Rheumatoid arthritis (RA) is characterized by chronic inflammation, synovial hyperplasia and progressive joint destruction. Rheumatoid arthritis synovial fibroblasts (RA-SF) are central effector cells in cartilage erosion and contribute actively to inflammation. RA-SF show an activated phenotype that is independent of the inflammatory environment. Although new aspects regarding RA-SF activation via TLR activation, inflammatory factors, matrix degradation products and others have been uncovered, the primarily pathophysiological processes in early arthritis leading to permanent activation are mostly unknown. New findings of RA-SF activation that contribute to their altered behaviour resulting in matrix destruction and inflammation as well as their increased migratory potential in RA will be summarized.
Disclosure of Interest None Declared
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