Osteoclast differentiation and bone resorption activity require stimulation by the receptor activator of nuclear factor-kappaB (RANKL) expressed on osteoblasts . In the present study, increased RANKL mRNA expression was observed in DPB-LPS-stimulated hFOB1.19 human osteoblast cells. In addition, DPB-LPS stimulated osteoclast formation and bone resorption under RANKL-limited conditions. These results are consistent with the results of previous studies showing that LPS stimulated osteoclastogenesis [35–37]. These results indicate that DPB-LPS promotes functional osteoclast formation through osteoblast-dependent and osteoblast-independent pathways. DPB-LPS-induced osteoclast formation and bone resorption were also significantly abolished by the EETC treatment.