关节软骨显著的低摩擦特性对关节功能至关重要。在骨关节炎(OA)中,软骨退化(例如,蛋白聚糖损失和胶原蛋白损伤)降低组织模量并增加渗透性。尽管这些变化损害了完全减压和缓慢滑动的软骨的润滑,新的证据表明,这种关系在生物保真滑动条件下可能不成立,更能代表体内遇到的那些。我们最近使用会聚固定接触区域(cSCA)配置的研究表明,关节(即,滑动)产生界面流体动力压力,能够通过称为摩擦学补水的机制补充软骨间质液/压力损失的压缩负荷。这种液体回收维持体内类似的动摩擦系数(在PBS中µk<0.02,在滑液中<0.005),对健康组织的机械性能几乎不敏感。然而,在生物保真滑动条件下受损软骨的摩擦力学功能仍然未知。这里,我们研究了软骨力学性质的OA样变化的影响,通过酶消化成熟的牛软骨建模,在CSCA滑动过程中的摩擦力学功能。我们发现幼稚和消化的cSCA软骨(在PBS或滑液中)之间的滑动驱动的摩擦学补液行为或µk没有差异。这表明OA样软骨保持足够的功能特性以支持在生物实体滑动条件下的原始流体回收和润滑。然而,由于在初始载荷施加期间增加的应变累积,OA样软骨积累了更大的总组织应变。一起,这些结果表明,与活动介导的应变或摩擦驱动的磨损相反,总组织应变的升高可能是软骨OA病理的关键生物力学介质.重要性声明:骨关节炎(OA)降低软骨的模量并增加其渗透性。虽然这些变化在低流体载荷支撑(FLS)条件下影响了台式测试的摩擦性能,目前尚不清楚此类观察结果是否在滑动条件下能够更好地代表体内关节动态FLS条件。这里,我们利用生物保真台式滑动实验——也就是说,那些模仿关节的天然滑动环境-检查机械性质的OA样变化如何影响软骨的自然润滑。我们发现,在初始软骨和OA样软骨之间,滑动介导的流体恢复或动摩擦行为没有差异。然而,OA样软骨在负载施加过程中经历了更大的应变积累,提示升高的组织应变(不是摩擦驱动的磨损)可能是OA病理的主要生物力学介质。
Articular cartilage\'s remarkable low-friction properties are essential to joint function. In osteoarthritis (OA), cartilage degeneration (e.g., proteoglycan loss and collagen damage) decreases tissue modulus and increases permeability. Although these changes impair lubrication in fully depressurized and slowly slid cartilage, new evidence suggests such relationships may not hold under biofidelic sliding conditions more representative of those encountered in vivo. Our recent studies using the convergent stationary contact area (cSCA) configuration demonstrate that articulation (i.e., sliding) generates interfacial hydrodynamic pressures capable of replenishing cartilage interstitial fluid/pressure lost to compressive loading through a mechanism termed tribological rehydration. This fluid recovery sustains in vivo-like kinetic friction coefficients (µk<0.02 in PBS and <0.005 in synovial fluid) with little sensitivity to mechanical properties in healthy tissue. However, the tribomechanical function of compromised cartilage under biofidelic sliding conditions remains unknown. Here, we investigated the effects of OA-like changes in cartilage mechanical properties, modeled via enzymatic digestion of mature bovine cartilage, on its tribomechanical function during cSCA sliding. We found no differences in sliding-driven tribological rehydration behaviors or µk between naïve and digested cSCA cartilage (in PBS or synovial fluid). This suggests that OA-like cartilage retains sufficient functional properties to support naïve-like fluid recovery and lubrication under biofidelic sliding conditions. However, OA-like cartilage accumulated greater total tissue strains due to elevated strain accrual during initial load application. Together, these results suggest that elevated total tissue strains-as opposed to activity-mediated strains or friction-driven wear-might be the key biomechanical mediator of OA pathology in cartilage. STATEMENT OF SIGNIFICANCE: Osteoarthritis (OA) decreases cartilage\'s modulus and increases its permeability. While these changes compromise frictional performance in benchtop testing under low fluid load support (FLS) conditions, whether such observations hold under sliding conditions that better represent the joints\' dynamic FLS conditions in vivo is unclear. Here, we leveraged biofidelic benchtop sliding experiments-that is, those mimicking joints\' native sliding environment-to examine how OA-like changes in mechanical properties effect cartilage\'s natural lubrication. We found no differences in sliding-mediated fluid recovery or kinetic friction behaviors between naïve and OA-like cartilage. However, OA-like cartilage experienced greater strain accumulation during load application, suggesting that elevated tissue strains (not friction-driven wear) may be the primary biomechanical mediator of OA pathology.