We explored the effects of dexamethasone on osteoclast precursors using BMMs. Dexamethasone inhibited the proliferation of BMMs. Furthermore, it stimulated the osteoclast formation via NFATc1 activation in the presence of RANKL. Since dexamethasone targeted the early stage of osteoclast formation, we investigated its effect on mRNA expression of GR and $IFN-{eta}$. Whereas dexamethasone had no effects on GR expression in the presence of RANKL, it reduced the expression of $IFN-{eta}$, suggesting that dexamethasone increased RANKL-induced osteoclast formation by modulating $IFN-{eta}$.