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

Christian Powell, Christopher Chang, M. Eric Gershwin

Research output: Contribution to journalArticle

61 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)102-113
Number of pages12
JournalClinical reviews in allergy & immunology
Volume41
Issue number1
DOIs
StatePublished - Aug 2011
Externally publishedYes

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Osteonecrosis
Steroids
Adrenal Cortex Hormones
Osteoblasts
Osteoclasts
Lipid Metabolism
Apoptosis
Calcium
Therapeutics
Research

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Current concepts on the pathogenesis and natural history of steroid-induced osteonecrosis. / Powell, Christian; Chang, Christopher; Gershwin, M. Eric.

In: Clinical reviews in allergy & immunology, Vol. 41, No. 1, 08.2011, p. 102-113.

Research output: Contribution to journalArticle

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