Measuring microscale strain fields in articular cartilage during rapid impact reveals thresholds for chondrocyte death and a protective role for the superficial layer

被引:71
作者
Bartell, Lena R. [1 ]
Fortier, Lisa A. [2 ]
Bonassar, Lawrence J. [3 ,4 ]
Cohen, Itai [5 ]
机构
[1] Cornell Univ, Sch Appl & Engn Phys, Ithaca, NY 14853 USA
[2] Cornell Univ, Dept Clin Sci, Ithaca, NY 14853 USA
[3] Cornell Univ, Dept Biomed Engn, Ithaca, NY 14853 USA
[4] Cornell Univ, Sibley Sch Mech & Aerosp Engn, Ithaca, NY 14853 USA
[5] Cornell Univ, Dept Phys, Ithaca, NY 14853 USA
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
PTOA; Indentation; Elastography; Arthritis initiation; Injury; MECHANICAL-BEHAVIOR; MATRIX DAMAGE; TISSUE STRAIN; PEAK-STRESS; CELL-DEATH; OSTEOARTHRITIS; COMPRESSION; VIABILITY; LOAD; INJURY;
D O I
10.1016/j.jbiomech.2015.05.035
中图分类号
Q6 [生物物理学];
学科分类号
071011 [生物物理学];
摘要
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 pm spatial resolution of both the cartilage deformation during a rapid (similar to 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. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码:3440 / 3446
页数:7
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