Our current concept of periodontal disease is that some mediators found in the gingival sulcus are able to penetrate the epithelial barrier and produce tissue destruction in the periodontium. Endotoxin, one such mediator, recently has been the subject of considerable study. The purpose of this investigation was to substantiate the role of endotoxin in the pathogenesis of periodontal disease by ascertaining its action on cellular and subcellular components. In order to accomplish this, cultured human gingival fibroblasts were exposed to media containing either 300 μg/ml or 500 μg/ml of endotoxin and untreated medium for a period of 24 hours. Cells were harvested and prepared for electron microscopy by conventional methods. Electron microscopic examination revealed alterations in mitochondria, Golgi apparatus, lysosomal‐like bodies, cytofilaments and plasma membrane. Relationship of these alterations to pathologic processes is discussed.
Twenty-five silver cones were removed from teeth which had been treated endodontically from 3 months to 20 years previously. Examination by the scanning electron microscope revealed that these cones were moderately to severely corroded. The corrosion patterns were described as ranging from pitting to deep crater formation with globular or spherical agglomerations. Examinations with the electron probe showed sulfur peaks on the corroded portions of the cones. X-ray diffraction analyses indicated that the chemical compounds formed were silver sulfides, silver sulfates, silver carbonates, and silver amine sulfate amide hydrates. Tissue culture studies indicated that the corrosion products were highly cytotoxic. The mechanisms for the formation of the corrosion products have been postulated as being due to plastic deformations and metal transfer to the silver cones, plus contact of the silver with tissue fluids.
An in vitro system was used to study the detoxifying potential of H2O2 on bacterial endotoxin. L929 fibroblasts were exposed to H2O2-treated and -untreated endotoxin. Growth and viability assays were made at 24, 48, 72, and 96 h. The cultures exposed to H2O2-treated endotoxin showed a normal growth rate, whereas the cultures exposed to untreated endotoxin displayed a substantial reduction in growth. Implications are presented as to the potential role of H2O2 in the pathogenesis and treatment of periodontal disease.
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