During normal bone remodeling, the supply of new osteoblasts and osteoclasts and the timing of the death of osteoclasts, osteoblasts and osteocytes by apoptosis are critical determinants of the initiation of new BMUs and the extension or reduction of the lifetime of existing ones. Many of the effects of chronic glucocorticoid administration on bone can be explained by decreased birth of osteoblast and osteoclast precursors and increased apoptosis of mature osteoblasts and osteocytes, disrupting the fine balance among these processes. Therapeutic agents that alter the prevalence of apoptosis of osteoblasts and osteoclasts can correct the imbalance in cell numbers that is the basis of the diminished bone mass and increased risk of fractures, found in glucocorticoid-induced osteoporosis.