Li Yingjie, Zhou Yinghong, Wang Yifan, Crawford Ross, Xiao Yin
State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST), Key Laboratory of Oral Biomedicine Ministry of Education (KLOBM), School and Hospital of Stomatology, Wuhan University, Wuhan, People's Republic of China.
The Australia-China Centre for Tissue Engineering and Regenerative Medicine (ACCTERM), Queensland University of Technology (QUT), Brisbane, QLD, 4000, Australia.
Biomed Mater. 2021 Dec 9;17(1). doi: 10.1088/1748-605X/ac3d74.
Inflammation is a critical process in disease pathogenesis and the restoration of tissue structure and function, for example, in joints such as the knee and temporomandibular. Within the innate immunity process, the body's first defense response in joints when physical and chemical barriers are breached is the synovial macrophages, the main innate immune effector cells, which are responsible for triggering the initial inflammatory reaction. Macrophage is broadly divided into three phenotypes of resting M0, pro-inflammatory M1-like (referred to below as M1), and anti-inflammatory M2-like (referred to below as M2). The synovial macrophage M1-to-M2 transition can affect the chondrogenic differentiation of mesenchymal stem cells (MSCs) in joints. On the other hand, MSCs can also influence the transition between M1 and M2. Failure of the chondrogenic differentiation of MSCs can result in persistent cartilage destruction leading to osteoarthritis. However, excessive chondrogenic differentiation of MSCs may cause distorted cartilage formation in the synovium, which is evidenced in the case of synovial chondromatosis. This review summarizes the role of macrophage polarization in the process of both cartilage destruction and regeneration, and postulates that the transition of macrophage phenotype in an inflammatory joint environment may play a key role in determining the fate of joint cartilage.
炎症是疾病发病机制以及组织结构和功能恢复过程中的关键过程，例如在膝关节和颞下颌关节等关节中。在固有免疫过程中，当物理和化学屏障被突破时，关节中机体的第一道防御反应是滑膜巨噬细胞，它是主要的固有免疫效应细胞，负责触发初始炎症反应。巨噬细胞大致分为静息M0、促炎M1样（以下简称M1）和抗炎M2样（以下简称M2）三种表型。滑膜巨噬细胞从M1向M2的转变会影响关节中间充质干细胞（MSC）的软骨形成分化。另一方面，MSC也会影响M1和M2之间的转变。MSC软骨形成分化失败会导致持续的软骨破坏，进而引发骨关节炎。然而，MSC过度的软骨形成分化可能会导致滑膜中软骨形成异常，滑膜软骨瘤病的病例就证明了这一点。本综述总结了巨噬细胞极化在软骨破坏和再生过程中的作用，并推测在炎症性关节环境中巨噬细胞表型的转变可能在决定关节软骨命运方面起关键作用。
