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A micromechanical model for the growth of collagenous tissues under mechanics-mediated collagen deposition and degradation

机译:机械介导的胶原沉积下胶原组织生长的微机械模型及降解

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In this study, we developed a micromechanical model for the growth and remodeling of a soft tissue based on the concurrent action of collagen deposition and degradation. We assumed in the model that collagen degradation causes a reduction in the fiber radius, while collagen deposition can increase both the radius and length of the collagen fibers growing under load. The latter arises from the assumption that collagen is deposited in an unstressed state, which increases the reference length of a fiber growing under mechanical load. The rate of collagen deposition and degradation can be stimulated and inhibited, respectively, by the fiber axial strain energy density. From these assumptions, we derived kinetic relationships for the fiber radial and axial growth stretch, and constitutive relations for the stress response and growth and remodeling of the tissues. We applied the model to study the growth of collagen fibers under a static and cyclic force. Cyclic force loading can drive the continual axial growth of collagen fiber, while the axial growth under a constant force eventually halts when an equilibrium state is reached. We then applied the model to investigate the development of stress and strain homeostasis of a spherical collagenous tissue membrane in response to a perturbation in the internal pressure. The model showed that an increase in the pressure produced growth in the tissue radius and thickness, such that the stress response was able to recover the equilibrium membrane stress before the pressure perturbation. Tissues composed of slender, or low-crimp collagen fibers also recovered the equilibrium mechanical stretch level before the perturbation. These results indicated that concurrent mechanics-stimulated collagen deposition and mechanics-inhibited degradation can produce stress homeostasis and for some fiber morphology strain homeostasis without prescribing a target stress or fiber strain.
机译:在这项研究中,我们基于胶原沉积和降解的同时作用,开发了一种用于软组织的生长和重塑的微机械模型。我们在模型中假设胶原蛋白降解导致纤维半径的降低,而胶原沉积可以增加在负载下生长的胶原纤维的半径和长度。后者源于假设胶原蛋白沉积在不秘密状态下,这增加了在机械负荷下生长的纤维的参考长度。通过纤维轴向应变能密度分别可以分别刺激和抑制胶原沉积和降解的速率。从这些假设中,我们衍生出用于纤维径向和轴向生长伸展的动力学关系,以及组织的应力响应和生长和重塑的组成关系。我们应用模型在静态和循环力下研究胶原纤维的生长。循环力负载可以驱动胶原纤维的连续轴向生长,而达到恒定力下的轴向生长最终在​​达到平衡状态时停止。然后,我们应用模型以研究球形胶原组织膜的应力和应变稳态的发展,以应对内部压力的扰动。该模型表明,增加压力在组织半径和厚度中产生的生长,使得应力响应能够在压力扰动之前恢复平衡膜应力。由细长或低压接胶原纤维组成的组织还在扰动之前恢复平衡机械拉伸水平。这些结果表明,并发力学刺激的胶原沉积和力学抑制的降解可以产生应激稳态和一些纤维形态应变稳态,而无需规定靶应激或纤维菌株。

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