An association between increased levels of endogenous glucocorticoids and osteoporosis was already described in 1932. Hench had administrated glucocorticoids to rheumatoid arthritis patients for the first time in 1948 and Nordin described increased prevalence of vertebral fractures in patients taking glucocorticoids in 1960. Glucocorticoids, for their antiinflammatory and immunosupressive effect, represent indispensable and widely used medicaments in rheumatology at the present time, but simultaneously the most frequent cause of secondary osteoporosis. Chronic inflammatory disorders, which we treat with glucocorticoids, might start in the childhood or in the young adulthood when glucocorticoids have negative effect on the reached peak bone density and later participate in an accelerated bone loss. The fastest drop in bone mineral density (BMD) values in association with glucocorticoid treatment occurs during the first 6–12 months of treatment, when it can reach even 5%per month. The majority of patients treated with glucocorticoids have low value of bone density and their prevalence of fractures is between 30–50%. Decreased value of bone density is the main risk factor of fractures. Their risk progressively increase in relation to decreasing values of BMD. An exponential increase of risk of fractures when T-score in BMD decreases under –2.5 SD is observed in patients with primary osteoporosis. That was the reason to declare this value as a diagnostic criterion for osteoporosis. Treatment with glucocorticoids shifts this threshold for the development of fractures higher, probably to the value of –1.5 SD in T-score, it means out of determination of osteoporosis. 1 SD decrease of BMD within the patients treated with glucocorticoids is followed by increased risk of vertebral body fractures compared with untreated individuals. This fact is due to the change of bone quality during the glucocorticoid treatment, which is not detectable by absorptiometry. The safe dose of glucocorticoids does not exist, that is why it is always necessary to use the lowest, but still effective dose, for as short time as possible. Everyadministration of prednisolon in a dose of 5 mg and more (or equivalent) for a period of 3 months should be complemented with preventive antiosteoporotic regimen. It should start together with the glucocorticoid treatment and last for the same period of time of its administration. In considering to possible GIOP development, every patient has to be carefully examined in the beginning of the treatment. Calcium and vitamin D supplementation, besides non-pharmacological interventions, are basic for the glucocorticoid induced osteoporosis (GIOP) prevention and treatment. Other medicaments are bisphosphonates, hormone replacement therapy, calcitonin and anabolic agents which have been approved to be effective in prevention and treatment of GIOP. The prevention of GIOP is essential, but when it is already present, the treatment is imperative. It is necessary to deal with all the risk factors. Calcium and vitamin D supplementation are basic for the treatment. Bisphosphonates are pharmacological agents of the first choice in the prevention and treatment of GIOP.Themost often discussed issue at the present time ishormone replacement therapy. Calcitonin is a drug of second choice whereas parathormon is a medicament of the future.

        Key words: glucocorticoid-induced osteoporosis, bone mineral density, calcium, vitamin D, bisphosphonates, hormone replacement therapy, calcitonin, parathormon