Triclosan (2,4,4'-trichloro-2'-hydroxydiphenyl ether) is an antibacterial and anti-inflammatory agent included in dentifrices, mouthrinses, as well as in soaps and cosmetics. Previously, we showed that triclosan reduces the production of PGE₂, IL-1b and IFN-g in gingival fibroblasts although the mechanism(s) is unclear. It has been suggested that the anti-inflammatory effect of triclosan is partly related to its inhibitory effect on PGE₂ biosynthesis. Objectives: In the present study, we investigated the effect of triclosan on the translocation of NF-kB and expression of COX-2 induced by TNFa in relation to PGE₂ production in gingival fibroblasts. Methods: Cultures of fibroblast cells were established from gingival biopsies obtained from three children with no clinical sign of periodontal disease. NF-kB translocation was analyzed by immunoblotting, COX-2 mRNA expression by colorimetric mRNA quantitation kit, COX-2 protein level by ELISA kits and the level of PGE₂ in the culture medium by Radioimmuno-assay. Results: TNFa increased the translocation of NF-kB, COX-2 mRNA expression, COX-2 protein level and PGE₂ production in gingival fibroblasts. Triclosan inhibited (p <0.01) the basal level as well as reduced (p<0.01) the stimulatory effect of TNFa on PGE₂ biosynthesis in gingival fibroblasts. Triclosan also reduced (p<0.05) the production of PGE₂ induced by exogenous arachidonic acid. The agent did not affect the translocation of NF-kB in controls or in TNFa stimulated cells. Furthermore, treatment of gingival fibroblasts with triclosan did neither affect the mRNA or the protein expression of COX-2 in gingival fibroblasts. Conclusion: These findings suggest that the inhibitory effect of triclosan on PGE₂ production may involve a signal pathway downstream of the transcription and the translation level of COX-2. This study was supported by the Swedish Patent Revenue Research Fund.

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