Triclosan alters antimicrobial and inflammatory responses of epithelial cells

Periodontal diseases are a class of pathologies wherein oral microbes induce harmful immune responses in a susceptible host. Therefore, an agent that can both reduce microbial burden and lessen pathogenesis of localized inflammation would have beneficial effects in periodontal disease; 2,4,4‐trichloro‐2‐hydroxydiphenyl‐ether [triclosan] is currently used in oral care products owing to broad spectrum antimicrobial and anti‐inflammatory properties.ObjectiveTo determine effects of triclosan on the response of oral epithelial cells to stimulation with the inflammatory microbial product lipopolysaccharide (LPS), a ligand for toll‐like receptor 4 [TLR4].Materials/MethodsPrimary human oral epithelial cells were stimulated with LPS in the presence and/or absence of triclosan after which expression of pro‐inflammatory cytokines, β‐defensins, micro‐RNAs [miRNAs], or TLR‐signaling pathway proteins were evaluated.ResultsHere, we demonstrate that triclosan is a potent inhibitor of oral epithelial cell LPS‐induced pro‐inflammatory responses by inducing miRNA regulation of the TLR‐signaling pathway. Triclosan was not a pan‐suppresser of oral epithelial cell responses as β‐defensin 2 [βD2] and βD3 were upregulated by triclosan following LPS‐stimulation.ConclusionsThese data demonstrate both a novel antimicrobial mechanism by which triclosan improves plaque control and an additional anti‐inflammatory property, which could have beneficial effects in periodontal disease resolution.