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Decrease in the mesenchymal stem-cell pool in the proximal femur in corticosteroid-induced osteonecrosis.

P Hernigou1, F Beaujean, J C Lambotte

  • 1Department of Orthopaedics, Hôpital Henri Mondor, Creteil, France.

The Journal of Bone and Joint Surgery. British Volume
|April 16, 1999
PubMed
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Corticosteroids reduce bone marrow stromal cell activity in the femur, potentially contributing to osteonecrosis. This study highlights a novel mechanism for glucocorticosteroid-induced bone damage.

Area of Science:

  • Bone biology
  • Cellular biology
  • Orthopedic research

Background:

  • Osteonecrosis, particularly in the femoral head, can lead to debilitating bone death.
  • Glucocorticosteroids and sickle-cell disease are known risk factors for osteonecrosis.
  • The underlying mechanisms of glucocorticosteroid-induced osteonecrosis are not fully understood.

Purpose of the Study:

  • To evaluate bone-marrow stromal cell activity in patients with corticosteroid-induced osteonecrosis.
  • To compare this activity with osteonecrosis in sickle-cell disease patients and healthy controls.
  • To investigate the potential role of glucocorticosteroids in reducing bone progenitor cells.

Main Methods:

  • Bone marrow was aspirated from the proximal femur (non-necrotic and intertrochanteric regions).

Related Experiment Videos

  • Stromal cell activity was assessed by culturing fibroblast colony-forming units (FCFUs).
  • FCFU counts were compared across patient groups (corticosteroid-induced osteonecrosis, sickle-cell osteonecrosis, controls).

    • Main Results:

    • A significant decrease in FCFUs was observed outside the necrotic area in the femoral heads of patients with corticosteroid-induced osteonecrosis.
    • This reduction in progenitor cells was more pronounced compared to sickle-cell disease and control groups.
    • The findings suggest an adverse effect of glucocorticosteroids on bone marrow progenitor cells.

    Conclusions:

    • Glucocorticosteroids may impair bone healing and contribute to osteonecrosis by reducing the number of bone marrow progenitor cells.
    • This mechanism offers a potential explanation for corticosteroid-induced osteonecrosis.
    • Further research is warranted to explore the therapeutic implications of these findings.