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Articular Cartilage Friction, Strain, and Viability Under Physiological to Pathological Benchtop Sliding Conditions
Cellular and Molecular Bioengineering ( IF 2.8 ) Pub Date : 2021-04-27 , DOI: 10.1007/s12195-021-00671-2
Margot S Farnham 1 , Kyla F Ortved 2 , David L Burris 1, 3 , Christopher Price 1, 3
Affiliation  

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.



中文翻译:

从生理到病理的台式滑动条件下的关节软骨摩擦、应变和活力

在体内,关节软骨对磨损、损伤和功能障碍具有极强的抵抗力。然而,在工作台上复制软骨惊人的体内摩擦力学(即高流体负载支持、低摩擦和应变)和力学生物学一直很困难,因为经典的测试方法倾向于最大限度地减少对组织功能的流体动力学贡献。我们的收敛静止接触区 (cSCA) 配置保留了流体动力学介导过程通过“摩擦再水化”促进间隙水化恢复和摩擦力学功能的能力。使用 cSCA,我们研究了如何在原位软骨细胞存活受到摩擦补液的影响,在玻璃反面与压缩加载的马 cSCA 软骨外植体相互滑动期间存在摩擦补液。当在测试过程中摩擦补液受到损害时,通过慢速滑动,观察到“病理生理学”摩擦力学环境和高表面细胞死亡。当通过高速滑动保留摩擦补液时,实现了“半生理”滑动环境和抑制细胞死亡。在测试期间加入滑液促进了与体内一致的“真正生理”滑动结果环境,但与 PBS 中的高速滑动相比,对细胞死亡的影响有限。随后,路径分析确定摩擦是细胞死亡的主要驱动因素,而应变是间接驱动因素,支持关节介导的补液可以有益于软骨的生物力学特性和生物稳态的论点。

更新日期:2021-04-28
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