Orthodontic tooth movement-activated sensory neurons contribute to enhancing osteoclast activity and tooth movement through sympathetic nervous signalling
Orthodontic tooth movement-activated sensory neurons contribute to enhancing osteoclast activity and tooth movement through sympathetic nervous signalling
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DOI：
10.1093/ejo/cjab072
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发表时间：
2021-10-13
影响因子：
2.6
通讯作者：
Togari, Akifumi
中科院分区：
文献类型：
--
作者：
Kondo, Hisataka;Kondo, Mayo;Togari, Akifumi
目的正畸牙齿运动（OTM）增加牙周组织的交感神经和感觉神经标志物。然而，交感神经系统和感觉神经系统在OTM中的关系尚不清楚。因此，本研究利用药理学方法探讨了中药激活的交感神经系统和感觉神经系统之间的关系。材料与方法比较C57BL6/J小鼠OTM过程中交感神经切除术与感觉神经损伤的影响。用辣椒素（Capsaicin， CAP）诱导感觉神经损伤。使用6-羟多巴胺进行交感神经切除术。为了研究β激动剂对感觉神经损伤的影响，我们给cap治疗的小鼠注射异丙肾上腺素（ISO）。此外，为了研究中枢神经系统在OTM中的作用，我们使用金硫葡萄糖消融下丘脑腹内侧核（VMH）。结果感觉神经损伤和交感神经切除术均能抑制OTM，降低牙周组织中破骨细胞覆盖的牙槽窝百分比。感觉神经损伤抑制牙周组织中otm诱导的降钙素基因相关肽（CGRP）免疫反应性（IR）（感觉神经元的标志）和酪氨酸羟化酶（TH） IR（交感神经元的标志）的增加。虽然交感神经切除术没有减少牙周组织中CGRP-IR神经元的数量，但otm诱导的TH-IR神经元数量的增加受到抑制。ISO治疗恢复了感觉神经损伤，抑制了牙齿运动和Oc.S/AS。此外，VMH（交感神经系统的中枢）的消融抑制了otm引起的牙齿运动和Oc.S/AS的增加。结论otm激活的感觉神经元通过交感神经信号促进破骨细胞活性和牙齿运动。
Objectives Orthodontic tooth movement (OTM) increases sympathetic and sensory neurological markers in periodontal tissue. However, the relationship between the sympathetic and sensory nervous systems during OTM remains unclear. Therefore, the present study investigated the relationship between the sympathetic and sensory nervous systems activated by OTM using pharmacological methods. Materials and Methods We compared the effects of sympathectomy and sensory nerve injury during OTM in C57BL6/J mice. Capsaicin (CAP) was used to induce sensory nerve injury. Sympathectomy was performed using 6-hydroxydopamine. To investigate the effects of a beta-agonist on sensory nerve injury, isoproterenol (ISO) was administered to CAP-treated mice. Furthermore, to examine the role of the central nervous system in OTM, the ventromedial hypothalamic nucleus (VMH) was ablated using gold thioglucose. Results Sensory nerve injury and sympathectomy both suppressed OTM and decreased the percent of the alveolar socket covered with osteoclasts (Oc.S/AS) in periodontal tissue. Sensory nerve injury inhibited increases in OTM-induced calcitonin gene-related peptide (CGRP) immunoreactivity (IR), a marker of sensory neurons, and tyrosine hydroxylase (TH) IR, a marker of sympathetic neurons, in periodontal tissue. Although sympathectomy did not decrease the number of CGRP-IR neurons in periodontal tissue, OTM-induced increases in the number of TH-IR neurons were suppressed. The ISO treatment restored sensory nerve injury-inhibited tooth movement and Oc.S/AS. Furthermore, the ablation of VMH, the centre of the sympathetic nervous system, suppressed OTM-induced increases in tooth movement and Oc.S/AS. Conclusions The present results suggest that OTM-activated sensory neurons contribute to enhancements in osteoclast activity and tooth movement through sympathetic nervous signalling.