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Current concepts on the pathogenesis and natural history of steroid-induced osteonecrosis.

Abstract
The pathophysiology of non-traumatic osteonecrosis is more complex than that of traumatic osteonecrosis, and corticosteroid-induced osteonecrosis presents the greatest challenge because of the multiple effects of corticosteroids on multi-system pathways; these pathways include the effects of corticosteroids on osteoblast differentiation, osteoblast and osteoclast apoptosis, lipid metabolism, coagulation pathways, and calcium metabolism. These pathways are frequently interrelated with each other, which makes the pathogenesis even more difficult to understand. Host factors and underlying disease have been shown to play a significant role in the risk of developing osteonecrosis, and our understanding of the pathogenesis must be able to explain why some patients are at greater risk than others. Identification of genetic variants that convey additional risk will also help to personalize the way we deliver care, both in the prevention and treatment of osteonecrosis. Further understanding of the intricate immunologic and genetic pathways contributing to osteonecrosis is at the forefront of research and may soon lead to viable and less invasive non-surgical therapeutic strategies.
AuthorsChristian Powell, Christopher Chang, M Eric Gershwin
JournalClinical reviews in allergy & immunology (Clin Rev Allergy Immunol) Vol. 41 Issue 1 Pg. 102-13 (Aug 2011) ISSN: 1559-0267 [Electronic] United States
PMID21161435 (Publication Type: Journal Article, Review)
Chemical References
  • Steroids
Topics
  • Apoptosis (drug effects)
  • Blood Coagulation (drug effects)
  • Bone and Bones (drug effects, pathology)
  • Genetic Predisposition to Disease
  • Humans
  • Lipid Metabolism (drug effects)
  • Osteogenesis (drug effects)
  • Osteonecrosis (chemically induced, epidemiology, genetics, immunology)
  • Polymorphism, Genetic
  • Practice Guidelines as Topic
  • Risk
  • Steroids (adverse effects, pharmacology)

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