PDF(Pubmed)
Abstract：
Soft tissue injuries (such as ligament, tendon, and meniscus tears) are the result of extracellular matrix damage from excessive tissue stretching. Deformation thresholds for soft tissues, however, remain largely unknown due to a lack of methods that can measure and compare the spatially heterogeneous damage and deformation that occurs in these materials. Here, we propose a full-field method for defining tissue injury criteria: multimodal strain limits for biological tissues analogous to yield criteria that exist for crystalline materials. Specifically, we developed a method for defining strain thresholds for mechanically-driven fibrillar collagen denaturation in soft tissues, using regional multimodal deformation and damage data. We established this new method using the murine medial collateral ligament (MCL) as our model tissue. Our findings revealed that multiple modes of deformation contribute to collagen denaturation in the murine MCL, contrary to the common assumption that collagen damage is driven only by strain in the direction of fibers. Remarkably, hydrostatic strain (computed here with an assumption of plane strain) was the best predictor of mechanically-driven collagen denaturation in ligament tissue, suggesting crosslink-mediated stress transfer plays a role in molecular damage accumulation. This work demonstrates that collagen denaturation can be driven by multiple modes of deformation and provides a method for defining deformation thresholds, or injury criteria, from spatially heterogeneous data. STATEMENT OF SIGNIFICANCE: Understanding the mechanics of soft tissue injuries is crucial for the development of new technology for injury detection, prevention, and treatment. Yet, tissue-level deformation thresholds for injury are unknown, due to a lack of methods that combine full-field measurements of multimodal deformation and damage in mechanically loaded soft tissues. Here, we propose a method for defining tissue injury criteria: multimodal strain thresholds for biological tissues. Our findings reveal that multiple modes of deformation contribute to collagen denaturation, contrary to the common assumption that collagen damage is driven by strain in the fiber direction alone. The method will inform the development of new mechanics-based diagnostic imaging, improve computational modeling of injury, and be employed to study the role of tissue composition in injury susceptibility.
摘要：
软组织损伤（如韧带，肌腱,和半月板撕裂）是过度组织拉伸导致的细胞外基质损伤的结果。软组织的变形阈值，然而,由于缺乏可以测量和比较这些材料中发生的空间异质损伤和变形的方法，因此在很大程度上仍然未知。这里,我们提出了一种定义组织损伤标准的方法：生物组织的多模态应变极限，类似于晶体材料的屈服标准。具体来说,我们开发了一种方法来定义软组织中机械驱动的原纤维胶原变性的损伤标准，使用区域多模态变形和损伤数据。我们使用鼠内侧副韧带（MCL）作为模型组织建立了这种新方法。我们的发现表明，多种变形模式有助于鼠MCL中的胶原蛋白变性，与胶原蛋白损伤仅由纤维方向的应变驱动的常见假设相反。值得注意的是,静水应变（这里用平面应变的假设计算）是韧带组织中机械驱动的胶原蛋白变性的最佳预测指标，表明交联介导的应激转移在分子损伤积累中起作用。这项工作表明，胶原蛋白变性可以由多种变形模式驱动，并提供了一种定义变形阈值的方法，或伤害标准，来自空间异构数据。重要性声明：软组织损伤(即，肌腱和半月板撕裂）是过度组织变形的结果。软组织的变形阈值，然而,由于缺乏可以测量和比较这些材料中发生的空间异质损伤和变形的方法，因此在很大程度上仍然未知。这里,我们提出了一种定义组织损伤标准的方法：生物组织的多模态应变极限，类似于晶体材料的屈服标准。我们的发现表明，多种变形模式有助于胶原蛋白变性，与胶原蛋白损伤仅由纤维方向的应变驱动的常见假设相反。所开发的方法将改善损伤的计算模型，并有助于研究组织成分如何影响损伤敏感性。
