SOA Arthritis / Source: Wikimedia Commons and GerardM

Researchers at McGill University have just published a study in the Journal of Neuroscience that confirms prior research indicating that the nervous system and nerve-growth factor (NGF) play a major role in arthritis. The findings also support the idea that reducing elevated levels of NGF—a protein that promotes the growth and survival of nerves, but also causes pain—may be an important strategy for developing treatment of arthritis pain.

In particular, they investigated changes in the nerves and tissues around the arthritic joint in rats by using specific markers to label the different types of nerve fibers and allow them to be visualized with a fluorescence microscope.

Under normal conditions, sympathetic nerve fibers regulate blood flow in blood vessels. Following the onset of arthritis in the rats, however, these fibers began to sprout into the inflamed skin over the joint and wrap around the pain-sensing nerve fibers instead. More sympathetic fibers were detected in the arthritic joint tissues, as well.

The results also showed a higher level in the inflamed skin of NGF, which mirrors the findings of human studies that have shown considerable increases in NGF levels in arthritis patients. To investigate the role of these abnormal sympathetic fibers, the McGill researchers used an agent to block the fibers’ function. They found that this reduced pain-related behavior in the animals.

“Our findings reinforce the idea that there is a neuropathic component to arthritis, and that sympathetic nerve fibers play a role in increasing the pain, ” said McGill doctoral student Geraldine Longo in the June 13, 2013 news release. Longo co-authored the paper with Professor Alfredo Ribeiro-da-Silva and postdoctoral fellow Maria Osikowicz.

“We are currently using drugs to prevent the production of elevated levels of NGF in arthritic rats; we hope that our research will serve as a basis for the development of a new treatment for arthritis in the clinic, ” said Professor Ribeiro-da-Silva.

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