Moore A C, Burris D L
Department of Biomedical Engineering, University of Delaware, Newark, DE, USA.
Department of Biomedical Engineering, University of Delaware, Newark, DE, USA; Department of Mechanical Engineering, University of Delaware, Newark, DE, USA.
Osteoarthritis Cartilage. 2017 Jan;25(1):99-107. doi: 10.1016/j.joca.2016.09.018. Epub 2016 Sep 30.
During exercise, cartilage recovers interstitial fluid lost during inactivity, which explains how tissue thickness and joint space are maintained over time. This recovery phenomenon is currently explained by a combination of osmotic swelling during intermittent bath exposure and sub-ambient pressurization during unloading. This paper tests an alternate hypothesis that cartilage can retain and recover interstitial fluid in the absence of bath exposure and unloading when physiological hydrodynamics are present.
Stationary cartilage-on-flat experiments were conducted to eliminate intermittent bath exposure as a potential contributor to fluid uptake. In situ compression measurements were used to monitor the loss, retention, and recovery of interstitial fluid during testing in saline. Samples were left larger than the contact area to preserve a convergence zone for hydrodynamic pressurization.
Interstitial fluid lost during static loading was recovered during sliding in the absence of unloading and contact migration; fluid recovery in a stationary contact cannot be explained by biphasic theory and suggests a fundamentally new contributor to the recovery process. We call the phenomenon 'tribological rehydration' because recovery was induced by sliding rather than by unloading or migration. Sensitivities to sliding speed, surface permeability, and nature of the convergence wedge are consistent with the hypothesis that hydrodynamic effects underlie the tribological rehydration phenomenon.
This study demonstrates that cartilage can retain and recover interstitial fluid without migration or unloading. The results suggest that hydrodynamic effects in the joint are not only important contributors to lubrication, they are likely equally important to the preservation of joint space.
在运动过程中，软骨会恢复不活动期间流失的组织间液，这解释了组织厚度和关节间隙如何随时间维持。目前，这种恢复现象是通过间歇性浸泡暴露期间的渗透肿胀和卸载期间低于环境压力的加压作用共同来解释的。本文检验了另一种假说，即在存在生理流体动力学的情况下，软骨在没有浸泡暴露和卸载时也能保留并恢复组织间液。
进行了固定的软骨-平面实验，以消除间歇性浸泡暴露作为液体吸收潜在因素的影响。在盐水中测试期间，使用原位压缩测量来监测组织间液的流失、保留和恢复情况。样本尺寸留得大于接触面积，以保留用于流体动力加压的汇聚区。
在没有卸载和接触迁移的滑动过程中，静态加载期间流失的组织间液得以恢复；固定接触中的液体恢复无法用双相理论来解释，这表明恢复过程有一个全新的影响因素。我们将这种现象称为“摩擦学再水化”，因为恢复是由滑动而非卸载或迁移引起的。对滑动速度、表面渗透率和汇聚楔性质的敏感性与流体动力效应是摩擦学再水化现象基础这一假说相符。
本研究表明，软骨无需迁移或卸载就能保留并恢复组织间液。结果表明，关节中的流体动力效应不仅是润滑的重要因素，对维持关节间隙可能同样重要。
