Although osteoarthritis (OA) pain was originally considered nociceptive in nature, recent studies have supported the role of sensitization as a key mechanism of pain. In fact, in the case of arthritis, sensitization and nociceptive input may actually reinforce each other because inflammation of the joint drives central sensitization and, thus, changes the way in which the nervous system perceives pain. More recently, research into the role of inflammation in pain perception has led to the hypothesis that a reduction in inflammation in patients with OA just may be able to decrease the progression of pain.
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David A. Walsh, MD, PhD, director of the Arthritis Research UK Pain Centre at the University of Nottingham, described the role of synovitis and pain sensitization in an editorial published in the March issue of Arthritis & Rheumatology.1 He elaborated on his perspective in an interview with The Rheumatologist and explained that the new understanding of pain could open doors for patients with OA.
“We already have a whole load of treatments that have been developed for rheumatoid arthritis,” he explains, adding that some of these anti-inflammatories and immunomodulators may be able to be successfully repurposed as long-term pain killers for OA. Clinical trials are also in progress with hydroxychloroquine and methotrexate, and Dr. Walsh explains that there is some interest in exploring the role of biologics in the treatment of OA. The expense and side effects associated with biologic drugs make them less palatable as treatments for pain, unless they have substantial and long-term benefits.
The editorial included a discussion of an epidemiological study that was published in the same issue of Arthritis & Rheumatology. The research performed by Tuhina Neogi, MD, PhD, associate professor of medicine at Boston University School of Medicine in Boston, and colleagues suggested that neuronal sensitization, once established, may be unresponsive to reductions in synovitis.2 Early prevention or treatment of sensitization might be paramount to reduce long-term OA pain. In their study, the investigators used synovitis/effusion as a marker of inflammation in knee OA. The authors explained that inflammation of the synovium activates the synovial membrane, leading to synovial thickening and/or joint effusion that can be imaged via magnetic resonance imaging (MRI). The Neogi paper studied a cohort of patients with, or at risk for, knee OA to identify whether or not synovitis may be contributing to their pain.
“In our exploratory analyses, we found that persistence of synovitis and persistence of effusion were associated with a decrease in PPT [pressure pain threshold] over time, primarily at the wrist, suggesting spreading sensitization over time,” write the authors in their paper. “In contrast, resolution of these inflammatory features on MRI did not result in a significant change in PPT, suggesting that perhaps once sensitization or heightened sensitivity has occurred, removal of the inflammatory stimulus may not be sufficient to alter the sensitization.”