The effect of triclosan on mediators of gingival inflammation

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Abstract
Triclosan (2,4,4′,‐trichloro‐2′‐hydroxydiphenylether) is a well‐known and widely used nonionic antibacterial agent which has recently been introduced in toothpastes and mouthrinses. The efficacy of triclosan‐containing 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 inflammation was due to its antimicrobial and anti‐plaque effect. It has now become apparent that triclosan may have a direct anti‐inflammatory effect 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 production of known mediators of inflammation such as the prostaglandins, leukotrienes and lipoxins. Triclosan inhibited both cyclooxygenase 1 and cyclo‐oxygenase 2 with IC–50 values of 43 μM and 227 μM, respectively. Triclosan also inhibited 5–lipoxygenase with an IC‐50 of 43 μM. The 15‐lipoxygenase was similarly inhibited by triclosan with an IC‐50 of 61 μM. Hence, triclosan has the ability to inhibit both the cyclo‐oxygenase and lipoxygenase pathways of arachidonic acid metabolism with similar efficacy. In cell culture experiments, it was found that triclosan inhibited IL‐1β induced prostaglandin E2 production by human gingival fibroblasts in a concentration dependent manner, and at relatively low concentrations. These data, taken together, indicate that triclosan can inhibit formation of several important mediators of gingival inflammation. The data further suggest that the necessary triclosan concentrations could probably be achieved in local tissues, such as the gingiva, from topical applications of triclosan‐containing toothpaste and mouthrinse.