The Role of Low-Level Sodium Fluoride in Periodontal Inflammation

Abstract

Fluoride has a wide range of physiological activities that may contribute to its beneficial effects against inflammation-related diseases. However, the molecular mechanisms underlying the anti-inflammatory activity of fluoride are not completely characterized, and many features remain to be elucidated. In this study, we investigated the molecular basis for the down-regulation of toll-like receptor 4 (TLR4) signal transduction by low-level fluoride (NaF) in periodontal ligament cells. In addition, the expression of asporin was investigated by quantitative real-time PCR as well as by immunohistochemical analysis of periodontal ligament cells, with or without fluoride treatment. P. gingivalis-derived lipopolysaccharide (LPS) markedly elevated the mRNA and protein expression levels of DEC1, a regulator of TLR signaling. LPS-induced expression of TLR4, DEC1 and Notch1 was inhibited by low-level NaF. Asporin and periostin were expressed in periodontal ligament cells as expected. Treatment with LPS decreased the expression levels of asporin and periostin in periodontal ligament cells and treatment with low-level NaF increased those levels both in vivo and in vitro. These novel findings provide new insights into understanding the regulatory mechanisms of the TLR4 signaling pathway and the pharmacological role of low-level NaF in the inflammatory response against the development and progression of periodontal disease.