Elevated Contact Stresses Compromise Activity-Mediated Cartilage Rehydration but not Lubrication.

Abstract

Purpose: Understanding how obesity-a key risk factor for osteoarthritis-effects articular cartilage function is critical to understand OA pathoetiology. Cartilage, a biphasic material, supports vanishingly low friction coefficients in vivo, but is tribomechanically compromised by load-induced interstitial pressure/lubrication loss. To maintain tribomechanical function, cartilage must recover fluid lost to habitual/average contact stresses, a problem obesity likely exacerbates. Recently, we have shown that articulation/sliding drives robust interstitial fluid recovery and indefinite maintenance of biofidelic tissue strains and frictions through generation of hydrodynamic pressures within cartilage contact interfaces, i.e., via 'tribological rehydration.' However, the impact of elevated contact stresses on tribological rehydration and cartilage's function/lubrication remains unknown.

Methods: Using our convergent stationary contact area (cSCA) testing approach on ovine stifle cartilage explants bathed in PBS, we aimed to elucidate several points: (1) the effect of elevated contact stress on tribological rehydration during high-speed articulation, and how (2) cartilage material properties and (3) sliding speed influence contact stress-dependent fluid exudation, rehydration, and lubrication.

Results: Overall, we identified that (i) contact stress, across a narrow range, and (ii) static loading time are key controllers of tribological rehydration magnitude, compression accumulation, and equilibrium/total compression under biofidelic cSCA loading and sliding conditions. However, over the range tested (i.e., 0.2-0.8 MPa), (iii) contact stresses had no appreciable effect on cartilage's remarkable lubricity in the cSCA.

Conclusions: These results show that obesity is likely to directly physically impair articular cartilage function, and that obesity-driven tissue compression/strain, and not friction per se, may be the primary mechanical driver of cartilage dysfunction and OA risk.