Glucocorticoid-induced osteoporosis: clinical and therapeutic aspects.

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. 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.

• Authors: Gherardo Mazziotti, Andrea Giustina, Ernesto Canalis, John P Bilezikian
• Journal: Arquivos brasileiros de endocrinologia e metabologia (Arq Bras Endocrinol Metabol) Vol. 51 Issue 8 Pg. 1404-12 (Nov 2007) ISSN: 0004-2730 [Print] Brazil
• PMID: 18209880 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Bone Density Conservation Agents
• Glucocorticoids
• Teriparatide

Topics

• Bone Density (drug effects)
• Bone Density Conservation Agents (therapeutic use)
• Glucocorticoids (adverse effects)
• Humans
• Osteoporosis (chemically induced, diagnosis, drug therapy)
• Teriparatide (therapeutic use)