Pulsed electromagnetic fields inhibit osteoclast differentiation in RAW264.7 macrophages via suppression of the protein kinase B/mammalian target of rapamycin signaling pathway.

When bone resorption, aided by the activity of osteoclasts, exceeds bone formation induced by ostcoblasts, bone metabolism loses equilibration, which results in the development of bone diseases, including osteoporosis. Pulsed electromagnetic fields (PEMFs) are known to be involved in various biological processes, including cell proliferation, differentiation and apoptosis. However, the exact mechanism of action of osteoclasts remains poorly understood. In the present study, the effects of PEMFs on osteoclast differentiation and associated signaling pathways were systematically investigated in RAW264.7 macrophages. RAW264.7 cells were induced by receptor activator of nuclear factor-kappa B ligand (RANKL) to obtain osteoclasts in vitro. The results of the present study demonstrated that PEMF exposure decreased osteoclast formation, limited tartrate-resistant acid phosphatase activity, contracted bone resorption area and inhibited osteoclastic specific gene and protein expression. Furthermore, western blot analysis indicated that PEMFs distinctly abolished the upregulation of phosphorylated-protein kinase B (Akt), -mammalian target of rapamycin (mTOR) and -ribosome S6 protein kinase (p70S6K) induced by RANKL, which was consistent with the effects of pharmacological inhibitor perifosine and rapamycin. Therefore, the present study suggested that PEMFs reduced osteoclast formation from RAW264.7 macrophages via inhibition of the Akt/mTOR signaling pathway. These findings provided novel insight into the mechanisms through which PEMFs suppress osteoclast differentiation.