Shi Jiahong, Wang Lulu, Shan Liliang, Zhu Meng, Chen Yu, Li Houxuan, Lei Lang
Department of Periodontics, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Department of Orthodontics, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
Prog Orthod. 2025 May 19;26(1):17. doi: 10.1186/s40510-025-00563-5.
This study aimed to elucidate metabolic alterations in gingival crevicular fluid (GCF) during orthodontic tooth movement (OTM) and investigate the role of the succinate-SUCNR1 axis in bone resorption and tooth movement.
OTM was accompanied by the change of TCA cycle and increase of succinate in the human GCF. Succinate accumulation was observed in periodontal ligament cells (PDLCs) under compressive force, accompanied by increase of glycolysis and decrease of succinic dehydrogenase activity. Suppression of the succinate-SUCNR1 axis reduced osteoclastogenesis in BMDMs. OTM slowed down in the SUCNR1/ mice when compared with wild mice.
OTM is accompanied by the increase of succinate in periodontal tissues. Compressive force induces metabolic reprogramming in PDLCs, leading to enhanced succinate production. Succinate promotes macrophage migration and osteoclast differentiation via the SUCNR1 axis, ultimately facilitating orthodontic tooth movement. These findings provide a new potential therapeutic target for regulating periodontal tissue remodeling during orthodontic treatment.
本研究旨在阐明正畸牙齿移动（OTM）过程中龈沟液（GCF）的代谢变化，并研究琥珀酸-SUCNR1轴在骨吸收和牙齿移动中的作用。
OTM伴随着人GCF中三羧酸循环的改变和琥珀酸的增加。在压缩力作用下，牙周膜细胞（PDLCs）中观察到琥珀酸积累，同时糖酵解增加，琥珀酸脱氢酶活性降低。抑制琥珀酸-SUCNR1轴可减少骨髓来源巨噬细胞（BMDMs）中的破骨细胞生成。与野生小鼠相比，SUCNR1基因敲除小鼠的OTM减慢。
OTM伴随着牙周组织中琥珀酸的增加。压缩力诱导PDLCs中的代谢重编程，导致琥珀酸产生增加。琥珀酸通过SUCNR1轴促进巨噬细胞迁移和破骨细胞分化，最终促进正畸牙齿移动。这些发现为正畸治疗期间调节牙周组织重塑提供了一个新的潜在治疗靶点。
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