Glucocorticoid-induced osteoporosis.
OBJECTIVE
To present an overview of the peer-reviewed literature relating to glucocorticoid-induced osteoporosis that has been published since January 2006.


RESULTS
Understanding the pathophysiology of bone loss resulting from glucocorticoid use has become clearer. The role of the receptor-activated nuclear factor kappaB-ligand-osteoprotogerin system has been clarified and will likely lead to better targeted therapies. Minimal trauma fractures occur in patients treated with glucocorticoids at higher bone mineral density than is seen with other primary or secondary causes of osteoporosis. Uncertainty still remains about the lowest dose of glucocorticoids that is not associated with bone loss. Bisphosphonates remain the treatment of choice for glucocorticoid-induced osteoporosis, but despite this effective therapy the disease remains under recognized and undertreated.


CONCLUSIONS
Glucocorticoid-induced osteoporosis is a leading cause of secondary osteoporosis, one of the more devastating consequences of glucocorticoid therapy. Bone mineral density underestimates the risk of fragility fractures in glucocorticoid-induced osteoporosis, which may account for the underrecognition and undertreatment of the disease prior to fracture.
Berris
Karen Koenig
KK
Department of Internal Medicine, Wayne State University, Detroit, Michigan, USA.
Repp
Anita Lopes
AL
Kleerekoper
Michael
M
D015519:Bone Density; D050071:Bone Density Conservation Agents / Q000627:therapeutic use; D004164:Diphosphonates / Q000627:therapeutic use; D050723:Fractures, Bone / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D010024:Osteoporosis / Q000139:chemically induced* / Q000150:complications / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology; D018570:Risk Assessment; D012307:Risk Factors
D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D005938:Glucocorticoids