Abstract
It has been reported that lipopolysaccharide (LPS) has the ability to induce inflammation and osteoclastogenesis. Osteoclast formation is dependent on macrophage‐colony‐stimulating factor (M‐CSF) and ligand for the receptor activator of necrosis factor‐kB. In this study, the effect of antibody against c‐Fms, which is the receptor of M‐CSF, on LPS‐mediated osteoclastogenesis was investigated in mice. LPS was administered with or without anti‐c‐Fms antibody into the supracalvaria of mice. The number of osteoclasts and the levels of mRNA for cathepsin K and tartrate‐resistant acid phosphatase, which are osteoclast markers, in mice administered both LPS and anti‐c‐Fms antibody were lower than those in mice administered LPS alone. The level of tartrate‐resistant acid phosphatase 5b as a marker of bone resorption in mice administered both LPS and anti‐c‐Fms antibody was also lower. Furthermore, the expression of the receptor activator of necrosis factor‐kB, which is receptor activator of nuclear factor kappa‐B ligand, was increased upon LPS administration, but the expression was inhibited by anti‐c‐Fms antibody. These results showed that anti‐c‐Fms antibody inhibits LPS‐induced osteoclast formation. In conclusion, M‐CSF and its receptor are potential therapeutic targets in bacterial infection‐induced osteoclastogenesis, and anti‐c‐Fms antibody might be useful for inhibition of bacterial infection‐induced bone destruction.