THE EFFECT OF TRICLOSAN ON MEDIATORS OF GINGIVAL INFLAMMATION

Triclosan (2,4,4',trichloro-2'-hydroxydiphenylether) is a well-known a nd widely used nonionic antibacterial agent which has recently been in troduced in toothpastes and mouthrinses. The efficacy of triclosan-con taining toothpaste and mouthrinse to reduce both plaque and gingivitis in long-term clinical trials has been well documented. Until recently , it was generally assumed that triclosan's effect on gingival inflamm ation was due to its antimicrobial and antiplaque effect. It has now b ecome apparent that triclosan may have a direct antiinflammatory effec t on the gingival tissues. Several in vitro studies were conducted to evaluate the effect of triclosan on 4 primary enzymes of the pathways of arachidonic acid metabolism, cyclo-oxygenase 1, cyclo-oxygenase 2, 5-lipoxygenase and 15-lipoxygenase. These pathways lead to the product ion of known mediators of inflammation such as the prostaglandins, leu kotrienes and lipoxins. Triclosan inhibited both cyclooxygenase 1 and cyclo-oxygenase 2 with IC-50 values of 43 mu M and 227 mu M, respectiv ely. Triclosan also inhibited 5-lipoxygenase with an IC-50 of 43 mu M. The 15-lipoxygenase was similarly inhibited by triclosan with an IC-5 0 of 61 mu M. Hence, triclosan has the ability to inhibit both the cyc looxygenase and lipoxygenase pathways of arachidonic acid metabolism w ith similar efficacy. In cell culture experiments, it was found that t riclosan inhibited IL-1 beta induced prostaglandin E(2) production by human gingival fibroblasts in a concentration dependent manner, and at relatively low concentrations. These data, taken together, indicate t hat triclosan can inhibit formation of several important mediators of gingival inflammation. The data further suggest that the necessary tri closan concentrations could probably be achieved in local tissues, suc h as the gingiva, from topical applications of triclosan-containing to othpaste and mouthrinse.