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Intravascular coagulation and osteonecrosis.

J P Jones1

  • 1Diagnostic Osteonecrosis Center, Kelseyville, California.

Clinical Orthopaedics and Related Research
|April 11, 1992
PubMed
Summary
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Intravascular coagulation (IC) is the likely cause of nontraumatic osteonecrosis (ON) by blocking blood flow. Evidence shows IC leads to bone death, particularly in the femoral head, progressing from fatty necrosis to ischemic degeneration.

Area of Science:

  • Orthopedics
  • Pathology
  • Vascular Biology

Background:

  • Nontraumatic osteonecrosis (ON) is a debilitating condition.
  • The precise mechanism leading to ON remains incompletely understood.
  • Intravascular coagulation (IC) is implicated as a potential pathway.

Purpose of the Study:

  • To investigate the role of intravascular coagulation (IC) as the final common pathway in the pathogenesis of nontraumatic osteonecrosis (ON).
  • To elucidate the progression of ON lesions from early fatty osteocytic necrosis to ischemic degeneration.

Main Methods:

  • Review of current evidence on IC and ON.
  • Analysis of lesion progression from Stage 1A to Stage 1B.
  • Consideration of factors contributing to IC, including fat overload, procoagulants, and impaired fibrinolysis.

Related Experiment Videos

  • Reference to animal models and cartography (embolic scintimetry, angiography).
  • Evaluation of plasma markers (fibrinopeptide A) and histologic findings.
  • Main Results:

    • Intravascular coagulation (IC) is identified as the most probable final common pathway for intraosseous fat embolism-induced osteonecrosis (ON).
    • ON lesion progression is linked to exceeding the ischemic threshold due to subchondral fat overload and impaired clearance of procoagulants.
    • Evidence supports IC initiation in the subchondral microcirculation, leading to devascularization and thrombosis.
    • Increased plasma fibrinopeptide A and histologic findings confirm intraosseous thromboses and IC's role.

    Conclusions:

    • Intravascular coagulation (IC) is the most likely final common pathway in nontraumatic osteonecrosis (ON).
    • The progression of ON involves exceeding ischemic thresholds, leading to IC and subsequent bone death.
    • Evidence from animal studies, imaging, and human cases supports the role of IC in ON pathogenesis.