Knee connective tissues are mainly responsible for joint stability and play a crucial role in restraining excessive motion during regular activities. The damage mechanism of these tissues is directly linked to the microscale collagen level. However, this mechanical connection is still unclear. During this investigation, a multiscale fibril‐reinforced hyper‐elastoplastic model was developed and statistically calibrated. The model is accounting for the structural architecture of the soft tissue, starting from the tropocollagen molecule that forms fibrils to the whole soft tissue. Model predictions are in agreement with the results of experimental and numerical studies. Further, damage initiation and propagation in the collagen fiber were computed at knee ligaments and located mainly in the superficial layers. Results indicated higher crosslink density required higher tensile stress to elicit fibril damage. This approach is aligned with a realistic simulation of a damaging process and repair attempt. To the best of our knowledge, this is the first model published in which the connective tissue stiffness is simultaneously predicted by encompassing the mesoscopic scales between the molecular and macroscopic levels.

Knee osteoarthritis (OA) is a growing source of pain and disability. Obesity is the most important avoidable risk factor underlying knee OA. The processes by which obesity impacts osteoarthritis are of tremendous interest to osteoarthritis researchers and physicians, where the joint mechanical load is one of the pathways generally thought to cause or intensify the disease process. In the current work, we developed a hybrid framework that simultaneously incorporates a detailed finite element model of the knee joint within a musculoskeletal model to compute lower extremity muscle forces and knee joint stresses in normal-weight (N) and obese (OB) subjects during the stance phase gait. This model accounts for the synergy between the active musculature and passive structures. In comparing OB subjects and normal ones, forces significantly increased in all muscle groups at most instances of stance. Mainly, much higher activation was computed with lateral hamstrings and medial gastrocnemius. Cartilage contact average pressure was mostly supported by the medial plateau and increased by 22%, with a larger portion of the load transmitted via menisci. This medial compartment experienced larger relative movement and cartilage stresses in the normal subjects and continued to do so with a higher level in the obese subjects. Finally, the developed bioengineering frame and the examined parameters during this investigation might be useful clinically in evaluating the initiation and propagation of knee OA.

Injuries to the knee anterior cruciate ligament (ACL) are common, with a known but poorly understood association with intrinsic and extrinsic risk factors. Some of these factors are enzymatically or mechanically mediated, creating acute focal injuries that may cause significant ligament damage. Understanding the relationship between the basic molecular structure and external loading of the ACL requires a hierarchical connection between the two levels. In the present study, a multi-domain frame was developed connecting the molecular dynamics of the collagen networks to the continuum mechanics of the ACL. The model was used to elucidate the effect of the two possible collagen degradation mechanisms on the aggregate ACL behaviour. Results indicated that collagen content and ACL stiffness were reduced significantly, regardless of the degradation mechanism. Furthermore, the volumetric degradation at the molecular level had a devastating effect on the mechanical behaviour of the ACL when it was compared with the superficial degradation. ACL damage initiation and propagation were clearly influenced by collagen degradation. To summarise, the new insights provided by the predicted results revealed the significance of the collagen network structural integrity to the aggregate mechanical response of the ACL and, hence, underlined the biomechanical factors that may help develop an engineering-based approach towards improving the therapeutic intervention for ACL pathologies.

The anterior cruciate ligament’s (ACL) mechanics is an important factor governing the ligament’s integrity and, hence, the knee joint’s response. Despite many investigations in this area, the cause and effect of injuries remain unclear or unknown. This may be due to the complexity of the direct link between macro- and micro-scale damage mechanisms. In the first part of this investigation, a three-dimensional coarse-grained model of collagen fibril (type I) was developed using a bottom-up approach to investigate deformation mechanisms under tensile testing. The output of this molecular level was used later to calibrate the parameters of a hierarchical multi-scale fibril-reinforced hyper-elastoplastic model of the ACL. Our model enabled us to determine the mechanical behavior of the ACL as a function of the basic response of the collagen molecules. Modeled elastic response and damage distribution were in good agreement with the reported measurements and computational investigations. Our results suggest that degradation of crosslink content dictates the loss of the stiffness of the fibrils and, hence, damage to the ACL. Therefore, the proposed computational frame is a promising tool that will allow new insights into the biomechanics of the ACL.

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Type I collagen is one of the most important proteins in the human body because of its role in providing structural support to the extracellular matrix of the connective tissues. Understanding its mechanical properties was widely investigated using experimental testing as well as molecular and finite element simulations. In this work, we present a new approach for defining the properties of the type I collagen fibrils by analytically formulating its response when subjected to a tensile load and investigating the effects of enzymatic crosslinks on the behavioral response. We reveal some of the shortcomings of the molecular dynamics (MD) method and how they affect the obtained stress–strain behavior of the fibril, and we prove that not only does MD underestimate the Young’s modulus and the ultimate tensile strength of the collagen fibrils, but also fails to detect the mechanics of some stretching phases of the fibril. We prove that non-crosslinked fibrils have three tension phases: (i) an initial elastic deformation corresponding to the collagen molecule uncoiling, (ii) a linear regime related to the stretching of the backbone of the tropocollagen molecules, and (iii) a plastic regime dominated by molecular sliding. We also show that for crosslinked fibrils, the second regime can be subdivided into three sub-regimes, and we define the properties of each regime. We also prove, analytically, the alleged MD quadratic relation between the ultimate tensile strength of the fibril and the concentration of enzymatic crosslinks (β).

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