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Pathophysiology and risk factors for osteonecrosis

  • Modern Surgical Treatment of Hip Avascular Necrosis (MA Mont, Section Editor)
  • Published:
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Abstract

Osteonecrosis, also known as avascular necrosis or AVN, is characterized by a stereotypical pattern of cell death and a complex repair process of bone resorption and formation. It is not the necrosis itself but rather the resorptive component of the repair process that results in loss of structural integrity and subchondral fracture. Most likely, a common pathophysiological pathway exists involving compromised subchondral microcirculation. Decreased femoral head blood flow can occur through three mechanisms: vascular interruption by fractures or dislocation, intravascular occlusion from thrombi or embolic fat, or intraosseous extravascular compression from lipocyte hypertrophy or Gaucher cells. In this review, we emphasize etiologic relationships derived mostly from longitudinal cohort studies or meta-analyses whose causal relationships to osteonecrosis can be estimated with confidence. Understanding risk factors and pathophysiology has therapeutic implications since several treatment regimens are available to optimize femoral head circulation, interrupt bone resorption, and preserve the subchondral bone.

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Kalpit N. Shah, Jennifer Racine, and Roy K. Aaron declare that they have no conflict of interest.

Lynne C. Jones is President of ARCO International. This is a medical society that promotes research and education regarding bone circulation and related diseases (including osteonecrosis). There is no financial reimbursement or pay associated with this position.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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Correspondence to Roy K. Aaron.

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This article is part of the Topical Collection on Modern Surgical Treatment of Hip Avascular Necrosis

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Shah, K.N., Racine, J., Jones, L.C. et al. Pathophysiology and risk factors for osteonecrosis. Curr Rev Musculoskelet Med 8, 201–209 (2015). https://doi.org/10.1007/s12178-015-9277-8

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