Measuring microscale strain fields in articular cartilage during rapid impact reveals thresholds for chondrocyte death and a protective role for the superficial layer.
Measuring microscale strain fields in articular cartilage during rapid impact reveals thresholds for chondrocyte death and a protective role for the superficial layer.
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DOI：
10.1016/j.jbiomech.2015.05.035
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发表时间：
2015-09-18
影响因子：
2.4
通讯作者：
Cohen I
中科院分区：
文献类型：
--
作者：
Bartell LR;Fortier LA;Bonassar LJ;Cohen I
关节软骨是一种异质性软组织，在哺乳动物关节中分散和分配负荷。虽然坚固，但软骨容易受到高速率或高强度载荷的损伤。这种有害的负荷与退行性变化有关，包括慢性骨关节炎（OA），这仍然是发达国家残疾的主要原因。尽管经过数十年的研究，创伤后OA发生的机制仍然知之甚少。事实上，尽管大块软骨力学在冲击过程中是可测量的，但目前的技术无法在那些快速的时间尺度上获得微尺度力学。我们的目的是通过成像的微观力学和相应的急性生物学变化的软骨响应快速加载来解决这个知识缺口。在这项研究中，我们利用快速相机和共聚焦显微镜，以实现大约85 μm的空间分辨率的软骨变形期间的快速（~3 ms），局部的影响和软骨细胞死亡的影响。我们的结果表明，在这些高速率下，应变和软骨细胞死亡高度相关（p<0.001），在任何细胞死亡发生之前，阈值为8%的微尺度应变标准。此外，软骨细胞死亡在撞击后两小时发生，这表明临床治疗的时间范围。此外，当表层被去除时，应变-以及随后的软骨细胞死亡-更深地渗透到样品中（p<0.001），这表明关节软骨的表层具有保护作用。结合起来，这些结果提供了关于驱动创伤后早期软骨细胞损伤的详细生物力学的见解，并强调了在微观尺度上理解软骨及其力学的重要性。
Articular cartilage is a heterogeneous soft tissue that dissipates and distributes loads in mammalian joints. Though robust, cartilage is susceptible to damage from loading at high rates or magnitudes. Such injurious loads have been implicated in degenerative changes, including chronic osteoarthritis (OA), which remains a leading cause of disability in developed nations. Despite decades of research, mechanisms of OA initiation after trauma remain poorly understood. Indeed, although bulk cartilage mechanics are measurable during impact, current techniques cannot access microscale mechanics at those rapid time scales. We aimed to address this knowledge gap by imaging the microscale mechanics and corresponding acute biological changes of cartilage in response to rapid loading. In this study, we utilized fast-camera and confocal microscopy to achieve roughly 85 μm spatial resolution of the cartilage deformation during a rapid (~3 ms), localized impact and the chondrocyte death following impact. Our results showed that, at these high rates, strain and chondrocyte death were highly correlated (p<0.001) with a threshold of 8% microscale strain norm before any cell death occurred. Additionally, chondrocyte death had developed by two hours after impact, suggesting a time frame for clinical therapeutics. Moreover, when the superficial layer was removed, strain – and subsequently chondrocyte death – penetrated deeper into the samples (p<0.001), suggesting a protective role for the superficial layer of articular cartilage. Combined, these results provide insight regarding the detailed biomechanics that drive early chondrocyte damage after trauma and emphasize the importance of understanding cartilage and its mechanics on the microscale.