Abstract

The present study has been performed to elucidate the mechanism of fibrinolysis of the crevicular epithelium in marginal periodontitis, on the gingival tissues including crevicular wall from the operated materials, pocket contents, and cultivated oral bacteria. For this purpose, fibrinolysis autography by Todd, Gram-Weigert staining for fibrin and bacteria, and control procedures by inhibitors and other factors were applied. The following results were obtained:1. In marginal periodontitis, fibrinolysis was observed in the crevicular epithelium in 100 per cent. However, there was no distinct correlation between fibrinolysis of the crevicular epithelium and perivascular fibrinolysis in subepithelial inflammatory focus of the crevicular wall.2. The fibrinolysis was found almost invariably in some part of all bacterial plaques examined, but not always in desquamated epithelial cells, polymorph nucleated leucocytes and macrophages.3. The fibrinolysis was not induced by cultivated Streptococci Group A and C alone which produce streptokinase, and by cultivated Bacteroides melaninogenicus alone which elavorates some kinase like streptokinase.4. Basing on these findings, it was concluded that the fibrinolysis of the crevicular epithelium has some relation with bacterial plaque in the pocket, but cannot be attributed to oral bacteria alone.5. The following possibility was discussed that the streptokinase from the bacterial plaque can combine with plasminogen present in pocket exsudate leading to production of a streptokinase-plasminogen complex, a potent activator and then the latter plays an important role in mechanism of the fibrinolysis of the crevicular epithelium in marginal periodontitis.6. Additionally, it was presumed that the plasmin activated from the plasminogen in the pocket also contributes to produce kinin and cloven products from the third component of complement, resulting in increased vascular permeability and chronic exudative inflammation in marginal periodontitis.

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