Sun Antonia RuJia, Udduttula Anjaneyulu, Li Jian, Liu Yanzhi, Ren Pei-Gen, Zhang Peng
Center for Translational Medicine Research and Development, Shenzhen Institutes of Advanced Technology, Chinese Academy of Science, Shenzhen, Guangdong, 518055, China.
Center for Energy Metabolism and Reproduction, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, 518055, China.
J Orthop Translat. 2020 Sep 28;26:3-15. doi: 10.1016/j.jot.2020.07.004. eCollection 2021 Jan.
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.
Altogether, this review delivers insight into obesity-induced OA and offers future research direction on the creation of tissue engineering-based therapies for obesity-induced OA.
骨关节炎（OA）是一种多因素关节疾病，其病理变化会影响整个关节组织。肥胖被认为是负重和非负重关节OA发生和进展的最具影响力的风险因素。肥胖诱导的OA是一个新定义的表型组，其中慢性低度炎症起核心作用。除了持续的慢性炎症外，负重关节因体重增加导致的异常机械负荷是肥胖诱导的OA发生和进展的原因。目前OA的治疗方法仍在不断发展。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患者由于异常的机械需求、细胞生物力学和生化活性改变、持续的慢性炎症以及其他与肥胖相关的因素，往往被排除在软骨修复尝试之外。随着全球肥胖人口数量的惊人增加，对于这一亚组患者来说，需要一种能够有效修复和恢复受损滑膜关节的创新治疗方法具有重要意义。在这篇综述中，我们讨论了全身和局部炎症反应在肥胖诱导的OA中的作用以及机械负荷改变对滑膜关节病理变化的影响。此外，我们研究了软骨组织工程的当前策略，并探讨了OA细胞治疗的关键挑战。此外，我们提供了创新方法和潜在策略的例子，以克服肥胖诱导的OA治疗中的障碍。
总之，这篇综述深入探讨了肥胖诱导的OA，并为创建基于组织工程的肥胖诱导的OA治疗方法提供了未来的研究方向。
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