A study involving mice found that the processing of pain in the joint contributes to arthritis. Pain itself may be actually what feeds the condition. University of Rochester researcher Stephanos Kyrkanides, DDS, PhD, and colleagues said that When a pain signal from an arthritic joint reaches the spine, there’s a burst of chemical signals. One result of this burst of signals is that the spine becomes inflamed in the area where the nerve from the joint attaches. Another result is that signals travel backward from the spine to the joint.
What researchers found was when the signal is interrupted there is less pain in the joint and the joint actually healed in the mice who had arthritis. Kyrkanides says:
“This cross talk is oil to the fire of arthritis. Trying to stop joint inflammation with the traditional drugs we have is inadequate — because it tries to address the joint but fails to address this newly discovered mechanism where pain is progressing along the nerve from the spine.”
In studies with arthritic mice, the researchers used a gene therapy to block a chemical messenger, IL-1B. The mice stopped their pain behavior. And their joints got better.
“It proves the processing of pain in the joint actually contributes to arthritis itself. We were very impressed to see we could control arthritis progression and allow for spontaneous if, by targeting IL-1B, we could control the pain at the spinal cord or along the sensory nerves.”
This research gives physicians a new outlook on treating arthritis. A osteoarthritis expert, Farshid Guilak, PhD, said that it’s a very exciting find because it opens up a whole new way of treating arthritis. Currently, physicians worry that if they just treat the pain in arthritis patients the joint damage will be worse because the patient will overuse their joints. With this study, it shows that by treating the pain it can actually affect the disease.