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TNFα blockade mediates bone protection in antigen-induced arthritis by reducing osteoclast precursor supply

Stephanie Uster1, Fernanda Matos Coelho2, Daniel Aeberli3

  • 1Department of Rheumatology, Immunology & Allergology, University Hospital, Bern, Switzerland; Theodor Kocher Institute, University of Bern, Bern, Switzerland; Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland.

Bone
|October 31, 2017
PubMed

Insights

Tumor necrosis factor-alpha (TNFα) inhibitors reduce bone damage in rheumatoid arthritis by decreasing osteoclast precursor cells (OPCs) in the blood and bone marrow, not by affecting their joint recruitment.

Area of Science:

  • Immunology
  • Rheumatology
  • Cell Biology

Background:

  • Rheumatoid arthritis (RA) involves bone erosion driven by osteoclasts.
  • Tumor necrosis factor-alpha (TNFα) inhibitors are effective RA treatments, believed to work by reducing osteoclast activity in joints.
  • The impact of TNFα inhibitors on the overall pool of osteoclast precursor cells (OPCs) remains unclear.

Purpose of the Study:

  • To investigate whether TNFα inhibition affects the number of peripheral osteoclast precursor cells (OPCs).
  • To determine the mechanism by which TNFα inhibition protects bone in antigen-induced arthritis (AIA).

Main Methods:

  • Mice with antigen-induced arthritis (AIA) were treated with etanercept, a TNFα inhibitor.
  • Osteoclast numbers, synovial inflammation, and OPC recruitment to the joint were assessed.
  • OPC populations in bone marrow and peripheral blood were quantified.

Main Results:

  • Etanercept treatment significantly reduced synovial bone lesions and osteoclasts in AIA mice.
  • Contrary to expectations, OPC recruitment to the arthritic joint and synovial inflammation were not reduced.
  • A significant decrease in OPC numbers was observed in the bone marrow and blood of etanercept-treated mice.

Conclusions:

  • TNFα inhibition protects against bone loss in early chronic AIA primarily by reducing the availability of peripheral osteoclast precursor cells (OPCs).
  • The protective effect is not mediated by reduced OPC recruitment to the joint or local anti-inflammatory actions within the synovium.
Keywords:
ArthritisBlockade of TNFαBone protectionOsteoclast precursors

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