Bone remodeling is regulated by systemic hormones and locally produced factors acting in concert to maintain bone mass (1). In the adult skeleton, bone remodeling is a tightly controlled process that occurs in the bone surface and results in bone turnover. Bone formation occurs only in areas of previously resorbed bone. The remodeling cycle consists of an activation phase, followed by bone resorption, a reversal phase, followed by bone formation, and a resting phase (2). Normally, bone formation and resorption are coordinated and in balance, but in conditions of persistently increased bone resorption or decreased bone formation, osteoporosis occurs. Glucocorticoids have marked effects on bone metabolism, and continued exposure of skeletal tissue to excessive amounts of these steroids results in osteoporosis. Although the exact mechanism of action of glucocorticoids in bone is uncertain, recent investigations have enhanced our understanding of the actions of glucocorticoids on skeletal tissue. This information will prove helpful for the eventual understanding of the pathogenesis of glucocorticoid-induced osteoporosis and for the development of new strategies to prevent and reverse the catabolic actions of glucocorticoids on the skeleton. Although in viva glucocorticoids have indirect actions on bone metabolism, there is sufficient evidence to believe that their direct actions on bone cells play a central role in determining their effects on bone mass and in the metabolic bone disease that follows glucocorticoid excess.