Glucocorticoid-induced osteoporosis: from basic mechanisms to clinical aspects

Neuroimmunomodulation. 2005;12(1):1-19. doi: 10.1159/000082360.

Abstract

Glucocorticoid (GC)-induced osteoporosis (GCOP) is the most common cause of osteoporosis in adults aged 20-45 years as well as the most common cause of iatrogenic osteoporosis. GC excess, either endogenous or exogenous, induces bone loss in 30-50% of cases. Indeed, bone loss leading to fractures is perhaps the most incapacitating, sometimes partially irreversible, complication of GC therapy. Nevertheless, GCOP is often underdiagnosed and left untreated. The following article provides an update on the cellular and molecular mechanisms implicated in the pathophysiology of GC-induced bone loss, as well as some guidelines on diagnostic, preventive and therapeutic strategies for this medical condition, in an effort to promote a better knowledge and greater awareness of GCOP by both the patient and the physician.

Publication types

  • Review

MeSH terms

  • Animals
  • Bone and Bones / drug effects*
  • Bone and Bones / metabolism
  • Bone and Bones / physiopathology
  • Glucocorticoids / adverse effects*
  • Glucocorticoids / metabolism
  • Growth Substances / metabolism
  • Humans
  • Osteoblasts / drug effects
  • Osteoblasts / metabolism
  • Osteoclasts / drug effects
  • Osteoclasts / metabolism
  • Osteogenesis / drug effects
  • Osteogenesis / physiology
  • Osteoporosis / chemically induced*
  • Osteoporosis / physiopathology
  • Osteoporosis / therapy

Substances

  • Glucocorticoids
  • Growth Substances