During the early phase of glucocorticoid (GC)-induced osteoporosis (GIO), GC increases the expression of receptor activator of NF-kappaB ligand (RANKL) in bone-forming cells and suppresses the production of interferon-beta in osteoclast progenitors, resulting in stimulation of bone resorption. On the other hand, GC represses the proliferation, differentiation and functional activities of bone forming cells, and finally induces their apoptosis throughout GIO, consequently causing the decrease in bone formation. In addition, as the number of bone-forming cells decrease, the osteoblast-dependent osteoclast formation also declines.