Arachidonic acid (AA) metabolites are known to play an important role in the development of inflammation and pathogenesis, of periodontal disease. The bone resorbing activity of PGE2 and elevated level of prostaglandins and thromboxane in inflamed gingiva, which are cyclooxygenase(C) products, has been well documented. However, since recent studies provide evidence that gingival tissue metabolizes AA mainly through lipoxygenase(L) path- way, we have started this study to show the exact profile of AA metabolism in gingival tissue.
Fourteen individual periodontal pocket tissue(PPT) samples were obtained from patients with advanced periodontitis and incubated separately with "CAA(0.2pCi). The tissue lipid extracts were separated by means of thin layer chromatography(TLC), and analyzed by means of autoradiography and TLC analyzer.
Our work show that "C-AA metabolism in PPT is mainly via the L pathway(L products/ C products=6.17) and that 12HETE & 15HETE(55.735yo of total formed metabolites), to a lesser extent 5HETE(6.21%), are the major L products formed. C products thromboxane B2 (4.3296), 6ketoPGF,,, & PGE2 (4.42%) were also detected in much smaller amounts than L products. Indomethacin wellknown C inhibitor, also inhibited L as well as C, that is the result similar to the reports of Paajanen et al.(1982) and Lessard et al.(1986). This phenomenon is being further investigated by use of partially purified L system.
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