Abstract

Prevention of glucocorticoid-induced osteoporosis (GIO) and the subsequent bone fractures is now essential for QOL. Direct inhibitory effect of glucocorticoid on bone formation and promotion of apoptosis of bone cells are currently thought to be the major mechanism of GIO. Bone resorption varies dependent on dose and length of administration of glucocorticoid, but the bone formation rate is considered to be always below the bone resorption rate. Most recent clinical guidelines have recommended bisphosphonates as the first choice for the treatment of GIO.

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