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Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
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Published on: March 18, 2019

M-CSF mediates TNF-induced inflammatory osteolysis.

Hideki Kitaura1, Ping Zhou, Hyun-Ju Kim

  • 1Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

The Journal of Clinical Investigation
|November 19, 2005
PubMed
Summary

Tumor necrosis factor-alpha (TNF-alpha) drives inflammatory bone loss by stimulating M-CSF production from stromal cells. Targeting the M-CSF receptor (c-Fms) effectively blocks this osteolysis, offering a potential therapeutic strategy.

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Area of Science:

  • Immunology
  • Cell Biology
  • Rheumatology

Background:

  • Tumor necrosis factor-alpha (TNF-alpha) is a key mediator of inflammatory osteolysis.
  • Understanding the cellular mechanisms by which TNF-alpha induces bone erosion is crucial for developing targeted therapies.

Purpose of the Study:

  • To elucidate the cellular sources and molecular pathways through which TNF-alpha mediates osteoclastogenesis.
  • To evaluate the therapeutic potential of targeting the M-CSF signaling pathway in inflammatory bone diseases.

Main Methods:

  • Chimeric mice studies to assess TNF receptor signaling in bone marrow stromal cells and osteoclast precursors.
  • In vivo experiments involving induction of inflammatory arthritis and TNF-alpha injection.
  • Treatment with a monoclonal antibody against the M-CSF receptor (c-Fms) and assessment of osteoclastogenesis and bone resorption markers.

Main Results:

  • Both bone marrow stromal cells and osteoclast precursors mediate TNF-alpha's osteoclastogenic effects, with stromal cells playing a greater role via M-CSF production.
  • TNF-alpha upregulates M-CSF expression in stromal cells, which in turn induces RANK in osteoclast precursors, promoting osteoclast formation and survival.
  • Anti-c-Fms antibody treatment completely inhibited pathological osteoclastogenesis and bone resorption in mouse models of inflammatory arthritis and TNF-alpha-induced osteolysis.

Conclusions:

  • M-CSF produced by TNF-responsive stromal cells is a critical mediator of TNF-alpha-induced osteoclastogenesis.
  • Targeting the M-CSF receptor (c-Fms) effectively blocks inflammatory bone erosion, presenting c-Fms as a promising therapeutic target for inflammatory bone diseases.