A study has shown that fibrin, the protein involved in blood clotting, plays a major role in the development of rheumatoid arthritis. The study, the first of its kind, carried out by researchers at Cincinnati Children's, showed that rheumatoid arthritis seems to occur due to the meeting of inflammatory cells with fibrin matrices through a specific integrin receptor, aMB2. The researchers have published an article in the November issue of Journal of Clinical Investigation, in which they suggest that therapies for arthritis can be designed so that the interaction between inflammatory cells and fibrin is interrupted.
"Our study establishes that fibrin is a powerful, although context-dependent, determinant of inflammatory joint disease," said Jay Degen, Ph.D., a researcher in Developmental Biology at Cincinnati Children's and the study's lead author. "These findings also suggest that pharmacologically interrupting the interaction of fibrin and aMB2 might be efficacious in the treatment of arthritic disease as well as many other inflammatory diseases, such as multiple sclerosis."
Affecting 2.1 million people in the United States, rheumatoid arthritis is a painful and debilitating disease involving chronic inflammation, tissue degeneration, loss of cartilage and bone and ultimately loss of joint mobility and function, according
to the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Although the disease's precise cause is not fully known, activation of specific components in the body's immune system seem to play a major role in its onset and early progression, according to researchers. Fibrin deposits are a prominent feature of arthritic joints and the protein appears to be a link between systems that control inflammation and bleeding within joints. Dr. Degen and his colleagues explained that in arthritic joints, the mesh-like matrices formed by fibrin to create blood clots may control local activity of inflammatory cells as well as support inappropriate tissue reorganization.