Journal article

Publication year: 2007

Journal: Arthritis Research and Therapy

Volume number: 9

Issue number: 2

ISSN: 1478-6354

eISSN: 1478-6362

Open access status: Gold

DOI Link: https://doi.org/10.1186/ar2140

Publisher: BioMed Central

Abstract: 
Synovial pathophysiology is a complex and synergistic interplay of different cell populations with tissue components, mediated by a variety of signaling mechanisms. All of these mechanisms drive the affected joint into inflammation and drive the subsequent destruction of cartilage and bone. Each cell type contributes significantly to the initiation and perpetuation of this deleterious concert, especially in rheumatoid arthritis. Rheumatoid arthritis synovial fibroblasts and macrophages, both cell types with pivotal roles in inflammation and destruction, but also T cells and B cells are crucial for complex network in the inflamed synovium. An even more complex cellular crosstalk between these key players maintains a process of chronic inflammation. As outlined in the present review, in the past year substantial progress has been made to elucidate further details of the rich pathophysiology of rheumatoid arthritis, which may also facilitate the identification of novel targets for future therapeutic strategies.

Harvard Citation style: Knedla, A., Neumann, E. and Mueller-Ladner, U. (2007) Developments in the synovial biology field 2006, Arthritis Research and Therapy, 9(2), Article 209. https://doi.org/10.1186/ar2140

APA Citation style: Knedla, A., Neumann, E., & Mueller-Ladner, U. (2007). Developments in the synovial biology field 2006. Arthritis Research and Therapy. 9(2), Article 209. https://doi.org/10.1186/ar2140