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.