Paper TR+BI-TuM4
Linking Cartilage Structure, Lubrication, and Osteoarthritis

Tuesday, October 30, 2012, 9:00 am, Room 19

Cartilage is known for exceptionally low friction coefficients during sliding, but its wear resistance is arguably more remarkable. Conventional wisdom suggests that cartilage wears gradually with use and that osteoarthritis is the inevitable consequence. This notion is refuted by the scientific literature. Dissections of mature, healthy, and active joints consistently reveal smooth, glossy, damage-free articulating surfaces that can only occur if tissue recovery matches wear. Cartilage recovery is extremely slow due to a lack of vasculature and numerous lubrication mechanisms have been proposed to explain extremely low in-vivo wear rates. Osteoarthritis (OA) is characterized by progressive wear and caused by a system destabilizing input (e.g. biochemistry, acute injury, altered loading, and joint instability). In certain joint-destabilized animal models, for example, a localized defect (~50 µm wide) is visible in as little as a week, and bone-on-bone contact occurs on the order of 6 months. Recent studies suggest that interstitial lubrication, a mechanism that reduces frictional and normal stresses by nearly 100X, is the dominant protective mechanism of cartilage. Localized surface damage can disrupt the very specific structural features responsible for the unique interstitial fluid pressurization mechanism. We hypothesize that localized surface damage can initiate OA-like degradation if it is sufficiently disruptive to the interstitial lubrication mechanism. In this paper, we present friction and wear measurements designed to explore this novel mechanical hypothesis of OA initiation and progression.