Loss of bone mass resulting from the treatment of chronic diseases is not unusual. However, osteoporosis in such patients is typically diagnosed too late, usually after a fracture appears. Particular attention should be given to glucocorticoids, which are commonly used in internal medicine. These hormones delay bone formation (via inhibition of osteoblast differentiation and osteoblast function) and activate bone resorption (through RANKL). Moreover, glucocorticoids inhibit calcium absorption from the intestines, which results in hypocalcemia. Following hyperparathyroidism further accelerates bone resorption. Severe damage to bone microstructure and its mechanical characteristics leads to atraumatic fractures. Bone loss sustained during glucocorticoid treatment occurs very early (3-5 % of bone mass in the first year and up to 1 % each year thereafter). Fortunately, most skeletal damage is reversible with early supplementation of vitamin D and calcium. Osteopenia (osteoporosis) complicates long-term treatment with supressive doses of thyroid hormone most often in females with hypoestrinism. L-thyroxine administered in doses > 0.093 mg/day leads to bone resorption, which is in part due to suppressed (low) levels ofTSH. Medications which pose a high risk of fracture are those which induce hypoestrinism (aromatase inhibitors) and antiandrogens (GnRH agonists). Similarly, some oral antidiabetics (such as thiazolindiones) promote adipogenesis to the detriment of osteogenesis, which increases bone loss. Fractures are also frequently observed in patients treated with selective serotonin reuptake inhibitors, anti-epileptics, diuretics, anticoagulation drugs and proton pump inhibitors. This review discusses the mechanisms of bone damage induced by the abovementioned pharmaceuticals.