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Glucocorticoids are a potent cause of osteoporosis and thus a potential source of substantial morbidity in patients who are already significantly disabled. They cause rapid bone loss within weeks of their introduction, and this loss continues even after many years of chronic use. Up to one-third of patients will develop fractures after glucocorticoid use over a 5-year period, those with lower initial bone densities (e.g., postmenopausal women) being at highest risk. Fracture risk can be assessed to some extent from a patient's age, body weight, the duration of steroid use, and the average dose, but in most cases bone density measurement at a trabecularrich site (e.g., the spine) is necessary. In those at high risk of fracture, bone density can be increased by use of sex hormone replacement (in those who have a demonstrable deficiency) or a bisphosphonate. Calcitriol, calcitonin, and fluoride may have roles as adjunctive therapies. It is incumbent on all physicians supervising long-term glucocorticoid therapy to ensure that a skeletal assessment is carried out and that osteoporosis prophylaxis is instituted where appropriate.