Mechanisms of bone resorption and new bone formation in spondyloarthropathies |
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Authors: | Willis Huang Edward M Schwarz |
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Institution: | (1) Department of Microbiology and Immunology, The Center for Musculoskeletal Research, University of Rochester Medical Center, 601 Elmwood Avenue, 14642 Rochester, NY, USA |
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Abstract: | Spondyloarthropathies (SpA) share clinical features such as sacroiliitis, axial immobility, and peripheral arthropathies.
They also share a strong association with human leukocyte antigen-B27, implicating T cells and antigen-presenting cells in
the disease process. Inflammation seems to underlie the pathogenesis of SpA, particularly in the axial skeleton and entheses.
Pathologic bone loss and formation occur simultaneously in inflamed regions, suggesting an inflammation-induced dysregulation
of osteoclast and osteoblast activity. Pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNFα) appear to be
central to the disease, because TNFα blockade has been shown to effectively improve clinical outcome. Other cytokines such
as transforming growth factor-beta, interferon-gamma (IFNγ), and interleukin-18 are also likely to be important in SpA. Activated
T cells have been shown to produce cytokines such as IFNγ and receptor activator of nuclear-factorkappaB ligand, with direct
effects on osteoclastogenesis. The dual role of T cells in immunobiology and skeletal biology provides a possible link between
human leukocyte antigen-B27, pro-inflammatory cytokines, and bone cells in SpA. |
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