Department of Orthopaedics & Traumatology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.
Department of Orthopaedics & Traumatology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China; Institute for Tissue Engineering and Regenerative Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.
Osteoarthritis Cartilage. 2022 Sep;30(9):1186-1197. doi: 10.1016/j.joca.2022.04.003. Epub 2022 Apr 27.
Osteoarthritis (OA) affects the entire joint, initially with a low degree of inflammation. Synovitis is correlated with the severity of OA clinical symptoms and cartilage degradation. The synovial lymphatic system (SLS) plays a prominent role in clearing macromolecules within the joint, including the pro-inflammatory cytokines in arthritic status. Scattered evidence shows that impaired SLS drainage function leads to the accumulation of inflammatory factors in the joint and aggravates the progression of OA, and the role of SLS function in OA is less studied.
This review summarizes the current understanding of synovial lymphatic function in OA progression and potential regulatory pathways and aims to provide a framework of knowledge for the development of OA treatments targeting lymphatic structure and functions.
SLS locates in the subintima layer of the synovium and consists of lymphatic capillaries and lymphatic collecting vessels. Vascular endothelial growth factor C (VEGF-C) is the most critical regulating factor of lymphatic endothelial cells (LECs) and SLS. Nitric oxide production-induced impairment of lymphatic muscle cells (LMCs) and contractile function may attribute to drainage dysfunction. Preclinical evidence suggests that promoting lymphatic drainage may help restore intra-articular homeostasis to attenuate the progression of OA.
SLS is actively involved in the homeostatic maintenance of the joint. Understanding the drainage function of the SLS at different stages of OA development is essential for further design of therapies targeting the function of these vessels.
骨关节炎（OA）影响整个关节，最初炎症程度较低。滑膜炎与 OA 临床症状的严重程度和软骨降解相关。滑膜淋巴系统（SLS）在清除关节内大分子物质方面发挥着重要作用，包括关节炎状态下的促炎细胞因子。零星证据表明，SLS 引流功能受损会导致关节内炎症因子的积累，从而加重 OA 的进展，而 SLS 功能在 OA 中的作用研究较少。
本文综述了 SLS 在 OA 进展中的作用及其潜在的调节途径，旨在为针对淋巴结构和功能的 OA 治疗方法的发展提供知识框架。
SLS 位于滑膜的亚内膜层，由淋巴管毛细血管和淋巴管收集管组成。血管内皮生长因子 C（VEGF-C）是调节淋巴管内皮细胞（LEC）和 SLS 的最关键因素。一氧化氮产生诱导的淋巴管平滑肌细胞（LMC）损伤和收缩功能障碍可能导致引流功能障碍。临床前证据表明，促进淋巴引流可能有助于恢复关节内的内稳态，从而减轻 OA 的进展。
SLS 积极参与关节的稳态维持。了解 SLS 在 OA 发展的不同阶段的引流功能对于进一步设计针对这些血管功能的治疗方法至关重要。
