© 2005 by BMJ Publishing Group Ltd & European League Against Rheumatism
LEADER
Antirheumatic treatment
The needle and the damage done*
Department of Rheumatology and Clinical Immunology, Charité University Hospital, Humboldt University of Berlin, Germany
Correspondence to:
Correspondence to:
Professor G-R Burmester
Department of Rheumatology and Clinical Immunology, Charité University Hospital, Humboldt University of Berlin, Schumannstr 20–21, D-10098 Berlin, Germany; gerd.burmester@charite.de
Evaluation of sublining macrophages by synovial needle biopsy, CD68 immunohistochemistry, and digital image analysis may help to establish evidence based treatments in RA.
Keywords: arthroscopy; biomarkers; macrophages; rheumatoid arthritis; synovial tissue; antirheumatic treatment
| The first 150 words of the full text of this article appear below. |
Despite decades of research, the aetiology of rheumatoid arthritis (RA) is still unknown. Early theories about its pathogenesis focused on autoantibodies and immune complexes, T cell mediated antigen-specific responses, a T cell independent cytokine network, and aggressive tumour-like behaviour of rheumatoid synovial tissue.1 Recently, B cell targeting approaches underline again the role of autoantibodies. None of these concepts alone could explain the chronic inflammation and progressive joint destruction characteristic of RA.
However, knowledge about the pathophysiological interplay of lymphocytes, macrophages, and local synovial fibroblasts within the synovial membrane has advanced over recent years. The success of treatments targeting tumour necrosis factor 
(TNF) and interleukin (IL) 1 suggest a key role for the monocyte-macrophage system in the pathophysiology of the disease. This is further supported by the fact, that macrophages are abundant within the rheumatoid synovial tissue.2 Moreover, both blood monocytes and tissue macrophages are activated and, in
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