Glucocorticoid therapy is associated with an appreciable risk of bone loss, which is most pronounced in the first few months of use. In addition, glucocorticoids increase fracture risk, and fractures occur at higher bone mineral density (BMD) values than occur in postmenopausal osteoporosis. The increased risk of fracture has been reported with doses of prednisone or its equivalent as low as to mg daily [ 1 ]. Thus, glucocorticoid-induced bone loss should be treated aggressively, particularly in those already at high risk for fracture (older, prior fragility fracture). In other individuals, clinical risk factor and bone density assessment may help guide therapy. The prevention and treatment of glucocorticoid-induced bone loss will be reviewed here. The clinical features are reviewed separately. (See "Pathogenesis, clinical features, and evaluation of glucocorticoid-induced osteoporosis" .)
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The most commonly used AAS in medicine are testosterone and its various esters (but most commonly testosterone undecanoate , testosterone enanthate , testosterone cypionate , and testosterone propionate ),  nandrolone esters (most commonly nandrolone decanoate and nandrolone phenylpropionate ), stanozolol , and metandienone (methandrostenolone).  Others also available and used commonly but to a lesser extent include methyltestosterone , oxandrolone , mesterolone , and oxymetholone , as well as drostanolone propionate , metenolone (methylandrostenolone), and fluoxymesterone .  Dihydrotestosterone (DHT; androstanolone, stanolone) and its esters are also notable, although they are not widely used in medicine.  Boldenone undecylenate and trenbolone acetate are used in veterinary medicine .