Institute of Continuum Mechanics, Leibniz University Hannover, An der Universität 1, 30823, Garbsen, Germany.
Department of Civil Engineering and Computer Science, University of Rome Tor Vergata, Via del Politecnico 1, 00133, Rome, Italy.
Biomech Model Mechanobiol. 2021 Aug;20(4):1297-1315. doi: 10.1007/s10237-021-01445-5. Epub 2021 Mar 26.
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.
软组织的愈合是一个在不同时间和长度尺度上发生的事件链。本工作提出了一个计算框架,用于捕捉和耦合愈合过程中的重要力学、化学和生物学方面。胶原中的分子级损伤,即层间离解,被视为组织中塑性变形的来源。这种机制引发了生化反应,启动了愈合链。特别是,损伤被认为是产生基质金属蛋白酶和生长因子的刺激物,而这些物质反过来又分别降解和产生胶原。由于胶原的转化,组织的体积发生变化,这可能导致正常或病理性愈合。为了在连续体尺度上捕捉这些机制,变形梯度被分解为非弹性和弹性变形梯度。最近提出的弹塑性公式通过生化模型与基于均匀化约束混合物的生长和重塑描述相耦合。在讨论了生物物种对损伤刺激的反应后,该框架被实现为一种混合非线性有限元公式,并对预拉伸平板组织样本进行了双轴拉伸和压痕试验。结果表明,该模型能够描述损伤后生长因子和基质金属蛋白酶的演变,以及随后在平衡方面的生长和重塑。愈合过程中发生的力学和化学生物学事件之间的相互作用被捕捉到,证明该框架是更详细模拟损伤诱导的组织反应的合适基础。