As researchers continue to make progress advancing our understanding of the pathogenesis of osteoarthritis (OA), the possibility of modifying the course of this common form of joint disease is getting closer to becoming a reality, according to Richard F. Loeser, Jr., MD, MACR, the Joseph P. Archie, Jr. Eminent Professor in the Division of Rheumatology, Allergy and Immunology, and the Director of the Thurston Arthritis Research Center at the University of North Carolina-Chapel Hill.
Dr. Loeser will discuss the potential of disease-modifying therapeutic interventions for OA when he delivers this year’s Oscar Gluck Memorial Lecture: Disease-Modification in Osteoarthritis: Will We Ever Get There? on Sunday, October 26, from 1–2 p.m. in Room W475A-B of McCormick Place. On-demand access to recorded presentations will be available to registered participants of ACR Convergence following the annual meeting through October 31, 2026.
“There are many people suffering from osteoarthritis who are receiving symptomatic therapies that will give them some benefit, but for many, many people, these therapies are just not sufficient,” Dr. Loeser said. “So, there really is a critical need to develop a disease-modifying therapy that will slow or stop the progression of OA. And while we don’t yet have an FDA-approved drug for disease modification in OA, the research has really taken off over the last 10 or 20 years.”
While OA was once thought of simply as a “wear-and-tear” degenerative disease, Dr. Loeser said that breakthroughs in understanding the biology of OA have shown it to be driven by complex biological processes that affect multiple joint tissues.
“We understand now that OA involves a host of pro-inflammatory mediators and matrix-degrading enzymes, and we’ve identified signaling pathways that seem to control all of this,” Dr. Loeser said. “Because of this improved understanding of the disease process, we have a lot more targets for therapies than we had in the past.”
Researchers also continue to learn more about the heterogeneity of OA and the presence of multiple phenotypes or endotypes in patients with the disease.
“When it comes to developing therapies, it’s not going to be a one-drug-fits-all therapy,” Dr. Loeser said. “It will need to be targeted to a particular subtype of osteoarthritis.”
Among the drugs currently being tested, he said that the Preventing Injured Knees from Osteoarthritis Severity Outcomes (PIKASO) clinical trial is looking at whether the diabetes drug metformin can slow or prevent OA progression in people with major knee injuries.
“If you have someone with an ACL tear, for example, starting them on an effective treatment, metformin in this case, might prevent them from getting osteoarthritis,” Dr. Loeser said. “The early research that was used to support this trial looked promising and really demonstrates the greater possibility and potential of identifying people who are at risk of getting OA and treating them at an early stage. We’re not there yet, but we’re getting close.”
Don’t Miss a Session
If you can’t make it to a live session during ACR Convergence 2025, make plans to watch the replay. All registered participants receive on-demand access to scientific sessions after the meeting through October 31, 2026.