Osteoarthritis (OA) is a degenerative joint disease that can affect any joint in the body and is one of the most common reasons for musculoskeletal pain. Although we can see objective evidence of OA through imaging findings such as joint space narrowing and thinning of joint cartilage, this doesn’t always correlate with a patient’s clinical symptoms. In addition, we don’t fully understand the true mechanism of pain with osteoarthritis, and there are believed to be multiple sources of pain generators. Understanding the mechanisms of pain with joint OA could lead to novel treatment methods for improving patient’s symptoms and quality of life. Recently, an international team of researchers spearheaded by Rush University Medical Center, published an article in the Journal of Clinical Investigation which shed light on a potentially new source for osteoarthritis pain after discovering a specific compound that is produced during the breakdown of cartilage.
The compound in question is known as 32-mer and is named so because it is made of thirty-two amino acids (building blocks of proteins). The above research team is the first to discover a relationship between 32-mer and arthritis pain. They figured out that the presence of 32-mer in joints activates a specific neurological pathway that is linked to knee pain. They validated this finding with laboratory cultures and experiments in mice that were genetically altered to develop osteoarthritis. They found that 32-mer in joints only caused pain in mice that had normal functioning of the Toll-like-recptor-2 (TLR2) pathway [a cell signaling pathway involved in transmitting pain signals].
Their study concluded, “Our findings suggest that the 32-mer fragment of aggrecan directly activates TLR2 expressed by nociceptors within the knee joint, driving the development of osteoarthritis-associated knee hyperalgesia.”
In very simple terms, this means that the presence of the 32 mer molecule activated a pain pathway in joints with osteoarthritis. Although more research is needed in the area of mer-32, these findings are an important step towards pinpointing the direct cause(s) of osteoarthritis pain and will help researchers in their quest for novel pain relieving treatments for joint OA. Future directions of the above research team include figuring out the exact location and type of nerve cells in the joint that produce pain in response to 32-mer. The Center for Disease Control (CDC) projects that by the year 2030, seventy-million people in the U.S. will have been diagnosed with arthritis. Unless a better and more cost-effective treatment for osteoarthritis is discovered, the financial burden is projected to rise from the 130 billion dollar mark that was noted in 2013. This study, among many others in the emerging volume of research in joint OA, highlights the need for continued collaboration and research efforts in the field.
