IBMS BoneKEy | Perspective

New insights into the biology of glucocorticoid-induced osteoporosis

Nancy E Lane
Wei Yao

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DOI:10.1138/20110511

Abstract

Glucocorticoid (GC) use results in rapid bone loss and elevated fracture risk. The excess bone fragility from GC treatment is multi-factorial. GCs alter calcium and phosphorus metabolism, which can result in elevation of parathyroid hormone (PTH) and early stimulation of osteoclast activity and bone remodeling, followed by a delayed but sustained reduction in osteogenesis, osteoblast activity and osteocyte metabolism. The changes in bone cell viability with GCs results in reduction of localized and whole bone strength. New data reveal that GC use may influence mineral metabolism through FGF23. The altered perilacunar mineralization around GC-treated osteocytes may be secondary to increased FGF23 production. In addition, low doses of GCs can induce self-preservation of osteocytes through the molecular mechanisms of autophagy, while higher doses of GCs induce osteocyte apoptosis. Osteocytic autophagy may allow for cell survival and then, with withdrawal of GCs, for the repair of lost bone tissue. Currently, both anti-resorptive and anabolic agents are prescribed to prevent or treat GC-induced bone loss. Additional studies are needed to further explore whether current treatments used for GC-induced bone loss alter osteocyte metabolism and how this influences localized and whole bone strength.

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