6-ketoprostaglandin-f1-alpha and Gingivitis

Prostaglandin E2 (PGE2) formation was studied in human gingival fibroblasts derived from three epileptic patients before and after 9 months of phenytoin (PHT) therapy. Interleukin 1 (IL-1 alpha; 0.3-6.0 ng/ml), (IL-1 beta; 10-1000 pg/ml) and tumour necrosis factor (TNF alpha; 0.01-0.1 microgram/ml) dose-dependently stimulated the formation of PGE2 in 24 h cultures. In fibroblasts, derived after 9 months of PHT therapy, IL-1 alpha, IL-1 beta and TNF alpha induced a significantly higher formation of PGE2 compared to that in fibroblasts derived before PHT therapy. IL-1 beta induced a significantly higher release also of 3H-arachidonic acid (3H-AA) from prelabelled PHT fibroblasts compared to that in prelabelled gingival fibroblasts isolated before the drug therapy. Addition of exogenous AA caused a spontaneous increase of PGE2 formation in PHT fibroblasts compared to that in fibroblasts isolated before the PHT treatment. The results indicate that PHT medication results in an upregulation of prostanoid formation in gingival fibroblasts partly due to an increased phospholipase A2 activity and partly due to an increased cyclooxygenase activity.

Topics: 6-Ketoprostaglandin F1 alpha; Arachidonic Acids; Cells, Cultured; Child; Dinoprostone; Dose-Response Relationship, Drug; Epilepsy; Fibroblasts; Gingiva; Gingival Hyperplasia; Gingivitis; Humans; Interleukin-1; Phenytoin; Tumor Necrosis Factor-alpha; Up-Regulation

This study was undertaken to determine the ability of inflamed and normal gingival tissues to synthesize prostaglandins (PGs) from the precursor arachidonic acid. Thirteen samples of inflamed human gingival tissue and six samples of normal human gingival tissue were studied. The inflammation was characterized histologically. After incubation of the tissue with [14C]arachidonate, PG metabolites were separated by thin-layer chromatography and identified by comparison with co-chromatographed standards. Inflamed gingival tissue synthesized significantly larger amounts, compared to normal tissue, of 6-keto-PGF1 alpha (P less than 0.05), thromboxane B2 (P less than 0.01), PGD2 (P less than 0.05), and PGA2 (P less than 0.001). Some unidentified metabolites, possibly lipoxygenase products were detected in significantly (P less than 0.001) larger amounts in inflamed than in normal tissue.

Topics: 6-Ketoprostaglandin F1 alpha; Arachidonic Acid; Arachidonic Acids; Carbon Radioisotopes; Dinoprost; Dinoprostone; Gingiva; Gingivitis; Humans; Periodontitis; Prostaglandin D2; Prostaglandins; Prostaglandins A; Prostaglandins D; Prostaglandins E; Prostaglandins F; Thromboxane B2