Effect of rheumatoid arthritis on bonesResearchers have claimed that they have been able to find out the reason behind relationship between rheumatoid arthritis (RA) and its effect on bones, according to published study in an edition of the Journal of Biological Chemistry.

The findings of this study have already guided attempts to design new drugs to reverse RA-related bone loss and provide a new ability to address more common forms of osteoporosis.

Rheumatoid arthritis is believed to affect more than two million Americans and can cause severe health risks such as pain and deformity in joints, swelling, and thinning of bone.

From News-Medical.Net:

While the new drugs are effective for many patients, others experience infections and even lymphoma in a few cases. The new drugs are based on bioengineered versions of proteins made by human immune cells called antibodies, and are very expensive to make. Thus, the field has been searching for smaller, simpler chemicals that would be effective, but with lower costs and fewer side effects.

“The significance of our study is that it identifies SMURF1 as the signaling partner through which TNF does damage in RA-related bone loss,” said Lianping Xing, Ph.D., assistant professor of Pathology and Laboratory Medicine at the University of Rochester Medical Center. “That has enabled researchers to begin designing small molecule drugs to shut down the action of Smurf 1 and its relatives. Furthermore, since mice engineered to have less Smurf1 expression develop thicker bones, future drugs that shut down Smurf1 may be also useful against more common forms of osteoporosis simply by changing the dose. Of course, this is early-stage work with many obstacles ahead, but it is exciting nonetheless.”

It was brought forward during the study that while traditional RA drugs like NSAIDs and steroids can be termed as effective for controlling symptoms, a newer class of drugs (e.g. Humira, Remicade and Enbrel) is efficacious for reversing the RA process by inhibiting TNF alpha activity.

Along with Xing, the study was led by Ruolin Guo, Motozo Yamashita, Laura Yanoso, Lan Zhao, Qian Zhang, Quan Zhou, Di Chen, David G. Reynolds, Hani Awad, Edward Schwarz, Ying Zhang and Brendan Boyce within the Department of Pathology and Laboratory Medicineat University of Rochester.

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