[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.
Dambacher
M A
MA
Forschungslabor für Calciumstoffwechsel, Orthopädischen Universitätsklinik Balgrist, Zürich.
Olah
A J
AJ
Maurer
H
H
Gampp
R
R
Rüegsegger
P
P
D001846:Bone Development; D001862:Bone Resorption; D002116:Calcitonin / Q000627:therapeutic use; D005459:Fluorides / Q000627:therapeutic use; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D006882:Hydroxyapatites / Q000627:therapeutic use; D010024:Osteoporosis / Q000139:chemically induced* / Q000503:physiopathology / Q000517:prevention & control
D005938:Glucocorticoids; D006882:Hydroxyapatites; D002116:Calcitonin; D005459:Fluorides
Pathogenese, Prophylaxe und Therapie der Steroid-Osteoporose.