Best Practice & Research Clinical Rheumatology
Volume 23, Issue 1 , Pages 37-48, February 2009

Current concepts in the pathogenesis of early rheumatoid arthritis

  • Arthur G. Pratt, BSc, MRCP (Doctor)

      Affiliations

    • Musculoskeletal Research Group, Institute for Cellular Medicine, School of Clinical Medical Sciences, Newcastle University, Newcastle NE2 4HH, UK
    • Corresponding Author InformationCorresponding author. Tel.: +44 191 222 5363.
  • ,
  • John D. Isaacs, PhD, FRCP (Professor)

      Affiliations

    • Musculoskeletal Research Group, Institute for Cellular Medicine, School of Clinical Medical Sciences, Newcastle University, Newcastle NE2 4HH, UK
  • ,
  • Derek L. Mattey, PhD (Doctor)

      Affiliations

    • Staffordshire Rheumatology Centre, Haywood Hospital, Stoke-on-Trent, Staffordshire ST6 7AG, UK
    • Institute of Science and Technology in Medicine, Keele University, UK

Rheumatoid arthritis (RA) is a systemic inflammatory disease with a predilection for symmetrically distributed diarthroidal joints. It is clinically heterogeneous, with particular disease phenotypes defined according to a complex interplay of genes and the environment. In this chapter we first summarize current knowledge of RA genetic susceptibility, a field which has been transformed in recent years by powerful modern genotyping technologies. The importance of a recently described subclassification for the disease based upon the presence or absence of circulating autoantibodies to citrullinated peptides has further informed genetic studies, and we consider the implications for our understanding of RA pathogenesis. We then review the cellular and molecular processes that initiate and perpetuate joint destruction.

Keywords: rheumatoid arthritis, early, genetics, aetiology, pathogenesis

 

PII: S1521-6942(08)00087-9

doi:10.1016/j.berh.2008.08.002

Best Practice & Research Clinical Rheumatology
Volume 23, Issue 1 , Pages 37-48, February 2009