[Cortisone-induced osteoporosis: from physiopathology to treatment]

Corticosteroid-induced osteoporosis, the principal cause of "secondary" osteoporosis, is usually observed in patients under prolonged systemic corticosteroid therapy and results from the multiple effects exerted by these drugs on bone cell metabolism. Corticosteroids reduce the intestinal absorption of calcium and its tubular reabsorption, thereby negativating the calcium balance and inducing a parathyroid reaction. This reaction is responsible for an increase in bone cell remodelling, but the main manifestation of the direct effect of corticosteroids on bone is osteoblast depression, so that there is disparity between bone resorption and formation, which in turn is responsible for bone tissue deficit. Sex hormone deficiency (due to menopause or treatment) and lack of physical activities (due to the causal disease or to iatrogenic myopathy) amplify bone rarefaction. By quantifying the bone loss, modern densitometry methods provide an early risk evaluation. Osteoporosis of varying intensity exposes some 20% of patients to fractures, vertebral collapse and rib fractures. Preventive measures are always recommended, including minimal effective dose corticosteroid therapy, sodium-free diet, calcium and vitamin D supplement, sex hormone replacement and pursuance of physical activities. Once the stage of fractures by osteoporosis has been reached, the "curative" treatment aims at reducing the incidence of new fractures, either by slowing down osteoclast resorption, or by restoring the bone tissue reserve through stimulation of the osteoblasts. The usefulness of these therapeutic measures in the preventive treatment of corticosteroid-induced osteoporosis remains controverted.