Kirschneck Christian, Nusser Hendrik, Jantsch Jonathan, Proff Peter, Schröder Agnes
Department of Orthodontics, University Hospital Regensburg, 93053 Regensburg, Germany.
Institute of Clinical Microbiology and Hygiene, University Hospital Regensburg, 93053 Regensburg, Germany.
J Clin Med. 2022 Mar 24;11(7):1796. doi: 10.3390/jcm11071796.
: Myeloid p38α/MAPK regulate and coordinate osteoclastogenesis. The present study was conducted to investigate the role of myeloid p38α/MAPK during orthodontic tooth movement. : Orthodontic tooth movement was performed in wildtype and mice lacking p38α/MAPK expression in myeloid cells. First, bone parameter as well as osteoblast and osteoclast number were determined in tibiae. RNA was isolated from the untreated and orthodontically treated maxillary jaw side and expression of genes involved in inflammation and bone remodelling were analysed. Finally, periodontal bone loss, alveolar bone density and extent of orthodontic tooth movement were assessed. : Bone density was increased in mice compared to wildtype mice in tibiae ( = 0.043) and alveolar bone ( = 0.003). This was accompanied by a reduced osteoclast number in tibiae ( = 0.005) and TRAP5b in serum ( = 0.015). Accordingly, expression of osteoclast-specific genes was reduced in mice. Extent of tooth movement was reduced in mice ( = 0.024). This may be due to the higher bone density of the p38αΔmyel mice. : Myeloid p38α/MAPK thus appears to play a regulatory role during orthodontic tooth movement by regulating osteoclastogenesis.
髓系p38α/丝裂原活化蛋白激酶(MAPK)调节并协调破骨细胞生成。本研究旨在探讨髓系p38α/MAPK在正畸牙齿移动过程中的作用。:在野生型小鼠和髓系细胞中缺乏p38α/MAPK表达的小鼠中进行正畸牙齿移动。首先,测定胫骨的骨参数以及成骨细胞和破骨细胞数量。从未经处理和正畸处理的上颌侧分离RNA,并分析参与炎症和骨重塑的基因表达。最后,评估牙周骨丧失、牙槽骨密度和正畸牙齿移动程度。:与野生型小鼠相比,p38αΔmyel小鼠胫骨(P = 0.043)和牙槽骨(P = 0.003)的骨密度增加。这伴随着胫骨中破骨细胞数量减少(P = 0.005)和血清中TRAP5b减少(P = 0.015)。因此,p38αΔmyel小鼠中破骨细胞特异性基因的表达降低。p38αΔmyel小鼠的牙齿移动程度降低(P = 0.024)。这可能是由于p38αΔmyel小鼠的骨密度较高。:因此,髓系p38α/MAPK似乎通过调节破骨细胞生成在正畸牙齿移动过程中发挥调节作用。