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Cartilage tissue engineering for obesity-induced osteoarthritis: Physiology challenges and future prospects

机译:肥胖诱发的骨关节炎的软骨组织工程:生理学挑战和未来的前景

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摘要

Osteoarthritis (OA) is a multifactorial joint disease with pathological changes that affect whole joint tissue. Obesity is acknowledged as the most influential risk factor for both the initiation and progression of OA in weight-bearing and non-weight-bearing joints. Obesity-induced OA is a newly defined phenotypic group in which chronic low-grade inflammation has a central role. Aside from persistent chronic inflammation, abnormal mechanical loading due to increased body weight on weight-bearing joints is accountable for the initiation and progression of obesity-induced OA. The current therapeutic approaches for OA are still evolving. Tissue-engineering-based strategy for cartilage regeneration is one of the most promising treatment breakthroughs in recent years. However, patients with obesity-induced OA are often excluded from cartilage repair attempts due to the abnormal mechanical demands, altered biomechanical and biochemical activities of cells, persistent chronic inflammation, and other obesity-associated factors. With the alarming increase in the number of obese populations globally, the need for an innovative therapeutic approach that could effectively repair and restore the damaged synovial joints is of significant importance for this sub-population of patients. In this review, we discuss the involvement of the systemic and localized inflammatory response in obesity-induced OA and the impact of altered mechanical loading on pathological changes in the synovial joint. Moreover, we examine the current strategies in cartilage tissue engineering and address the critical challenges of cell-based therapies for OA. Besides, we provide examples of innovative ways and potential strategies to overcome the obstacles in the treatment of obesity-induced OA.
机译:骨关节炎(OA)是一种多因素关节疾病,具有影响全关节组织的病理变化。肥胖被认为是负重和非负载接头中OA的起始和进展的最有影响力的危险因素。肥胖诱导的OA是一种新定义的表型组织,其中慢性低级炎症具有核心作用。除了持续的慢性炎症之外,由于负重接头上的体重增加而异的机械负荷是对肥胖诱导的OA的启动和进展负责。 OA目前的治疗方法仍在发展。基于组织工程的软骨再生策略是近年来最有前途的治疗突破之一。然而,肥胖诱导的OA患者通常被排除在软骨修复尝试之外,由于机械需求异常,细胞的生物力学和生化活性改变,持续的慢性炎症和其他肥胖相关因素。随着全球肥胖人群数量的令人震惊的增加,需要一种可以有效修复和恢复受损的滑膜关节的创新治疗方法对该患者的亚群具有重要意义。在本综述中,我们探讨了系统性和局部炎症反应在肥胖症诱导的OA中的累积以及改变机械负载改变对滑膜接头的病理变化的影响。此外,我们研究了软骨组织工程中的当前策略,并解决了对OA的细胞疗法的关键挑战。此外,我们提供了创新的方式和潜在策略的例子,以克服肥胖诱导的OA治疗的障碍。

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