Glucocorticoid-induced osteonecrosis is a common and severe adverse event. Glucocorticoid use is one of the most important causes of osteonecrosis. In patients receiving long-term therapy, glucocorticoids induce fractures in 30 to 50% and osteonecrosis in 9 to 40%. The pathogenesis of glucocorticoid-induced osteonecrosis is not fully understood but postulated mechanisms include hyperlipidemia, fat emboli and intravascular coagulation that reduce the supply of blood to the bones. Since not all patients who are treated with steroids develop osteonecrosis, the presence of additional risk factors or individual variation of glucocorticoids sensitivity has been suggested. The risks of this disease include advancing age, prolonged duration of treatment, increased daily dosage and cumulative dose, low body mass index, underlying disease, and polymorphisms in the glucocorticoid receptor. Bisphosphonates are first-line options for glucocorticoid-induced osteoporosis and may also be useful in glucocorticoid-induced osteonecrosis. It has been indicated that bisphosphonates may rapidly reduce pain, and delay joint collapse in patients with osteonecrosis.
