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Many arachidonic metabolites have been shown to have marked potent biological effects in animals. The cyclooxygenase and lipoxygenase products of arachidonate metabolism are known to play a key role in the development of inflammatory symptoms and signs. Reports published during past decades indicate that cyclooxygenase products of arachidonic acid metabolism are present in much higher concentrations in inflamed than in healthy periodontal tissues. Since information about the role of lipoxygenase products of arachidonic acid metabolism in human periodontal disease is lacking, the objective of this study was to determine the ability of diseased and non-diseased gingival tissue to synthesize lipoxygenase products from the precursor arachidonic acid. Twenty-six samples of diseased tissue and nine samples of non-diseased tissue were included in our data analysis. After incubation of the tissue with 100,000 cpm [3H]-arachidonic acid, lipoxygenase products were separated by high performance liquid chromatography (HPLC) and identified by comparison with cochromatographed standards. Our results showed that inflamed gingival tissue synthesized significantly larger amounts, of LTB4(p < 0.01), LTC4(p < 0.01), LTD4(p < 0.01), LTE4(p < 0.01), 5-HETE(p < 0.05), 12-HETE(p < 0.01), and 15-HETE(p < 0.01), compared to non-diseased tissue. The lipoxygenases are more active in inflamed gingival tissue than in non-diseased gingival tissue. 12-HETE and 15-HETE were the the major metabolites formed by lipoxygenases in diseased and non-diseased human gingiva. Since we did not functionally determine the fractions separated by HPLC, our present data may only provided indirect evidence for the existence of lipoxygenase products in periodontal tissue. However, our study did establish a research model for the investigation of arachidonic acid metabolism in the pathogenesis of periodontal disease.