Abstract
Epidemiological data indicate twofold increase of low impact fractures (spine, hip, ribs, distal forearm, and shoulder) in patients on glucocorticoid treatment compared with untreated subjects. These risks are mainly independent of BMD and prevalent fracture.
Early direct inhibitory effect of glucocorticoid on bone formation and promotion of apoptosis of bone cells are thought to be the major mechanism of glucocorticoid-induced osteoporosis (GIO). Despite differences in pathogenesis of postmenopausal osteoporosis, GIO, and other types of osteoporosis, the algorithm of treatment of GIO should be based on the assessment of the individual absolute risk of fracture (FRAX) according to the WHO recommendations.
Glucocorticoid-induced bone loss should be prevented, and if present, should be treated.