Triclosan reduces prostaglandin biosynthesis in human gingival fibroblasts challenged with interleukin-1 in vitro

The effect of the toothpaste ingredient triclosan (2,4,4'-trichloro-2'-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1 beta (IL-1 beta) or tumor necrosis factor alpha (TNF alpha) was studied in vitro. When gingival fibroblasts were treated simultaneously with triclosan and IL-1 beta, the stimulatory effect of IL-1 beta on prostaglandin E(2) (PGE(2)) and PGI(2) formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE(2) formation induced by TNF alpha. Furthermore, the capacity of IL-1 beta to induce release of [H-3] arachidonic acid from prelabelled gingival fibroblasts was reduced in the presence of triclosan. Addition of exogenous unlabelled arachidonic acid (AA) to the cells resulted in enhanced PGE(2) formation which was reduced by triclosan. The upregulation of the metabolism of AA to PGE(2) induced by IL-1 beta, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1 beta on prostanoid formation (PGE(2) PGI(2)) in human gingival fibroblasts was diminished in the presence of triclosan partly at the level of phospholipase A(2) and partly at the level of cyclooxygenase. The present data that triclosan, in vitro, inhibits the production of inflammatory mediators such as prostaglandins suggests that this can be an aspect of its clinical effect on gingivitis, in addition to its antibacterial effect.