Osteoarthritis (OA) is a Disease of Bone
Monday, March 12
4:30 PM – 5:30 PM
The ORS Program Committee invites you to participate in our second Annual Meeting Debate. ORS Past President David Burr will propose the motion that osteoarthritis is a disease of bone, specifically the subchondral bone at the joint. Professor Christopher Little will argue that joint pathology in osteoarthritis is driven by cartilage changes. Dr. Tamara Alliston will set the context for the debate, lead the questioning and keep the debaters honest. Audience participation is critical to the session, including questions from the floor and audience votes before and after the debaters have each made their case. Come join us and get involved in the ORS Great Debate!
Moderator:
Tamara Alliston, PhD
University of California San Francisco, Department of Orthopaedic Surgery
Arguing for the Motion:
David B. Burr, PhD
Indiana University School of Medicine
The role of subchondral bone in the progression of osteoarthritis has been controversial for 50 years. The observation that subchondral sclerosis was nearly always present in end-stage disease led to the conclusion that the increased stiffness caused by a thicker subchondral bone plate detracted from the bone’s ability to attenuate the loads imposed on the joint cartilage, increasing cartilage stresses and initiating the process of joint deterioration. We have been misled by this observation, leading some to conclude that early bone changes are not part of the pathogenic process because subchondral densification is not apparent prior to cartilage loss. But the observation that increased plate thickness occurs subsequent to the initiation of cartilage deterioration does not address whether other changes to subchondral bone that occur prior to overt cartilage deterioration contribute to the disease. There is now accumulating evidence that preventing the physiologic increase in remodeling rate in the early phases of joint disease before detectable cartilage changes will delay or prevent progressive deterioration. Moreover, bone marrow lesions are apparent before the radiologic appearance of OA, and have been shown to be a strong predictor of progressive disease. Such studies provide fundamental evidence that OA is very much a bone disease for without bone changes, joint destruction does not occur.
Arguing Against the Motion:
Christopher Little, BVMS, PhD
University of Sydney
This debate hinges on reasoning issues that are central to the human condition: we tend to believe only what we can see, and we infer causality based on the temporal appearance of these observations. In Psychology, these internalized cognitive processes contribute to the theories of ‘confirmation bias” and “illusory correlation”. So, what’s the relevance to this debate? Because we have always had imaging tools that allow us to “see” change in bone before cartilage, we infer both primacy and causality to bone in OA pathophysiology. As scientists, you would think we should know better, but evolutionary Psychology will tell us that reasoning is a developed and learned human response that emerged to resolve the problems posed by living in collaborative groups, not to solve abstract, logical problems or draw conclusions from new data. You will need to fight this evolutionarily engrained “reasoning”, and rather use the experimental rather than observational data that will be presented, that allows causality rather than illusory correlation to be apportioned. The results may surprise or even disturb you, but as fully evolved OARSI scientists you will only be able to reach one conclusion: osteoarthritis is a disease initiated in and driven by change in cartilage.
