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This study focused on the suppressive effects of SMFs on receptor activator of nuclear factor \u03baB ligand (RANKL)\u2010induced osteoclastogenesis and bone resorption. Direct SMFs inhibit RANKL\u2010induced multinucleated osteoclast formation, tartrate\u2010resistant acid phosphatase activity, and bone resorption in mouse bone marrow\u2010derived macrophage cells. The conditioned medium from osteoblasts treated with SMFs also resulted in the inhibition of osteoclast differentiation as well as resorption. The RANKL\u2010induced expression of osteoclast\u2010specific transcription factors, such as c\u2010Fos and NFATc1, was remarkably downregulated by SMF at 15\u2009mT. In addition, SMF inhibited RANKL\u2010activated Akt, glycogen synthase kinase 3\u03b2 (GSK3\u03b2), extracellular signal\u2010regulated kinase, c\u2010jun N\u2010terminal protein kinase, mitogen\u2010activated protein kinase (MAPK), and nuclear factor\u2010\u03baB (NF\u2010\u03baB) formation. These findings indicate that SMF\u2010mediated attenuation of RANKL\u2010induced Akt, GSK3\u03b2, MAPK, and NF\u2010\u03baB pathways could contribute to the direct and indirect inhibition of osteoclast formation and bone resorption. Therefore, SMFs could be developed as a therapeutic agent against periprosthetic or peri\u2010implant osteolysis. Additionally, these could be used against osteolytic diseases such as osteoporosis and rheumatoid arthritis. 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