[Pathogenesis, prevention and therapy of steroid osteoporosis]

The pathogenesis of glucocorticoid osteoporosis is complex. Numerous, controversial mechanisms have been postulated. However, there is certainly both a reduction in bone formation as well as an increase in resorption. The increase in resorption probably occurs before the reduction in formation. As of a threshold dose of approx. 7.5% prednisone equivalents per day, administered for approx. 1 year, a loss of cancellous bone occurs; the reduction in compact bone is far less pronounced. Histologically, bone matrix synthesis appears to be uniformly reduced, while resorption varies considerably. The cancellous bone structure has a filigree appearance which is also recognizable by the glass-like appearance on radiographs. The development of new glucocorticoid preparations such as Deflazacort, which promotes osteoporosis less than, e.g., prednisone, is very promising. For the prevention and treatment of glucocorticoid-induced osteoporosis, frequently used drugs today are fluorides, ossein-hydroxy-apatite complexes and, especially in acute glucocorticoid osteoporosis, calcitonin.