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Pathogenese, Prophylaxe und Therapie der Steroid-Osteoporose

2008; Thieme Medical Publishers (Germany); Volume: 128; Issue: 03 Linguagem: Inglês

10.1055/s-2008-1039986

1438-941X

M. A. Dambacher, Attila Oláh, H. Maurer, R. Gampp, P. Rüegsegger,

Blood disorders and treatments

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.