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Computational model of damage-induced growth in soft biological tissues considering the mechanobiology of healing
Biomechanics and Modeling in Mechanobiology ( IF 3.5 ) Pub Date : 2021-03-26 , DOI: 10.1007/s10237-021-01445-5
Meike Gierig 1 , Peter Wriggers 1 , Michele Marino 2
Affiliation  

Healing in soft biological tissues is a chain of events on different time and length scales. This work presents a computational framework to capture and couple important mechanical, chemical and biological aspects of healing. A molecular-level damage in collagen, i.e., the interstrand delamination, is addressed as source of plastic deformation in tissues. This mechanism initiates a biochemical response and starts the chain of healing. In particular, damage is considered to be the stimulus for the production of matrix metalloproteinases and growth factors which in turn, respectively, degrade and produce collagen. Due to collagen turnover, the volume of the tissue changes, which can result either in normal or pathological healing. To capture the mechanisms on continuum scale, the deformation gradient is multiplicatively decomposed in inelastic and elastic deformation gradients. A recently proposed elasto-plastic formulation is, through a biochemical model, coupled with a growth and remodeling description based on homogenized constrained mixtures. After the discussion of the biological species response to the damage stimulus, the framework is implemented in a mixed nonlinear finite element formulation and a biaxial tension and an indentation tests are conducted on a prestretched flat tissue sample. The results illustrate that the model is able to describe the evolutions of growth factors and matrix metalloproteinases following damage and the subsequent growth and remodeling in the respect of equilibrium. The interplay between mechanical and chemo-biological events occurring during healing is captured, proving that the framework is a suitable basis for more detailed simulations of damage-induced tissue response.



中文翻译:

考虑愈合力学生物学的软生物组织损伤诱导生长的计算模型

软生物组织的愈合是一系列不同时间和长度尺度的事件。这项工作提出了一个计算框架来捕捉和耦合愈合的重要机械、化学和生物方面。胶原中的分子水平损伤,即链间分层,被认为是组织中塑性变形的来源。这种机制会引发生化反应并开始愈合链。特别是,损伤被认为是基质金属蛋白酶和生长因子产生的刺激物,它们依次降解和产生胶原蛋白。由于胶原蛋白的更新,组织的体积发生变化,这可能导致正常或病理性愈合。为了捕捉连续尺度的机制,变形梯度乘法分解为非弹性和弹性变形梯度。最近提出的弹塑性配方通过生化模型与基于均质约束混合物的生长和重塑描述相结合。在讨论了生物物种对损伤刺激的反应之后,该框架以混合非线性有限元公式实现,并在预拉伸的扁平组织样本上进行了双轴拉伸和压痕测试。结果表明,该模型能够描述生长因子和基质金属蛋白酶在损伤后的演变以及随后在平衡方面的生长和重塑。捕捉到愈合过程中发生的机械和化学生物学事件之间的相互作用,

更新日期:2021-03-26
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