文献类型：期刊文献

英文题名：Synovial immune control failure in osteoarthritis: from maintenance of tissue homeostasis to inflammatory niche formation

作者：Hu, Kangyi[1];Song, Yongjia[1];Pan, Jiaxing[1];Wang, Zhiqiang[1];Li, Weiran[1];Yan, Chaoqun[1];Xue, Yongpeng[1];Jia, Xiao[1];Yu, Luhao[1];Song, Min[1];Bao, Jiamin[2]

第一作者：Hu, Kangyi

通信作者：Song, M[1];Bao, JM[2]

机构：[1]Gansu Univ Chinese Med, Clin Coll Tradit Chinese Med, Lanzhou, Peoples R China;[2]Shanghai Univ Tradit Chinese Med, Sch Rehabil Sci, Shanghai, Peoples R China

第一机构：甘肃中医药大学中医临床学院

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Clin Coll Tradit Chinese Med, Lanzhou, Peoples R China;[2]corresponding author), Shanghai Univ Tradit Chinese Med, Sch Rehabil Sci, Shanghai, Peoples R China.|[10735ccd4a8840d96ab71]甘肃中医药大学中医临床学院;[10735]甘肃中医药大学;

年份：2026

卷号：17

外文期刊名：FRONTIERS IN IMMUNOLOGY

收录：;Scopus(收录号：2-s2.0-105050442826);WOS:【SCI-EXPANDED(收录号:WOS:001873734600001)】；

基金：The author(s) declared that financial support was received for this work and/or its publication. National Natural Science Foundation (grant numbers 82505631 to JB); This work was supported by the Gansu University of Chinese Medicine talent research start-up fund (2024YJRC-09), The 2024 Gansu Basic Research Program-Natural Science Funds-Youth Science and Technology Fund (24JRRA567), Gansu Province Youth Talent - Individual Project (2025QNGR09), and the National Natural Science Foundation (82505631).

语种：英文

外文关键词：fibroblast-like synoviocytes; inflammatory niche; macrophages; osteoarthritis; synovial immune control failure; synovium

摘要：Osteoarthritis (OA) is a whole-joint disease involving cartilage, synovium, subchondral bone, and neurovascular structures. Synovitis, damage-associated molecular patterns, and interactions between macrophages and fibroblast-like synoviocytes have been widely studied. However, a tissue-level explanation is still lacking for how low-grade and fluctuating synovial responses become persistent inflammation. We therefore propose a framework of synovial immune control failure. In this framework, the synovium does more than participate in inflammation. By clearing intra-articular damage-related material, limiting the duration of inflammation, maintaining stromal homeostasis, and regulating the entry of peripheral immune cells, it helps determine whether local joint inflammation can return to a low-level state. When damage-related inputs persist and debris clearance, inflammatory resolution, and resetting of cellular states do not occur in parallel, macrophages, fibroblast-like synoviocytes, and the vascular-interstitial interface may form a mutually sustaining pathological cellular network. Disease-associated cellular states and their interactions may then be retained locally in the synovium, forming what this article defines as an inflammatory niche. This niche may form bidirectional feedback with cartilage degeneration and subchondral bone remodeling. However, the synovium is not the common initiating tissue in all patients with OA. This framework may be most relevant to disease subtypes with persistent or recurrent synovitis, myeloid cell activation, and abnormal stromal remodeling. We further discuss the evidence base, boundaries, testable predictions, and potential implications of this model for OA patient stratification and synovium-targeted intervention.