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

机译:通过炎症细胞因子和机械刺激模拟损伤软骨降解的力学模型

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摘要

Post-traumatic osteoarthritis is a musculoskeletal disorder where inflammatory processes and abnormal joint loading predispose articular cartilage to degradation after a mechanical injury. Since inflamed and injured cartilage cannot be reversed back to healthy state, prevention of osteoarthritis progression is advisable, a prestigious goal where computational models could serve as tools. The current literature is short of computational models combining both biochemical and biomechanical aspects of osteoarthritis. Thus, here we implemented inflammation of living cartilage tissue followed by biochemical perturbations of tissue homeostasis and shear strain-induced biomechanical degradation in novel cell-to-tissue-level finite element models. The models presented in this paper and enriched by our experimental findings/previous literature provide profound new mechanobiological insights and predictions about cartilage degradation in injured and inflamed tissue under physiologically relevant mechanical loading. We suggest that mechanobiological computational models could be applied as in silico analysis tools that provide clinicians information of the personalized progression of post-traumatic osteoarthritis and decision-making guidance for treatment of the disease.
机译:创伤后骨关节炎是一种肌肉骨骼障碍,炎症过程和异常关节载荷易于在机械损伤后降解关节软骨。由于发炎和受伤的软骨不能逆转到健康状态,因此建议预防骨关节炎进展,这是一个具有较为代表性的目标,其中计算模型可以作为工具。目前的文献是缺乏骨关节炎的生物化学和生物力学方面的计算模型。因此,在这里,我们实施了活性软骨组织的炎症,然后进行了组织稳态和剪切应变诱导的生物力学降解在新型细胞对组织级有限元模型中的生化扰动。本文提出的模型和我们的实验结果富集/以前的文献提供了对生理相关机械载荷的受损和发炎组织中的软骨降解的深刻新的力学洞察和预测。我们建议,机械化计算模型可以应用于硅分析工具中,提供临床医生信息的临床医生信息的临床学家的术后骨关节炎和治疗疾病的决策指导。

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