Department of Orthodontics, Center of Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany.
Department of Periodontology and Operative Dentistry, University Medical Center, University of Mainz, 55131 Mainz, Germany.
Int J Mol Sci. 2021 Jan 8;22(2):591. doi: 10.3390/ijms22020591.
The aim of the study was to clarify whether orthodontic forces and periodontitis interact with respect to the anti-apoptotic molecules superoxide dismutase 2 (SOD2) and baculoviral IAP repeat-containing protein 3 (BIRC3). SOD2, BIRC3, and the apoptotic markers caspases 3 (CASP3) and 9 (CASP9) were analyzed in gingiva from periodontally healthy and periodontitis subjects by real-time PCR and immunohistochemistry. SOD2 and BIRC3 were also studied in gingiva from rats with experimental periodontitis and/or orthodontic tooth movement. Additionally, SOD2 and BIRC3 levels were examined in human periodontal fibroblasts incubated with and/or subjected to mechanical forces. Gingiva from periodontitis patients showed significantly higher SOD2, BIRC3, CASP3, and CASP9 levels than periodontally healthy gingiva. SOD2 and BIRC3 expressions were also significantly increased in the gingiva from rats with experimental periodontitis, but the upregulation of both molecules was significantly diminished in the concomitant presence of orthodontic tooth movement. In vitro, SOD2 and BIRC3 levels were significantly increased by , but this stimulatory effect was also significantly inhibited by mechanical forces. Our study suggests that SOD2 and BIRC3 are produced in periodontal infection as a protective mechanism against exaggerated apoptosis. In the concomitant presence of orthodontic forces, this protective anti-apoptotic mechanism may get lost.
本研究旨在阐明正畸力与牙周炎之间是否存在相互作用,以及这种相互作用是否与抗凋亡分子超氧化物歧化酶 2(SOD2)和杆状病毒 IAP 重复蛋白 3(BIRC3)有关。通过实时 PCR 和免疫组织化学分析了牙周健康和牙周炎患者牙龈中的 SOD2、BIRC3 以及凋亡标志物半胱天冬酶 3(CASP3)和 9(CASP9)。还研究了实验性牙周炎和/或正畸牙齿移动大鼠的牙龈中的 SOD2 和 BIRC3。此外,还检查了在与人牙周成纤维细胞孵育的 和/或受到机械力作用的 SOD2 和 BIRC3 水平。牙周炎患者的牙龈中 SOD2、BIRC3、CASP3 和 CASP9 的水平明显高于牙周健康的牙龈。实验性牙周炎大鼠的牙龈中 SOD2 和 BIRC3 的表达也明显增加,但在同时存在正畸牙齿移动的情况下,这两种分子的上调明显减少。在体外, 显著增加了 SOD2 和 BIRC3 的水平,但机械力也显著抑制了这种刺激作用。我们的研究表明,SOD2 和 BIRC3 在牙周感染中产生,作为对抗过度凋亡的保护机制。在正畸力的共同作用下,这种保护性抗凋亡机制可能会丧失。