Multiscale Model Predicts Tissue-Level Failure From Collagen Fiber-Level Damage

Abstract

Excessive tissue-level forces communicated to the microstructure and extracellular matrix of soft tissues can lead to damage and failure through poorly understood physical processes that are multiscale in nature. In this work, we propose a multiscale mechanical model for the failure of collagenous soft tissues that incorporates spatial heterogeneity in the microstructure and links the failure of discrete collagen fibers to the material response of the tissue. The model, which is based on experimental failure data derived from different collagen gel geometries, was able to predict the mechanical response and failure of type I collagen gels, and it demonstrated that a fiber-based rule (at the micrometer scale) for discrete failure can strongly shape the macroscale failure response of the gel (at the millimeter scale). The model may be a useful tool in predicting the macroscale failure conditions for soft tissues and engineered tissue analogs. In addition, the multiscale model provides a framework for the study of failure in complex fiber-based mechanical systems in general.

Multiscale cartilage biomechanics: technical challenges in realizing a high-throughput modelling and simulation workflow

“…It should be noted that such a feedback loop is not necessary to obtain the mechanical environment of cartilage and chondrocytes for a given tissue state. It will be necessary when constitutive properties change as a result of tissue growth and damage [31]. Nonetheless, the tools presented in this study can be adapted for such purposes.…”

“…incorporating the cytoskeleton (actin and tubulin) [30], to understand the mechanical load transmission to intracellular components, in particular to the nucleus. Similar submodelling can be performed for the extracellular matrix, for example, to evaluate microstructural-level loading of collagen fibres, which may provide the relationship between macroscopic tissue damage accumulation and microscale fibre failure [31]. At all spatial scales, it is also possible to increase the fidelity of mechanical representation; in terms of physics (nonlinear elasticity, multiphasic response) [32], with additional anatomical components, and by using more advanced constitutive relationships [24,33].…”

“…Finally, computational homogenization strategies can be employed [45], where average mechanical response of a representative volume element (in this case, the tissue-cell scale model) can be calculated from simulations of uniform loading cases, and a surrogate macroscopic constitutive law can be fitted to determine homogenized material properties for the joint-tissue scale model. This approach may be beneficial for complicated and dense cellular arrangements [17] and for explicit fibre-based modelling of the tissue matrix microstructurally [31]. The gross impact of tissue heterogeneity and the contributions of cells and fibres on tissue behaviour can be incorporated within the continuum mechanics framework.…”

Prefailure and Failure Mechanics of the Porcine Ascending Thoracic Aorta: Experiments and a Multiscale Model

“…A previous study also indicated that intrinsic elastic properties dictate distensibility of the aorta [34]. In addition, a collagen-based fiber network would not be able to achieve a stretch of 2.0 since collagen fibers have a k crit closer to 1.4 [17], while elastin can reach stretches up to 3 [35]. Histological evidence supports a large elastin contribution as studies have shown more elastin than collagen exists in the ascending aorta (by dry weight 35% elastin, 22% collagen [19]).…”

“…2, Refs. [14,15,17]) was made up of elements at three scales: the finite element (FE) domain at the millimeter (mm) scale, representative volume elements (RVE) at the micrometer (lm) scale, and the fibers with radii at the Each element consists of eight Gauss points that dictate its stress-strain response. Each Gauss point consists of representative volume elements (RVE) that consist of a nanoscale fiber network in parallel with a nearly incompressible neoHookean matrix.…”