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Cellular and molecular pathways of structural damage in rheumatoid arthritis

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Abstract

Structural damage of cartilage and bone tissue is a hallmark of rheumatoid arthritis (RA). The resulting joint destruction constitutes one of the major disease consequences for patients and creates a significant burden for the society. The main cells executing bone and cartilage degradation are osteoclasts and fibroblast-like synoviocytes, respectively. The function of both cell types is heavily influenced by the immune system. In the last decades, research has identified several mediators of structural damage, ranging from infiltrating immune cells and inflammatory cytokines to autoantibodies. These factors result in an inflammatory milieu in the affected joints which leads to an increased development and function of osteoclasts and the transformation of fibroblast-like synoviocytes towards a highly migratory and destructive phenotype. In addition, repair mechanisms mediated by osteoblasts and chondrocytes are strongly impaired by the presence of pro-inflammatory cytokines. This article will review the current knowledge on the mechanisms of joint inflammation and the destruction of bone and cartilage.

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Authors and Affiliations

  1. Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Department of Internal Medicine 3 – Rheumatology and Immunology, Universitätsklinikum Erlangen, Ulmenweg 18, 91054, Erlangen, Germany

    Ulrike Harre & Georg Schett

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  1. Ulrike Harre
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  2. Georg Schett
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Correspondence to Georg Schett.

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This article is a contribution to the special issue on Immunopathology of Rheumatoid Arthritis - Guest Editors: Cem Gabay and Paul Hasler

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Harre, U., Schett, G. Cellular and molecular pathways of structural damage in rheumatoid arthritis. Semin Immunopathol 39, 355–363 (2017). https://doi.org/10.1007/s00281-017-0634-0

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