3/18/2019

Joint Tissue Findings Offer Potential Insight into Rheumatoid Arthritis

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 within individuals with arthritis is actually providing investigators a better understanding of the antibodies involved in rheumatoid arthritis (RA), a condition in which chronic 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 tissue.

The NIH Explains that Two Autoantibodies

Rheumatoid factor and anti-cyclic citrullinated peptide (anti-CCP) - becoming more common in the blood of many people with RA have been useful for diagnosing RA and predicting it's severity, but experts have little understanding of what these autoantibodies actually do in the joint, or 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 tests of joint tissue samples taken from 18 patients with RA.

While their investigation failed to necessarily find a "third antibody," the researchers did realize 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 relate with Dna in the formation of chromosomes. The histone deposits may be derived from cells that died and spilled their items, which be a consequence of 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 seldom removed in the course of surgery, the scientists compared their findings to those from samples from eight patients with osteoarthritis (OA, a form of arthritis not generally associated with autoantibodies). The variations between the OA and RA samples were striking; the OA cartilage samples were not covered in histones. Right now, the actual scientists can't say whether histones sitting down on the cartilage surface are binding to be able to antihistone antibodies and adding to swelling, but that is a possibility, says Doctor. Monach.

He says in the event that 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 provides potentially damaging enzymes to the cartilage surface. Dr. Monach believes that following up on these and other hypotheses may eventually lead to the development of drugs that would get involved in or block the process, as well as thereby slow down shared inflammation and damage in RA.

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  • These conclusions 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 medical scientists to carry out this research, and the dissemination of information on research progress in these diseases. For more information about NIAMS, contact the data Clearinghouse (877) 22-NIAMS or go to the NIAMS Web site at http://www.niams.nih.gov.

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