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<p>Temporomandibular joint (TMJ) arthritis is a craniofacial disorder characterized by joint dysfunction and orofacial pain. Lymphatic regulation and function in TMJ remain unknown. Using genetic reporter mice, human tissues, tissue clearing, 3D volume imaging, and functional studies, we identified a synovial lymphatic system in TMJ. In a mouse model of TMJ arthritis, inflammation induces extensive lymphatic remodeling and leads to synovial lymphatic dysfunctions. Functional genetics and single-cell RNA sequencing (scRNA-seq) revealed that lymphatic deficiency induces a population of fibroblast-macrophage hybrid cells and enhances inflammation, exacerbating cartilage defects, bone loss, synovitis, and pain behaviors in TMJ arthritis mice. Conversely, lymphatic function promotion via a hydrogel-mediated VEGF-C delivery prevents TMJ pain, inflammation, and arthritis-like pathogenesis. Thus, we identified synovial lymphatics in TMJ and found that lymphatic dysfunction drives TMJ arthritis and pain, suggesting its potential as a therapeutic target.</p>

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Identification of synovial lymphatic system in the temporomandibular joint and their roles in arthritis and pain

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月25日

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  • Yang Shu,
  • Qing Chang,
  • Ziying Lin,
  • Pao-Fen Ko,
  • Jingyi Chen,
  • Yuyueyang Qiu,
  • Feixiang Chen,
  • Zhen Zhao,
  • Glenn Thomas Clark,
  • Anette Vistoso Monreal,
  • David Ahn,
  • Zhaoyang Liu,
  • Jian Xu,
  • Jian-Fu Chen

摘要

Temporomandibular joint (TMJ) arthritis is a craniofacial disorder characterized by joint dysfunction and orofacial pain. Lymphatic regulation and function in TMJ remain unknown. Using genetic reporter mice, human tissues, tissue clearing, 3D volume imaging, and functional studies, we identified a synovial lymphatic system in TMJ. In a mouse model of TMJ arthritis, inflammation induces extensive lymphatic remodeling and leads to synovial lymphatic dysfunctions. Functional genetics and single-cell RNA sequencing (scRNA-seq) revealed that lymphatic deficiency induces a population of fibroblast-macrophage hybrid cells and enhances inflammation, exacerbating cartilage defects, bone loss, synovitis, and pain behaviors in TMJ arthritis mice. Conversely, lymphatic function promotion via a hydrogel-mediated VEGF-C delivery prevents TMJ pain, inflammation, and arthritis-like pathogenesis. Thus, we identified synovial lymphatics in TMJ and found that lymphatic dysfunction drives TMJ arthritis and pain, suggesting its potential as a therapeutic target.