Under physiological contact pressures, joint spaces thin as interstitial fluid is driven from articular cartilage. Because cartilage relies on interstitial fluid for its mechanical and lubrication functions, unbalanced exudation necessarily leads to increased friction, cartilage wear, and joint disease. Fortunately, cartilage and joint space actually thicken during physical activity due to the recovery of interstitial fluid in healthy joints. The only, and accepted, hypothesis for this recovery is that "dehydrated" cartilage regions passively uptake fluid when they become exposed to the bath by contact migration. However, recent in-situ studies have shown activity-induced recovery comparable to that observed in-vivo without ever exposing the contact to the bath; the phenomenon is called "tribological rehydration" because it is induced by sliding rather than migration. These preliminary results suggested that the balance between interstitial fluid loss and recovery in active joints is regulated by the interaction between interstitial (within cartilage) and hydrodynamic (between cartilage) pressure fields. The present study tests this hypothesis using explant tribology experiments with in-situ confocal imaging to elucidate the mechanisms involved in tribological rehydration. The anticipated results will help reveal why physical activity is so important to joint health while informing ongoing efforts to design the next generation of bio-inspired joint replacement devices. The investigators will recruit local high school seniors to participate in this research through the University of Delaware College of Engineering's K12 Outreach program.
Recent in-situ studies of cartilage in a convergent stationary contact area configuration have shown that friction decreases with increased speed, which supports the fluid film theory of joint lubrication. However, they also showed that cartilage simultaneously recovered interstitial fluid, which suggests that hydrodynamic pressures serve to restore hydration (via tribological rehydration) and the interstitial lubrication mechanism. Because existing theory relies on contact migration to expose dehydrated zones to the bath for recovery, the result also implies a fundamentally new mechanism by which joints maintain and recover joint space during activity. By quantifying the effects of physiological articulation amplitudes and contact stresses on passive and active recovery of cartilage, directly interrogating the interfacial and interstitial microfluidics associated with active-rehydration via in-situ confocal microscopy, and evaluating the influence of cartilage degradation on the rehydration of cartilage, this study aims to identify the limits of passive recovery and tribological rehydration in the physiological context and elucidate the mechanism underlying tribological rehydration. The anticipated results of this study will provide new insights into joint mechanics, disease etiology, and the design of new bio-inspired joint replacement systems.
