Glucocorticoid-induced osteoporosis is one of the major complications of long-term exposure to supraphysiological doses of glucocorticoid. It has been recognized that bone loss is rapid, particularly in the first 6 months of the therapy. The skeletal effects are both dose and duration dependent; daily glucocorticoid therapy at doses of 7.5 mg/day of prednisolone or above leads to decrease bone mass and increase risk of fractures. The mechanisms which glucocorticoid induces osteoporosis are suppression of bone formation and increase of bone resorption. Hypogonadism also contributes to this pathological condition via direct suppression of sex steroids and indirect suppression through decreased secretion of pituitary hormones. Estrogen, vitamin D and its active analogues, and calcitonin, have been therefore used to prevent glucocorticoid-induced osteoporosis; however, the effectiveness is somehow limited. Treatment with newly developed anti-resorptive amino-containing bisphosphonates such as alendronate and risedronate, showed significant increase of bone mineral density for both the prevention and the treatment of glucocorticoid-induced osteoporosis, as well as risk reduction of fractures in the patients. These bisphosphonates provide a better consequence for the treatment of glucocorticoid-induced osteoporosis.