Publications by authors named "Malek Adouni"

This research demonstrates a systematic curve fitting approach for acquiring parametric values of hyperelastic constitutive models for both healthy and enzymatically mediated degenerated cartilage to facilitate finite element modeling of cartilage. Several widely used phenomenological hyperelastic constitutive models were tested to adequately capture the changes in cartilage mechanics that vary with the differential/unequal abundance of matrix metalloproteinases (MMPs). Trauma and physiological conditions result in an increased production of collagenases (MMP-1) and gelatinases (MMP-9), which impacts the load-bearing ability of cartilage by significantly deteriorating its extracellular matrix (ECM).

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Background: Obesity is a crucial factor that increases the risk of initiating and advancing knee osteoarthritis. However, it remains unclear how obesity directly impacts the biomechanical experience of the lower limb joints, potentially triggering or exacerbating joint degeneration. This study investigated the interactive effects of BMI augmentation on lower limb kinematics, kinetics, and muscle activations during walking.

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Knee osteoarthritis (OA) and obesity are major public health concerns that are closely intertwined. This intimate relationship was documented by considering obesity as the most significant preventable risk factor associated with knee OA. To date, however, the effects of obesity on the knee joint's passive-active structure and cartilage loading have been inconclusive.

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Understanding the mechanics behind knee joint injuries and providing appropriate treatment is crucial for improving physical function, quality of life, and employability. In this study, we used a hybrid molecular dynamics-finite element-musculoskeletal model to determine the level of loads the knee can withstand when landing from different heights (20, 40, 60 cm), including the height at which cartilage damage occurs. The model was driven by kinematics-kinetics data of asymptomatic subjects at the peak loading instance of drop landing.

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A characteristic feature of arthritic diseases is cartilage extracellular matrix (ECM) degradation, often orchestrated by the overexpression of matrix metalloproteinases (MMPs) and other proteases. The interplay between fibril level degradation and the tissue-level aggregate response to biomechanical loading was explored in this work by a computational multiscale cartilaginous model. We considered the relative abundance of collagenases (MMP-1) and gelatinases (MMP-9) in surrogate models, where the diffusion (spatial distribution) of these enzymes and the subsequent, co-localized fibrillar damage were spatially randomized with Latin Hypercube Sampling.

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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.

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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.

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The purpose of this study is to understand the effect of essential surgical design parameters on collateral and cruciate ligaments behavior for a Bone-Patellar-Tendon-Bone (BPTB) anterior cruciate ligament reconstruction (ACL-R) surgery. A parametric finite element model of biomechanical experiments depicting the ACL-R surgery associated with a global sensitivity analysis was adopted in this work. The model parameters were six intraoperative variables, two-quadrant coordinates of femoral tunnel placement, femoral tunnel sagittal and coronal angles, graft pretension, and the joint angle at which the BPTB graft is tensioned (fixation angle).

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In this study, we aimed to develop an in-silico synthesis of the effect of critical surgical design parameters on articular contact behavior for a bone-patellar-tendon-bone anterior cruciate ligament reconstruction (ACL-R) surgery. A previously developed finite element model of the knee joint consisting of all relevant soft tissues was employed. The knee model was further updated with additional features to develop the parametric FE model of the biomechanical experiments that depicted the ACL-R surgery.

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Matrix metalloproteinases (MMPs) play a crucial role in enzymatically digesting cartilage extracellular matrix (ECM) components, resulting in degraded cartilage with altered mechanical loading capacity. Overexpression of MMPs is often caused by trauma, physiologic conditions and by disease. To understand the synergistic impact MMPs have on cartilage biomechanical properties, MMPs from two subfamilies: collagenase (MMP-1) and gelatinase (MMP-9) were investigated in this study.

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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.

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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.

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Knee articular cartilage is characterized by a complex mechanical behavior, posing a challenge to develop an efficient and precise model. We argue that the cartilage damage, in general, can be traced to the fibril level as a plastic deformation, defined as micro-defects. To investigate these micro-defects, we have developed a detailed finite element model of the entire healthy tibiofemoral joint (TF) including a multiscale constitutive model which considers the structural hierarchies of the articular cartilage.

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The pathogenesis and pathophysiological underpinnings of cartilage degradation are not well understood. Either mechanically or enzymatically mediated degeneration at the fibril level can lead to acute focal injuries that will, overtime, cause significant cartilage degradation. Understanding the relationship between external loading and the basic molecular structure of cartilage requires establishing a connection between the fibril-level defects and its aggregate effect on cartilage.

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Anterior cruciate ligament (ACL) reconstructive surgeries, employing a total of 48 models, were conducted by virtually removing the ACL and then modeling the surgical preparation, tunnel architecture, graft pre-tensioning and fixation angle of a bone-patellar-tendon-bone autograft. Multifactorial sensitivity analyses were performed to assess the relative influence of these surgical factors on the intraoperative joint laxity, graft-tunnel contact mechanics and graft forces. The sensitivity results indicated that the combined variation in tunnel architecture and graft pre-tension at the time of fixation accounts for most of the estimated variance of the three outcomes.

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Collagen damage is one of the earliest signs of cartilage degeneration and the onset of osteoarthritis (OA), but the connection between the microscale damage and macroscale tissue function is unclear. We argue that a multiscale model can help elucidate the biochemical and mechanical underpinnings of OA by connecting the microscale defects in collagen fibrils to the macroscopic cartilage mechanics. We investigated this connection using a multiscale fibril reinforced hyperelastoplastic (MFRHEP) model that accounts for the structural architecture of the soft tissue, starting from tropocollagen molecules that form fibrils, and moving to the complete soft tissue.

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