Treating the Pain of Osteoarthritis — Where Do We Go from Here?

Abstract

Pain is the overriding clinical issue in osteoarthritis (OA). Pain is what motivates patients to seek medical care, and pain is what drives patients to have total joint replacement surgery1. Although rheumatologists deal with OA patients and their pain on a daily basis, we are often ineffective in our attempts to address what many consider a very straightforward complaint. This may be because, as Mease and colleagues describe in their article in this issue of The Journal 2, the mechanisms underlying the pain of OA are surprisingly complex. OA pain has traditionally been viewed as peripherally mediated nociceptive pain. Noxious stimuli from the damaged joint stimulate peripheral nerve endings, triggering the ascending and descending neuronal pathways, which results in pain perception. However, this model provides only a starting point for understanding the pathophysiology — even the basic relationship between bony changes and pain is unclear. For example, bone marrow lesions (BML), which represent a heterogeneous group of morphologic changes in the subchondral bone, are readily seen on magnetic resonance imaging. These lesions contain peripheral nociceptors, and many investigators have shown a clear correlation between BML and pain in patients with OA3. However, significant BML can be seen in pain-free subjects without OA, and intriguingly, the presence of BML predicts the development of pain in these patients4. There is clearly more to OA pain than local osseous damage. Peripheral nociceptors are located not only on periosteum and subchondral bone, but also on ligaments, the synovial capsule, and menisci — soft tissue structures that comprise the “joint organ.” In fact, as Mease and colleagues point out, cartilage itself is aneural, and … Address correspondence to Dr. Mandl; E-mail: MandlL{at}hss.edu