Schröder Agnes, Nazet Ute, Neubert Patrick, Jantsch Jonathan, Spanier Gerrit, Proff Peter, Kirschneck Christian
Department of Orthodontics, University Hospital Regensburg, Regensburg, Germany.
Institute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.
Eur J Oral Sci. 2019 Oct;127(5):386-395. doi: 10.1111/eos.12643. Epub 2019 Jun 29.
Increased salt (NaCl) consumption triggers chronic diseases such as hypertension or osteopenia. Its impact on orthodontic tooth movement and periodontitis, however, has not been investigated, although both processes are related to the immune system, with periodontal ligament fibroblasts (PDLFs) playing a key mediating role. Here, we investigated the impact of NaCl on the expression pattern of PDLFs in a model of simulated compressive orthodontic strain. Periodontal ligament fibroblasts were preincubated for 24 h with additional 0 or 40 mM NaCl and concurrently treated for another 48 h with or without compressive strain of 2 g cm . We analyzed the expression of genes and proteins involved in orthodontic tooth movement by reverse transcription quantitative polymerase chain reaction (RT-qPCR), ELISA, and immunoblot. Co-culture experiments were performed to observe PDLF-mediated osteoclastogenesis. A higher (40 mM) concentration of NaCl in the culture medium resulted in increased secretion of prostaglandin, expression of alkaline phosphatase, and expression of genes involved in extracellular matrix remodeling, but decreased compression-induced expression of the interleukin-6 (IL6) gene. The 40 mM concentration of NaCl also enhanced receptor activator of nuclear factor kappa-B ligand (RANKL) but reduced that of osteoprotegerin (OPG), resulting in upregulated PDLF-mediated osteoclastogenesis. A high NaCl concentration in the periodontal ligament, corresponding to a high-salt diet in vivo, may influence orthodontic tooth movement and periodontitis through increased secretion of prostaglandins by PDLFs and upregulated PDLF-mediated osteoclastogenesis, possibly accelerating orthodontic tooth movement and propagating periodontitis and periodontal bone loss.
盐（氯化钠）摄入量增加会引发高血压或骨质减少等慢性疾病。然而，尽管正畸牙齿移动和牙周炎这两个过程都与免疫系统有关，且牙周膜成纤维细胞（PDLFs）起着关键的介导作用，但盐对它们的影响尚未得到研究。在此，我们在模拟正畸压缩应变模型中研究了氯化钠对PDLFs表达模式的影响。将牙周膜成纤维细胞分别在添加0或40 mM氯化钠的条件下预孵育24小时，然后在有或无2 g/cm压缩应变的情况下再处理48小时。我们通过逆转录定量聚合酶链反应（RT-qPCR）、酶联免疫吸附测定（ELISA）和免疫印迹分析了参与正畸牙齿移动的基因和蛋白质的表达。进行共培养实验以观察PDLF介导的破骨细胞生成。培养基中较高浓度（40 mM）的氯化钠导致前列腺素分泌增加、碱性磷酸酶表达以及参与细胞外基质重塑的基因表达增加，但压缩诱导的白细胞介素-6（IL6）基因表达降低。40 mM浓度的氯化钠还增强了核因子κB受体激活剂配体（RANKL）的表达，但降低了骨保护素（OPG）的表达，导致PDLF介导的破骨细胞生成上调。牙周膜中高浓度的氯化钠，相当于体内的高盐饮食，可能通过PDLFs前列腺素分泌增加和PDLF介导的破骨细胞生成上调来影响正畸牙齿移动和牙周炎，可能会加速正畸牙齿移动并加剧牙周炎和牙周骨丧失。
