen in the connective tissue close to the pocket epithelium is dissolved and there are relatively fewer fibroblasts compared to healthy periodontal conditions. The mechanisms behind the tissue damage appear to associate with the release of metalloproteinases from accumulated

leukocytes and substances from the local immune process in the gingiva. The actual attachment loss is believed to be caused by the dissolution of collagen fibers which allow the epithelium to proliferate over the tooth surface. 2. The progression rate of periodontal attachment loss varies. In some periods the destruction of the attachment is rapid in others more slow. The lack of appropriate methodology prevents the registration of minor progressions and it is only when the loss of attachment has reached a certain level that it can be registred clinically. Changes in attachment level of 2 mm or more is generally indicative of that a progression has taken place. The pathological periodontal pocket is characterized by an ongoing inflammatory reaction which will vary over time. On the tooth surface there are accumulations of dental plaque.The composition of the subgingival microflora varies but around 10 bacterial species have been suggested to be particular periodontal pathogens. The composition varies both in the lateral and apical coronal direction. The subgingival ecology is different on the tooth surface, in the pocket exudate and on the epithelium of the pocket lining. It is therefore difficult to take a microbial sample which is reflecting the tissue response in relation to the composition of the flora. 3. In addition current research have demonstrated that the subgingival bacteria also may invade dentinal tubules in areas where the disease process has removed the cementum. Such intradental reservoirs of microorganisms may favor recolonization of the tooth surface after treatment. Calculus formation subgingivally creates increased surfaces for bacterial colonization and subgingival calculus may contribute indirectly to the etiology of periodontitis. A continuous migration of leukocytes into the pocket occur. The polymorphonuclear

leukocytes predominate this cellular exudate. The leukocytes form a wall between the gingival tissues and the surface of the tooth associated dental plaque. The leukocytes protect the gingival tissues towards major invasion of bacteria, There is only a short junctional epithelium at the apical part of the pocket.