Hydroxy fatty acids and prostaglandin formation in diseased human periodontal pocket tissue

The lipoxygenase and cyclooxygenase products of arachidonic acid (AA) metabolism are known to play a key role in the development of inflammatory signs and symptoms. Periodontal pocket tissues (PPT) provide an ideal model to study the nature of mediators of inflammation in periodontal disease. Eight individual PPT samples were obtained from patients with advanced periodontitis and incubated separately with 14C‐AA. The tissue lipid extracts were analyzed by means of TLC and HPLC. It was found that PPT in all samples metabolizes AA mainly through the lipoxygenase pathways and that 12‐HETE and 15‐HETE are the major lipoxygenase products formed. Cyclooxygenase products PGE2, TXB2, and 6‐keto‐PGF1α were detected in much smaller amounts than the lipoxygenase products. Since both lipoxygenase and cyclooxygenase products are associated with inflammatory processes, the findings suggest that in treatment of inflammation in periodontal disease, drugs which inhibit the formation of both lipoxygenase and cyclooxygenase metabolites of AA would be more beneficial than those which inhibit only the cyclooxygenase products, PGs.