The primary pathophysiologic feature of advanced osteonecrosis is a zone of necrotic bone containing trabeculae with dead osteocytes associated with marrow necrosis and fibrosis . This pathognomonic feature led to the use of the expression “avascular necrosis,” although the international society for the study of the circulation to bone and its disorders, ARCO International (Association Internationale pour la Recherche sur la Circulation Osseuse), recommends using the term “osteonecrosis.” There are several theories regarding the pathogenesis of osteonecrosis [ON], as discussed in several outstanding review articles [2–6]. These can be categorized as (1) extraosseous, (2) intraosseous, or (3) direct cellular. There are many other theories as well, such as intravascular or extravascular pathologies. John Paul Jones, Jr., suggested that multiple etiologies may lead to a final common pathway of intravascular coagulation. He hypothesized that intravascular coagulation is an “intermediary mechanism” in the development of ON . The evidence that intravascular coagulation plays an integral role in the pathogenesis of ON is both direct and indirect and will be the focus of this chapter.
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