State Key Laboratory of Oral and Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School and Hospital of Stomatology, Wuhan University, Wuhan, China; The Affiliated Stomatological Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China; Jiangxi Province Key Laboratory of Oral Biomedicine. Jiangxi Province Clinical Research Center for Oral Diseases, Nanchang, China.
State Key Laboratory of Oral and Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School and Hospital of Stomatology, Wuhan University, Wuhan, China; Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Wuhan University, Wuhan, China.
Am J Pathol. 2024 Feb;194(2):296-306. doi: 10.1016/j.ajpath.2023.11.010.
This study investigates the regulatory mechanisms of synovial macrophages and their polarization in the progression of temporomandibular joint osteoarthritis (TMJOA). Macrophage depletion models were established by intra-articular injection of clodronate liposomes and unloaded liposomes. TMJOA was induced by intra-articular injection of 50 μL Complete Freund's Adjuvant and the surgery of disc perforation. The contralateral joint was used as the control group. The expression of F4/80, CD86, and CD206 in the synovium was detected by immunofluorescence staining analysis. Hematoxylin and eosin staining and TMJOA synovial score were detected to show the synovial changes in rat joints after TMJOA induction and macrophage depletion. Changes in rat cartilage after TMJOA induction and macrophage depletion were shown by safranin fast green staining. The bone-related parameters of rats' joints were evaluated by micro-computed tomography analysis. The TMJOA model induced by Complete Freund's Adjuvant injection and disc perforation aggravated synovial hyperplasia and showed a significant up-regulation of expression of F4/80-, CD86-, and CD206-positive cells. F4/80, CD86, and CD206 staining levels were significantly decreased in macrophage depletion rats, whereas the synovitis score further increased and cartilage and subchondral bone destruction was slightly aggravated. Macrophages were crucially involved in the progression of TMJOA, and macrophage depletion in TMJOA synoviocytes promoted synovitis and cartilage destruction.
本研究探讨了滑膜巨噬细胞的调控机制及其在颞下颌关节骨关节炎(TMJOA)进展中的极化。通过关节内注射氯膦酸脂质体和空载脂质体建立巨噬细胞耗竭模型。通过关节内注射 50 μL 完全弗氏佐剂和盘穿孔手术诱导 TMJOA。对侧关节作为对照组。通过免疫荧光染色分析检测滑膜中 F4/80、CD86 和 CD206 的表达。通过苏木精和伊红染色以及 TMJOA 滑膜评分检测 TMJOA 诱导和巨噬细胞耗竭后大鼠关节滑膜的变化。通过番红快绿染色显示 TMJOA 诱导和巨噬细胞耗竭后大鼠软骨的变化。通过微计算机断层扫描分析评估大鼠关节的骨相关参数。完全弗氏佐剂注射和盘穿孔诱导的 TMJOA 模型加重了滑膜增生,并显示 F4/80-、CD86-和 CD206 阳性细胞的表达显著上调。巨噬细胞耗竭大鼠的 F4/80、CD86 和 CD206 染色水平显著降低,而滑膜炎评分进一步增加,软骨和软骨下骨破坏略有加重。巨噬细胞在 TMJOA 的进展中起着至关重要的作用,TMJOA 滑膜细胞中的巨噬细胞耗竭促进了滑膜炎和软骨破坏。