SAN DIEGO — Acting on modifiable factors such as obesity and joint injury prevention could have a huge impact on osteoarthritis pathogenesis and incidence, according to a presentation at Congress of Clinical Rheumatology West.
David Hunter, PhD, Florance and Cope Chair of Rheumatology, and chair of the Institute of Bone and Joint Research at the University of Sydney, addressed a cross-section of broad topics pertaining to OA, including definitions of the disease; how the evolution of the human race is impacting OA pathogenesis; the burden of disease; risk factors for onset; reasons for pain and other symptoms; and an update on phenotypes that referenced the lumpers-splitters debate.
Understanding of OA has changed over the course of just a few decades, according to Hunter. “Historically, osteoarthritis was a cartilage-centric disease,” he said. “But we now know that OA is a failure of the whole synovial joint organ. Cartilage itself does not contain susceptive nerve fibers, so it can’t be responsible for the symptoms. You have to have bones to develop OA.”
With this understanding in mind, Hunter zeroed in on how changes in human behavior over time may be increasing OA risk. For example, different types of footwear and the prevalence of concrete may explain increased mechanical load on joints. “We are walking on firmer ground,” he said.
Acting on modifiable factors such as obesity and joint injury prevention could have a huge impact on OA pathogenesis and incidence, according to a presentation.
But the much larger issue to consider is the global overweight/obesity epidemic that dwarfs footwear or concrete as a risk factor for increased mechanical load. For Hunter, the matter is of the utmost urgency.
“We need to make policy changes to impact what is happening here in terms of obesity,” he said. “We saw what policy and tax changes did in reducing smoking incidence. There are measures we can take.”
Some of those measures include taxing unhealthy or fatty foods and banning advertisements for junk food that target children, according to Hunter. “At the moment, there are huge missed opportunities to take action on overweight and obesity,” he said.
The other important modifiable factor Hunter addressed is joint injury prevention. “The mean age of a cruciate ligament tear is 22 years,” he said. Individuals — a disproportionate number of them young men — who suffer this injury around this age, are considerably more likely to develop OA in their 30s or early 40s, according to Hunter.
But this burden, too, can be modified, if not prevented. Organizations like FIFA offer exercise regimens to help young athletes strengthen their joints and prevent cruciate tears. He encouraged rheumatologists to advise their young patients on these techniques.
The talk closed with Hunter suggesting that there is a strong movement toward splitting, as opposed to lumping, in the OA community. “We have not paid particular heed to why people develop this disease until now,” he said. “Increasingly, we are very interested in phenotypes, and why they are important.”
This dovetails with the discussion of modifiable factors because understanding whether a patient has developed OA due to obesity, a ligament injury, or some other reason, can help clinicians target interventions. “Increasing understanding of pathogenesis can help us tailor interventions in clinical practice,” he said. “It can also help us in prevention.” – by Rob Volansky
Hunter D. Recent changes in the pathogenesis of osteoarthritis. Presented at: Congress of Clinical Rheumatology West. Sept. 25-29, 2019; San Diego, Calif.
Disclosure: Hunter reports consulting for Lilly, Merck Serono, Pfizer, TLCBio, and Zynerba.