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Biomedical subjects

F A DeRenzis

Publications and source records attributed to F A DeRenzis.

9 recordsLinked to original sources

Ultrastructural study of cultured human gingival fibroblasts exposed to endotoxin.

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 micrograms/ml or 500 micrograms/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.

Adolescent↗

Endotoxin-inactivating potency of hydrogen peroxide: effect on cell growth.

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.

Cell Division↗

On the possible mechanism of cyanoacrylate histotoxicity.

The loss of tissue fluid as a possible mechanism of cyanoacrylate histotoxicity was studied in vitro. There appears to be no statistical difference in the rates of fluid removal between methyl, isobutyl and N-octyl 2-cyanoacrylates, nor is there any correlation between fluid removed and the observed in vivo tissue damage. It is suggested that tissue fluids play a dual role in initiating polymerization and in polymer degradation; and that tissue damage depends upon the rate of polymer decomposition with the formation of toxic degradation products.

Analysis of Variance↗