Articular Cartilage Friction, Strain, and Viability Under Physiological to Pathological Benchtop Sliding Conditions.

In vivo, articular cartilage is exceptionally resistant to wear, damage, and dysfunction. However, replicating cartilage's phenomenal in vivo tribomechanics (i.e., high fluid load support, low frictions and strains) and mechanobiology on the benchtop has been difficult, because classical testing approaches tend to minimize hydrodynamic contributors to tissue function. Our convergent stationary contact area (cSCA) configuration retains the ability for hydrodynamically-mediated processes to contribute to interstitial hydration recovery and tribomechanical function via 'tribological rehydration'. Using the cSCA, we investigated how in situ chondrocyte survival is impacted by the presence of tribological rehydration during the reciprocal sliding of a glass counterface against a compressively loaded equine cSCA cartilage explant. When tribological rehydration was compromised during testing, by slow-speed sliding, 'pathophysiological' tribomechanical environments and high surface cell death were observed. When tribological rehydration was preserved, by high-speed sliding, 'semi-physiological' sliding environments and suppressed cell death were realized. Inclusion of synovial fluid during testing fostered 'truly physiological' sliding outcomes consistent with the in vivo environment but had limited influence on cell death compared to high-speed sliding in PBS. Subsequently, path analysis identified friction as a primary driver of cell death, with strain an indirect driver, supporting the contention that articulation mediated rehydration can benefit both the biomechanical properties and biological homeostasis of cartilage. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12195-021-00671-2.

Effects of mechanical injury on the tribological rehydration and lubrication of articular cartilage.

Healthy articular cartilage is crucial to joint function, as it provides the low friction and load bearing surface necessary for joint articulation. Nonetheless, joint injury places patients at increased risk of experiencing both accelerated cartilage degeneration and wear, and joint dysfunction due to post-traumatic osteoarthritis (PTOA). In this study, we used our ex vivo convergent stationary contact area (cSCA) explant testing configuration to demonstrate that high-speed sliding of healthy tissues against glass could drive consistent and reproducible recovery of compression-induced cartilage deformation, through the mechanism of 'tribological rehydration'. In contrast, the presence of physical cartilage damage, mimicking those injuries known to precipitate PTOA, could compromise tribological rehydration and the sliding-driven recovery of cartilage function. Full-thickness cartilage injuries (i.e. fissures and chondral defects) markedly suppressed sliding-driven tribological rehydration. In contrast, impaction to cartilage, which caused surface associated damage, had little effect on the immediate tribomechanical response of explants to sliding (deformation/strain, tribological rehydration, and friction/lubricity). By leveraging the unique ability of the cSCA configuration to support tribological rehydration, this study permitted the first direct ex vivo investigation of injury-dependent strain and friction outcomes in cartilage under testing conditions that replicate and maintain physiologically-relevant levels of fluid load support and frictional outcomes under high sliding speeds (80 mm/s) and moderate compressive stresses (~0.3 MPa). Understanding how injury alters cartilage tribomechanics during sliding sheds light on mechanisms by which cartilage's long-term resilience and low frictional properties are maintained, and can guide studies investigating the functional consequences of physical injury and joint articulation on cartilage health, disease, and rehabilitation.