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Mechanisms of glucocorticoid-induced osteoporosis

Canalis, Ernesto MD

Current Opinion in Rheumatology: July 2003 - Volume 15 - Issue 4 - p 454-457
Metabolic bone disease
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Glucocorticoids modify osteoblastic cell differentiation, number, and function. Glucocorticoids stimulate osteoclastogenesis and increase the expression of receptor activator of Nuclear factor-κB ligand and colony-stimulating factor-1, and decrease the expression of osteoprotegerin. However, the most significant effect of glucocorticoids in bone is an inhibition of bone formation. This inhibition is caused by a decrease in the number of osteoblasts secondary to a shift in the differentiation of mesenchymal cells away from the osteoblastic lineage, and an increase in the death of mature osteoblasts. Glucocorticoids decrease the function of the remaining osteoblasts directly and indirectly through the inhibition of insulin-like growth factor I expression. The stimulation of bone resorption is likely responsible for the initial bone loss after glucocorticoid exposure. Eventually, the inhibition of bone formation will cause a decrease in bone remodeling and a continued increased risk of fractures.

Department of Research, Saint Francis Hospital and Medical Center, Hartford, Connecticut, USA, and the University of Connecticut School of Medicine, Farmington, Connecticut, USA.

Correspondence to Ernesto Canalis, MD, Department of Research, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, CT 06105-1299, USA; e-mail: ecanalis@stfranciscare.org

Work from the authors' laboratory was supported by grant DK 45227 from the National Institute of Diabetes Digestive and Kidney Diseases.

© 2003 Lippincott Williams & Wilkins, Inc.