A computational algorithm to simulate disorganization of collagen network in injured articular cartilage

Abstract

Cartilage defects are a known risk factor for osteoarthritis. Estimation of structural changes in these defects could help us to identify high risk defects and thus to identify patients that are susceptible for the onset and progression of osteoarthritis. Here, we present an algorithm combined with computational modeling to simulate the disorganization of collagen fibril network in injured cartilage. Several potential triggers for collagen disorganization were tested in the algorithm following the assumption that disorganization is dependent on the mechanical stimulus of the tissue. We found that tensile tissue stimulus alone was unable to preserve collagen architecture in intact cartilage as collagen network reoriented throughout the cartilage thickness. However, when collagen reorientation was based on both tensile tissue stimulus and tensile collagen fibril strains or stresses, the collagen network architecture was preserved in intact cartilage. Using the same approach, substantial collagen reorientation was predicted locally near the cartilage defect and particularly at the cartilage-bone interface. The developed algorithm was able to predict similar structural findings reported in the literature that are associated with experimentally observed remodeling in articular cartilage. The proposed algorithm, if further validated, could help to predict structural changes in articular cartilage following post-traumatic injury potentially advancing to impaired cartilage function.

Computational evaluation of altered biomechanics related to articular cartilage lesions observed in vivo

“…Here, the effect of changes in material properties of cartilage were not modeled because we assumed that tissue properties do not change immediately after injury. Nevertheless, it has been reported previously that both the disruption of the collagen network and the loss of proteoglycan content can lead to increased strains in cartilage and that the increased strains can further contribute to the progressive loss of tissue integrity and function in an iterative manner . Therefore, it is expected that the inclusion of changes in cartilage structure and composition would have only emphasized the effect of cartilage lesions in the present study.…”

“…In addition to measuring strain values, stress‐based failure criteria have been used in evaluation of cartilage degeneration around lesions . However, since maximum principal stresses in cartilage have been suggested to be connected to degeneration caused by chronic overloading, we prioritized our analyses to the strain measures that have experimentally shown to be related to tissue degeneration, i.e., cell death or proteoglycan loss, close to lesions …”

“…Arthrographic CT allows also quantifying spatial distribution of subchondral bone mineral density . Based on imaging data, finite element (FE) modeling can be applied to simulate the biomechanical function of the knee under physiologically relevant loading conditions . Simulation of knee joint function can reveal diagnostically valuable information on the status of the joint; for instance, strain or stress levels and distributions in the cartilage can be applied to estimate the failure of the tissue .…”

Maximum shear strain-based algorithm can predict proteoglycan loss in damaged articular cartilage

“…Such loading values have been used in a previous computational study as well . Unconfined compression was chosen due to its easy experimental setup and because it has been commonly used in other studies (Gratz et al 2009;Szarko and Xia 2012;Li et al 2013;Tanska et al 2018). The lesion had the width of the explant since such lesions could be reproduced experimentally.…”

“…Only the FCD loss was considered, since substantial reduction in the PG content has been observed after a trauma (Fick et al 2016), as opposed to a negligible change in the collagen content (Nelson et al 2006). Potential collagen fibrillation or disorganization was neglected as the collagen orientation angle was not suggested to alter in the superficial and transitional zones near the cartilage injury (Rolauffs et al 2010;Tanska et al 2018). The loss of the FCD via fluid flow or diffusion was not directly modeled, since the literature is lacking the corresponding parameter values.…”