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Ischemia and Reperfusion Injury in Bone

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Osteonecrosis

Abstract

Bone cells may be killed in a variety of ways, from radiation to poison. But the clinical phenomenon that has become most identified with the term “osteonecrosis” is associated with ischemia. Ischemic osteonecrosis (ION) is the preferred term, although clinicians traditionally use AVN (avascular necrosis) in spite of the fact that the absence of vessels has never been histologically confirmed (ischemic vessels are still vessels just as a dead body is still a body). It is generally agreed that ION results from two main causes of ischemia: (1) hypercoagulation that is associated with a wide range of diseases, leading to the name of this category as “idiopathic” ION, and (2) physical damage to bone blood vessels resulting from impact—high energy or compression—known as “traumatic” ION. This review is divided into three sections: (a) idiopathic ION, (b) traumatic ION and reperfusion, and (c) intravital microscopic investigation of both.

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Authors and Affiliations

  1. Departments of Orthopaedic Surgery and Bioengineering, University of California, Los Angeles, CA, USA

    Howard Winet

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  1. Howard Winet
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Correspondence to Howard Winet .

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Editors and Affiliations

  1. Department of Orthopaedic Surgery, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Seongnam, Kyonggi-do, Korea, Republic of (South Korea)

    Kyung-Hoi Koo

  2. Rubin Institute for Advanced Orthopedics, Center for Joint Preservation and Replacement, Sinai Hospital of Baltimore, Baltimore, Maryland, USA

    Michael A. Mont

  3. Department of Orthopaedic Surgery, Department of Orthopaedic Surgery, Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

    Lynne C. Jones

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© 2014 Springer-Verlag Berlin Heidelberg

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Winet, H. (2014). Ischemia and Reperfusion Injury in Bone. In: Koo, KH., Mont, M., Jones, L. (eds) Osteonecrosis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-35767-1_3

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  • DOI: https://doi.org/10.1007/978-3-642-35767-1_3

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  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-35766-4

  • Online ISBN: 978-3-642-35767-1

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