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Glucocorticoid-induced osteoporosis: clinical and therapeutic aspects.

MAZZIOTTI, Gherardo;GIUSTINA, Andrea;
2007-01-01
2007
Ateneo di appartenenza
LS7_7 Surgery
LS7_6 Gene therapy, stem cell therapy, regenerative medicine
LS4_5 Metabolism, biological basis of metabolism
LS4_3 Endocrinology
ARQUIVOS BRASILEIROS DE ENDOCRINOLOGIA E METABOLOGIA
2-s2.0-38649136320
WOS:000256344300028
Inglese
51
1404
1412
8
18209880
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. Glucocorticoids have direct and indirect effects on the skeleton. They 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 the most effective of the various therapies that have been assessed for the management of GIO. Anabolic therapeutic strategies are under investigation. Teriparatide seems to be also efficacious for the treatment of patients with GIO.
Bone Density; Bone Density Conservation Agents; Glucocorticoids; Humans; Osteoporosis; Teriparatide
4
info:eu-repo/semantics/article
262
Mazziotti, Gherardo; Giustina, Andrea; Canalis, E; Bilezikian, Jp
1 Contributo su Rivista::1.1 Articolo in rivista
none
1.1 Articolo in rivista
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11379/31935
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