Joint Tissue Findings Offer Potential Insight into Rheumatoid Arthritis
According to the National Institutes of Health, new research supported in part by the national Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) looking directly at joint tissue in people with arthritis is actually offering investigators a better understanding of the antibodies involved in rheumatoid arthritis (RA), a condition in which longterm inflammation causes pain, stiffness and damage to the joints. Antibodies are molecules that participate in the immune system's protection of the body by recognizing harmful antigens such as viruses and bacteria. In RA, antibodies called autoantibodies are directed against a person's personal healthy tissues.
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Rheumatoid factor and anti-cyclic citrullinated peptide (anti-CCP) - becoming more common in the blood of lots of people with RA have been useful for diagnosing RA and also predicting it's severity, but experts have little idea of what these autoantibodies actually do in the joint, or even whether the joints themselves might have clues to other antibodies contributing to the disease. To find some answers, NIAMS-supported researchers, Paul A. Monach, M.D., and also Diane Mathis, Ph.D., and their colleagues conducted complex checks of joint tissue samples taken from 18 patients with RA.
While their research did not necessarily find a "third antibody," the researchers did find that antibodies that came out of the joints actually bound to a lot of products associated with joint cartilage and also to histones, intracellular proteins from your cell nucleus that connect with Dna in the formation of chromosomes. The histone debris may be derived from cells that died and spilled their items, which result from the disease problem. Furthermore, they found that cartilage in RA is actually coated with histones, regardless of whether RA was active or not.
Because normal joint tissue is hardly ever removed in the course of surgery, the scientists compared their findings to those from samples from eight patients with osteoarthritis (OA, a kind of arthritis not generally associated with autoantibodies). The differences between the OA as well as RA samples were striking; the OA cartilage samples were not covered in histones. Right now, the particular scientists can not say whether histones seated on the cartilage surface are joining to be able to antihistone antibodies and causing irritation, but that is a possibility, says Doctor. Monach.
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He says when histones are a contributor to joint damage, there are also other theories about their role. One is that they stimulate immune cells through a class of proteins called Toll-like receptors (TLRs). Another is that they may be key in a process that offers potentially damaging enzymes to the cartilage surface. Doctor. Monach believes that following up on these and other hypotheses may eventually lead to the development of medication that would intervene in or prevent the process, and also thereby slow down combined swelling and damage in RA.
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These findings were published in the Proceedings of the National Academy of Sciences.
The mission of the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), a part of the U.S. Department of Health and Human Services' National Institutes of Health, is to support research into the causes, treatment, and prevention of arthritis and musculoskeletal and skin diseases, the training of basic and scientific researchers to carry out this research, and the dissemination of information on research progress in these diseases. For more information about NIAMS, phone the information Clearinghouse (877) 22-NIAMS or visit the NIAMS Web site at http://www.niams.nih.gov.
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