Involvement of arachidonic acid metabolites in experimental pulpal inflammation in rats

Abstract

The purpose of the present study was to elucidate the role of the arachidonic acid metabolites in the development of pulpal inflammation. Bacterial lipopolysaccharide (LPS) -induced pulpitis was generated in the rat upper incisor. The arachidonic acid metabolism in the dental pulp was determined by measuring the conversion of the exogenously added arachidonic acid by pulp homogenates. The changes in the vascular permeability and the PMNL infiltration in the dental pulp were also examined. The results obtained were as follows: 1) The inflamed pulp could produce 12-hydroxy-eicosatetraenoic acid (12-HETE) >6-ketoprostaglandin (PG) F1α>thromboxane B2, PGE2, 12-hydroxy-5, 8, 10-heptadecatrienoic acid and 11-HETE. 2) The production of 12-HETE reached the peak at one hour after the application of LPS whereas the others reached at 12-24 hours. 3) The vascular permeability reached the maximum level at 12 hours. 4) The PMNL infiltration was found most markedly at 12-24 hours. 5) Indomethacin dose-dependently inhibited the production of PGE2 and 6-keto-PGF1α and decreased the vascular permeability in the inflamed dental pulp. 6) BW755C, an inhibitor of lipoxygenase, inhibited the production of HETEs and decreased the number of infiltrated PMNLs. These results suggest that PGE2 and PGI2 are involved in the increase in vascular permeability and HETEs are involved in PMNL infiltration in pulpal inflammation.