Department of Biomedical Dental Sciences, College of Dentistry, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, 31441, Dammam, Saudi Arabia.
Department of Preventive Dental Sciences, College of Dentistry, Imam Abdulrahman Bin Faisal University, P.O. Box 1982, 31441, Dammam, Saudi Arabia.
Prog Orthod. 2023 Oct 16;24(1):33. doi: 10.1186/s40510-023-00486-z.
Renin-angiotensin system and its ACE2/Ang(1-7)/Mas receptor axis regulates skeletal response to multiple physiological and pathological conditions. Recent research suggested a vital role of Ang(1-7) in regulating alveolar bone metabolism and remodeling. In this context, this study evaluated the effects of the Ang(1-7)/Mas receptor axis on orthodontic tooth movement (OTM) and the alveolar bone response to mechanical load.
A coil spring was placed between the right maxillary first molar and the anterior tooth of Wistar rats to apply bidirectional mechanical force. Ang(1-7) with or without a specific Mas receptor antagonist (A779) was infused using subcutaneous osmotic pumps (200 and 400 ng/kg/min: respectively). Animals were killed after 5 and 14 days from the OTM procedure after the clinical evaluation of tooth movement and mobility. Morphometric analysis of alveolar bone structure was conducted using micro-CT and the histological picture was evaluated after H&E staining. Moreover, collagen fiber distribution was assessed using Picro-Sirius red stain. In addition, bone samples were collected from the pressure and tension sites around the anterior tooth for gene expression analysis.
Ang(1-7) infusion suppressed the tooth movement and mobility after 14 days of the orthodontic force application. Additionally, Ang(1-7) infusion preserved the morphometric and histological structure of the alveolar bone at pressure and tension sides. These effects were abolished by adding A779 infusion. Collagen fiber distribution was dysregulated mainly by the A779 Mas receptor blockage. Ang(1-7) affected the bone formation, remodeling- and vascularity-related genes in the pressure and tension sides, suggesting a prominent suppression of osteoclastogenesis. Ang(1-7) also improved osteoblasts-related genes on the tension side, whereas the osteoclasts-related genes were augmented by A779 on the pressure side.
Collectively, the activation of Ang(1-7)/Mas receptor axis appears to hinder tooth movement and regulates alveolar bone remodeling in response to mechanical force.
肾素-血管紧张素系统及其 ACE2/Ang(1-7)/Mas 受体轴调节多种生理和病理条件下的骨骼反应。最近的研究表明，Ang(1-7)在调节肺泡骨代谢和重塑中起着重要作用。在这种情况下，本研究评估了 Ang(1-7)/Mas 受体轴对正畸牙齿移动（OTM）和牙槽骨对机械负荷的反应的影响。
在 Wistar 大鼠的右上颌第一磨牙和前牙之间放置螺旋弹簧，以施加双向机械力。使用皮下渗透泵（分别为 200 和 400 ng/kg/min）输注 Ang(1-7)和/或特定的 Mas 受体拮抗剂（A779）。在 OTM 手术后 5 和 14 天，从临床评估牙齿移动和活动性后，处死动物。使用 micro-CT 进行牙槽骨结构的形态计量分析，并在 H&E 染色后评估组织学图片。此外，使用 Picro-Sirius red 染色评估胶原纤维分布。此外，从前牙周围的压力和张力部位采集骨样本，用于基因表达分析。
Ang(1-7)输注抑制了正畸力应用后 14 天的牙齿移动和活动性。此外，Ang(1-7)输注保留了牙槽骨在压力和张力侧的形态计量和组织学结构。这些作用通过添加 A779 输注而被消除。胶原纤维分布主要通过 A779 Mas 受体阻断而失调。Ang(1-7)影响压力和张力侧的骨形成、重塑和血管生成相关基因，表明破骨细胞生成明显受到抑制。Ang(1-7)还改善了张力侧的成骨细胞相关基因，而 A779 则增加了压力侧的破骨细胞相关基因。
总的来说，激活 Ang(1-7)/Mas 受体轴似乎会阻碍牙齿移动，并调节机械力作用下的牙槽骨重塑。
