Effects of phenol and other dental medicaments on endogenous arachidonic acid metabolism in isolated rat dental pulp.

Abstract

Phenolic compounds such as phenol or eugenol are widely used as topical medicaments in dentistry for the treatment of pulp inflammation. The effects of these drugs on the endogenous biosynthetic capacity of isolated dental pulp to form prostaglandin (PG) E2, PGF2α, PGI2 and thromboxane (TX) A2 were investigated. Dental pulp tissues excised from rat incisors were incubated in Krebs-Henseleit buffer, and PGs and TX in the medium were determined by radioimmunoassay. The most abundant PG released from the pulp tissue was PGI2 (assayed as 6-keto-PGF1α), followed by TXA2 (assayed as TXB2), PGF2α and PGE2. Phenolic compounds used as dental medications were found to inhibit dose-dependently the endogenous production of PGI2 in the order eugenol > thymol > guaiacol > phenol. Phenol also reduced dose-dependently the ionophore A23187-stimulated formation of all cyclooxygenase metabolites to a similar extent. Pretreatment with 10 mM phenol, which could almost completely inhibit PGI2 release, did not influence the capacity of PGI2 production induced by A23187, suggesting that the inhibitory effect is reversible and may not be due to nonspecific denaturation of enzyme proteins. These results suggest that the anodyne effects of these phenolic compounds may result from their ability to inhibit cyclooxygenase activity or deacylation of its substrate from phospholipids.