Effective biologics have improved outcomes from rheumatoid arthritis (RA) due to their better disease control, but osteoarthritis (OA) typically does not respond to these drugs. Work is being done to better understand and target the pathobiology of OA, including erosive OA, as well as central pain syndromes in RA and OA.

In the current treatment era, since the introduction of methotrexate and biologics, evidence suggests that the rates of hip and knee arthroplasties have declined significantly among patients with RA. This is significant progress, because I recall that, when I was a fellow, we would meet regularly with the orthopedic surgeon in our group about tendon ruptures and repair, wrist arthroplasties and joint fusions, and the need for hip or knee arthroplasty in my patients. Now, orthopedic surgeons are less involved in the management of RA because, in many people, we are able to prevent or delay the joint damage that can ultimately require arthroplasty.

While these advances have been made in the treatment of RA, there are still areas of unmet need related to preserving the joints of those with OA. Unlike RA, OA tends to have different mechanisms, causes, and prognoses for each of the joints affected (eg, knee, finger, or hip). While some patients have what we call generalized OA, which may be related to metabolic or genetic abnormalities, for most people, OA is joint specific and should be addressed in a joint-specific way.

Erosive OA, a subset of hand OA, tends to have an inflammatory ingredient in addition to the well-known and appreciated familial or genetic component. However, anti-inflammatory, antirheumatic, and immunosuppressive drugs have been tried in this setting with limited success. So, we think that the inflammatory component of erosive OA may partially be a result of OA rather than a cause of it. Current research is investigating whether cartilage pathobiology is involved in the inflammation and if impact loading is contributing to the subchondral bone erosion.

Something interesting that has come up recently is the use of GLP-1 receptor agonists, which have significant metabolic effects, as a potential OA therapy. Weight loss slows the progression of knee OA. This may be due not only to a reduction in impact loading but also, potentially, to an anti-inflammatory effect of the weight loss itself. Therefore, GLP-1 receptor agonists may help reduce the progression of knee OA and may potentially help delay or eliminate the need for patients to receive knee arthroplasties. These studies are underway.

Patient-reported central pain (often referred to as nociplastic pain) remains an important issue for both OA and RA because it will persist in patients even after the arthritis is controlled. We do not know with certainty why this occurs, but the simplest explanation is that it could be partially related to the damage that has already occurred to the surfaces of the affected joints. However, most researchers think—and emerging studies support—that psychosocial factors (eg, social disadvantage or isolation) may also play a role because the degree of pain in these patients is not necessarily correlated to the degree of damage or inflammation in the joints. It is important to try to identify the source of the pain, and, once identified, treat it in a way that addresses the root cause or source, even if it comes from a central mechanism. I may refer a patient to a psychologist or pain management specialist for additional suggestions for a comprehensive approach.