Relative conversion of arachidonic acid through lipoxygenase and cyclooxygenase pathways by homogenates of diseased periodontal tissues

Abstract

The present study shows that 14C‐arachidonic acid metabolism in gingiva of patients with periodontal disease is mainly via the lipoxygenase pathway. In two pools of gingival tissue homogenates the lipoxygenase products contained 22.65% and 23.38%, while the prostaglandins (PGs), products of the cyclooxygenase pathway, contained only 4.85% and 3.98% of the total radioactivity incubated. 12‐hydroxy‐eicosatetraenoic acid (12‐HETE), a lipoxygenase product, was detected as a major metabolite of arachidonic acid in gingiva.

Measurement of eight prostaglandins in human gingival and periodontal disease using high pressure liquid chromatography and radioimmunoassay

“…Although it was recently reported that arachidonic acid is mainly metabohzed by the lipooxygenase pathway in inflamed human gingiva (Sidhagen, Hamberg & Fredholm 1982, El Attar & Lin 1983, this study shows that products of the cyclooxygenase pathway play an important role in the development of inflammatory periodontal disease in humans.…”

Influence of cigarette smoking on synthesis of eicosanoids, isoprostanes and lipoxygenase metabolites in apical periodontitis

“…28 14 C-AA in gingiva of patients with periodontal disease is mainly metabolized via the LOX-pathway. 29 As confirmed by our results extracted granuloma converted a significantly higher percentage of the total radioactivity to LOXproducts as compared to PGs synthesized via the COX-pathway. The amount of products of the LOX-pathway were influenced by smoking.…”

Inhibition of human periodontal prostaglandin E2 synthesis with selected agents

“…Goodson et al [1] have shown that prostaglandin E 2 (PGE2) concentrations are increased in inflamed periodontal tissues. Subsequently, E1Attar and others [2][3][4][5][6] demonstrated that homogenates of inflamed periodontal tissues have an increased PGE2 synthetic capacity when compared to homogenates of healthy tissues. This suggests that there is an activation process which enhances tis-sue CO activity.…”