Cell migration is a central part of physiological and pathophysiological 
processes including wound healing, immune defense, matrix remodeling and organ 
homeostasis. Different cell types have migratory potential including cells of 
the immune system and cells required in wound healing and tissue repair. These 
cells migrate locally through the tissue to the site of damage. The fibroblast 
is a central cell type of wound healing. In rheumatoid arthritis (RA), activated 
synovial fibroblasts (SFs) have the ability to invade joint cartilage, actively 
contributing to joint destruction in RA. Recently, RASFs have been shown to be 
able to migrate to non-affected areas and joints through the blood stream and to 
invade distant cartilage. RASFs most likely use similar mechanisms comparable to 
lymphocytes and tumor cells for long-distance and vascular trans-migration. 
Future experiments will address the goal to keep the transformed-appearing 
fibroblasts in the affected joints using therapeutical strategies that inhibit 
the pathophysiological changes of transformed-appearing RASFs but do not 
interfere with the physiological processes of 'normal' fibroblasts.