One of the most important of the secondary causes of osteoporosis is chronic exposure to glucocorticoids, which are used for an extraordinarily large number of disorders. The adverse effects of hypercortisolism on bone metabolism were recognized more than half a century ago (1). Today, glucocorticoid exposure in the context of medicinal use has become far more common than excess endogenous exposure (Cushing’s syndrome). Glucocorticoid-induced osteoporosis (GIO) is the third most common cause of osteoporosis, trailing only postmenopausal and age-related osteoporosis (2). As many as 50% of individuals on chronic glucocorticoid therapy will suffer an osteoporotic fracture (3). Recently, a large-scale retrospective cohort study by Van Staa et al.(4) in England clearly demonstrated that fracture risk is increased across virtually the entire dosage range of oral glucocorticoids. A large number of subjects with a history of glucocorticoid exposure (n 244,235) were matched to the same number of control patients who had no history of glucocorticoid exposure. The average age of the subjects was 57 yr; respiratory diseases were the common indication for therapy, being prescribed in 40% of the patients (4). Referent to nonglucocorticoid users, subjects with a history of glucocorticoid therapy had significantly greater risk for fractures at the spine (rr 2.6), the hip (rr 1.6), and at any nonvertebral site (rr 1.3). The magnitude of the fracture risk was directly related to dosage, with subjects receiving as little as 2.5 mg of prednisolone at significantly greater risk than control subjects (4). Bone loss from glucocorticoid use was also found to occur rapidly, within the first 3 months of treatment. A similarly precipitous loss of bone mass has also been observed prospectively when glucocorticoids are used in the setting of organ transplantation (5, 6), and in other clinical situations (7–10). Even inhaled steroids have been implicated as a cause of bone loss (11, 12).