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Osteoporosis International
Erschienen in: Osteoporosis International 10/2007

01.10.2007 | Review

Glucocorticoid-induced osteoporosis: pathophysiology and therapy

verfasst von: E. Canalis, G. Mazziotti, A. Giustina, J. P. Bilezikian

Erschienen in: Osteoporosis International | Ausgabe 10/2007

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Abstract

Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Fractures, which are often asymptomatic, may occur in as many as 30–50% of patients receiving chronic glucocorticoid therapy. Vertebral fractures occur early after exposure to glucocorticoids, at a time when bone mineral density (BMD) declines rapidly. Fractures tend to occur at higher BMD levels than in women with postmenopausal osteoporosis. In human subjects, the early rapid decline in BMD is followed by a slower progressive decline in BMD. Glucocorticoids have direct and indirect effects on the skeleton. The primary effects are on osteoblasts and osteocytes. Glucocorticoids impair the replication, differentiation and function of osteoblasts and induce the apoptosis of mature osteoblasts and osteocytes. These effects lead to a suppression of bone formation, a central feature in the pathogenesis of GIO. Glucocorticoids also favor osteoclastogenesis and as a consequence increase bone resorption. Bisphosphonates are effective in the prevention and treatment of GIO. Anabolic therapeutic strategies are under investigation.
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Metadaten
Titel
Glucocorticoid-induced osteoporosis: pathophysiology and therapy
verfasst von
E. Canalis
G. Mazziotti
A. Giustina
J. P. Bilezikian
Publikationsdatum
01.10.2007
Verlag
Springer-Verlag
Erschienen in
Osteoporosis International / Ausgabe 10/2007
Print ISSN: 0937-941X
Elektronische ISSN: 1433-2965
DOI
https://doi.org/10.1007/s00198-007-0394-0

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