Regulation of inflammation and innate immunity by TLR agonists

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Bacteria are a common cause of periodontitis, in which accelerated alveolar bone resorption may ultimately lead to tooth loss. It is well established that bacteria interact with host cells through components of their cell wall by binding to corresponding Toll-like receptors (TLRs). Among these, LPS, a ligand for TLR4, is the most clearly defined molecule as a potent inducer of osteoclastogenesis and bone resorption. On the other hand, the fact that TLR2, in addition to TLR4, was prominently expressed in both precursors and differentiated osteoclasts, raised the possibility that TLR2 is involved in periodontitis-associated osteolysis. In the present study, we studied whether Pam3CSK4, a ligand for TLR2, caused bone resorption in vivo. The results showed that Pam3CSK4 caused even severer alveolar bone resorption as compared to LPS, indicating that transition time from inflammation to innate immunity was prolonged in Pam3CSK4-induced osteolysis compared to that of LPS.