@article{06714460b23b4964815aa4ece2279a65,
title = "Computational frame of ligament in situ strain in a full knee model",
abstract = "The biomechanical function of connective tissues in a knee joint is to stabilize the kinematics-kinetics of the joint by augmenting its stiffness and limiting excessive coupled motion. The connective tissues are characterized by an in vivo reference configuration (in situ strain) that would significantly contribute to the mechanical response of the knee joint. In this work, a novel iterative method for computing the in situ strain at reference configuration was presented. The framework used an in situ strain gradient approach (deformed reference configuration) and a detailed finite element (FE) model of the knee joint. The effect of the predicted initial configuration on the mechanical response of the joint was then investigated under joint axial compression, passive flexion, and coupled rotations (adduction and internal), and during the stance phase of gait. The inclusion of the reference configuration has a minimal effect on the knee joint mechanics under axial compression, passive flexion, and at two instances (0% and 50%) of the stance phase of gait. However, the presence of the ligaments in situ strains significantly increased the joint stiffness under passive adduction and internal rotations, as well as during the other simulated instances (25%, 75% and 100%) of the stance phase of gait. Also, these parameters substantially altered the local loading state of the ligaments and resulted in better agreement with the literature during joint flexion. Therefore, the proposed computational framework of ligament in situ strain will help to overcome the challenges in considering this crucial biological aspect during knee joint modeling. Besides, the current construct is advantageous for a better understanding of the mechanical behavior of knee ligaments under physiological and pathological states and provide relevant information in the design of reconstructive treatments and artificial grafts.",
keywords = "Finite element, In situ strain, Knee, Ligaments, Optimization",
author = "Malek Adouni and Faisal, {Tanvir R.} and Dhaher, {Yasin Y.}",
note = "Funding Information: This work is supported by a grant (# U01 EB015410-01A1 ) from the National Institute of Health NIH . Funding Information: Considering the optimal configuration of the in situ strains (Fig. 2) at full knee extension and under 2000 N of axial compression, the relative displacements of the joint decreased by approximately 1, 0.3, and 0.2 mm in the anterior, lateral, and proximal directions, respectively (Fig. 4a). Accordingly, a peak ligament force of 105 N was supported by the ACL and decreased to 96 N with the optimal configuration (with in situ strains). Under the same loading condition, the force in the collateral ligaments (MCL and LCL) was augmented by approximately 11%. Less than 5 N was computed for the rest of the ligaments (Fig. 4a). However, the inclusion of the in situ strains had a negligible effect on the predicted contact force/area, with a difference of less than 2%. This led to approximately the same cartilage stress/strain distributions within the contact region (Fig. 4b and d).During the passive flexion of the tibiofemoral joint, the ACL force reached the maximum values of 36 N and 24 N at approximately full extension with and without ligament in situ strains, respectively (Fig. 5). This force diminished during flexion and reached approximately the same minimum (20 N) in both cases (with and without in situ strain). This result appears to be consistent with previously observed small forces in the ACL throughout the flexion range [ 64?66]. This ACL force variation during flexion was almost equally supported between the ACL bundles in the absence of in situ strains. However, by considering the optimal map of the in situ strain distribution, the ACL force was mostly supported by the ACL-pl bundle at full extension and gradually shifted to ACL-am with knee flexion. This trend is in agreement with previously reported measurements [7]. The results of this study were also confirmed by the reported measured increase in the ACL-am strain with knee joint flexion higher than 40? [42,43]. Moreover, the force in the PCL initiated with the joint flexion and reached 16 N at 90?. This result is consistent with the results obtained by previous studies that have reported the augmentation of PCL force/strain during knee flexion [54, 66?69]. The in situ strain in the PCL increased the stiffness of this ligament in the flexion range between full extension and 60?. In the collateral ligaments, LCL and MCL, the forces increased with the joint flexion, which provides a clear indication of their significant role at larger flexion angles. These findings corroborate those of Hull et al. [46], who reported a substantial strain increase in the MCL during knee flexion. However, the result obtained by this study is different to the previous observation of collateral ligament isometry reported by Victor et al. [70]. This difference is attributed to the slight deviation in the adopted boundary conditions (experimental set-up) and/or to certain weaknesses, which are mainly related to the technique used to measure the ligament length. The ligament in situ strain slightly affected the MCL force during flexion. However, higher resistance was observed in the LCL, particularly after 40? of flexion. Notably, most of the effects on the ligament forces when considering the in situ strains occurred in the range of 20??60? of knee flexion. This justifies the greater contact force/stress calculated in the same flexion range when the in situ strains were considered (Fig. 6). One explanation for the more considerable change in the mechanics of the knee joint within the flexion range of 20??60? is the screw-home mechanism. This is adequately characterized by the obvious augmentation of the coupled rotations (adduction and internal rotations) in the range of 10??60? of flexion, which are considered as essential factors affecting the knee joint stiffness [71].This work is supported by a grant (#U01 EB015410-01A1) from the National Institute of Health NIH. Publisher Copyright: {\textcopyright} 2020 Elsevier Ltd",
year = "2020",
month = nov,
doi = "10.1016/j.compbiomed.2020.104012",
language = "English (US)",
volume = "126",
journal = "Computers in Biology and Medicine",
issn = "0010-4825",
publisher = "Elsevier Limited",
}