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

Abstract

Chondral lesions provide a potential risk factor for development of osteoarthritis. Despite the variety of in vitro studies on lesion degeneration, in vivo studies that evaluate relation between lesion characteristics and the risk for the possible progression of OA are lacking. Here, we aimed to characterize different lesions and quantify biomechanical responses experienced by surrounding cartilage tissue. We generated computational knee joint models with nine chondral injuries based on clinical in vivo arthrographic computed tomography images. Finite element models with fibril-reinforced poro(visco)elastic cartilage and menisci were constructed to simulate physiological loading. Systematically, the lesions experienced increased peak values of maximum principal strain, maximum shear strain, and minimum principal strain in the surrounding chondral tissue (p < 0.01) compared with intact tissue. Depth, volume, and area of the lesion correlated with the maximum shear strain (p < 0.05, Spearman rank correlation coefficient r ¼ 0.733-0.917). Depth and volume of the lesion correlated also with the maximum principal strain (p < 0.05, r ¼ 0.767, and r ¼ 0.717, respectively). However, the lesion area had non-significant correlation with this strain parameter (p ¼ 0.06, r ¼ 0.65). Potentially, the introduced approach could be developed for clinical evaluation of biomechanical risks of a chondral lesion and planning an intervention. Statement of Clinical Relevance:In this study, we computationally characterized different in vivo chondral lesions and evaluated their risk of cartilage degeneration. This information is vital in decision-making for intervention in order to prevent post-traumatic

Mechanobiological model for simulation of injured cartilage degradation via pro-inflammatory cytokines and mechanical stimulus

“…The computational models should also be brought from tissue to joint level in order to predict PTOA progression for clinical relevance. This could be possible with synovial fluid or serum data on biochemical mediators [ 93 , 94 ] combined with subject-specific joint models obtained via medical imaging [ 18 ]. For example, it would be interesting to include predictions of inflammation and biomechanically-driven degradation of ACL injured patients.…”

“…Biomechanical degradation of PG content was associated with increased levels of intra-tissue shear strain during loading, since shear strains have been suggested to increase near chondral lesions [ 16 – 18 , 77 ] and may induce cartilage matrix breakdown [ 19 ] and chondrocyte apoptosis [ 78 – 80 ]. Ultimately, this leads to loss of FCD content.…”

“…The first mechanism involves joint inflammation [ 3 , 6 , 7 ] and the resulting diffusion of pro-inflammatory cytokines from the synovial fluid into cartilage [ 8 – 11 ], leading to proteolysis of cartilage matrix. The second mechanism involves biomechanical factors [ 12 ] including induction of chondral defects and aberrant loading characteristics in the knee joint milieu [ 13 – 15 ], leading to elevated shear strains near chondral lesions [ 16 – 18 ]. While these mechanisms have been recognized for years, current healthcare approaches lack effective tools to identify patients with increased risk of PTOA development.…”

Study on the Potential Active Components and Molecular Mechanism of Xiao Huoluo Pills in the Treatment of Cartilage Degeneration of Knee Osteoarthritis Based on Bioinformatics Analysis and Molecular Docking Technology

“…The enrichment analysis of target genes GO/KEGG indicated that "Oxygen levels", "mechanical stimulus", "collagen-containing extracellular matrix", "TNF signaling pathway", "PI3K-Akt signaling pathway", and "Fluid shear stress" may be a potential way of XHLP treatment of KOA. Many studies [55][56][57] have revealed that the mechanical stress environment of joints is a signi cant factor affecting the activity of cartilage cells in the body, and accelerates the catabolism of osteoarthritis cartilage by interacting with pro-in ammatory factors. TNF-α can inhibit the synthesis of matrix macromolecules, stimulate the synthesis and secretion of cartilage degrading enzymes, prostaglandin (PGE2), and promote the synthesis of in ammatory factors, leading to cartilage destruction, increased in ammation, and nally degeneration of KOA cartilage [58,59].…”

Rapid CT-based Estimation of Articular Cartilage Biomechanics in the Knee Joint Without Cartilage Segmentation

“…As an alternative to MRI, a contrast-enhanced CT (CECT) imaging method has been used for generating knee and hip joint FE models. 4,6,17,33,47 Compared to MRI, CECT has superior resolution and contrast, and enables better characterization of cartilage lesions. 32 However, this method has not yet been extensively applied clinically.…”