Modulation of orthodontic tooth movement though diet and electrolyte metabolism

对于正畸牙齿移动，机械力施加到牙齿上，在牙周膜(PDL)中产生压力和张力区，在那里发生骨吸收和骨定位过程，从而使牙齿向力的方向移动。尽管正畸治疗对患者的健康很重要，但许多方面仍然知之甚少。由于牙齿移动是一个无菌炎症的免疫过程，因此有许多潜在的全身和外部影响。在我们自己的前期工作中，已经研究了各种外源性调节剂(雷尼酸锶、尼古丁、美洛昔康)对正畸牙移动的影响。除了药物以外，某些生活习惯，如饮食，也会产生调制作用。除其他外，钠和钾等电解质在当今社会通常以高的、非生理性的数量消耗，作为一种膳食补充剂(例如在成品中)。因此，它们可以通过电解质平衡和局部组织浓度发挥药理免疫作用。在我们自己的初步工作中，我们可以证明富钠营养导致皮肤中的Na+沉积，并伴随着巨噬细胞的渗透。这些细胞越来越多地表达转录因子NFAT5(渗透压保护基因转录增加)。在初步实验中，hPDL成纤维细胞中Na+浓度的增加导致NFAT5和与细胞外基质和RANKL/OPG系统重塑有关的基因的诱导。由于Na+直接影响巨噬细胞和hPDL成纤维细胞等免疫细胞的活性，因此可以推测牙周组织中的局部氯化钠浓度也会对正畸牙齿移动引起的无菌炎症反应产生影响。然而，到目前为止，电解质的免疫调节特性在这方面的作用还没有被研究。因此，氯化钠可能会导致正畸牙齿移动的意外加速或抑制，但也会增加或减少与之相关的牙根吸收、牙周骨丢失或移动牙齿向初始位置的早期复发。除了为正畸治疗期间的食盐消耗制定第一个预防建议外，对这些关系的探索也可能使有针对性地使用氯化钠作为辅助治疗。因此，拟议项目的目的是调查富盐/贫盐饮食对正畸牙移动的影响和相关的副作用，以及潜在的分子过程，特别是通过NFAT5可能的调节。

For orthodontic tooth movement, a mechanical force is applied to a tooth creating pressure and tension zones in the periodontal ligament (PDL), where bone resorption and bone apposition processes take place, thus enabling tooth movement in the direction of force. Despite the importance of orthodontic treatment for patient health, many aspects are yet poorly understood. Since tooth movement is a sterile-inflammatory, immunological process, there are many potential systemic and exogenous influences. In our own preliminary work, the effect of various exogenous modulators on orthodontic tooth movement has already been investigated (strontium ranelate, nicotine, meloxicam). In addition to pharmaceuticals, modulation is also to be expected by certain lifestyle habits such as diet. Among other things, electrolytes such as sodium and potassium are generally consumed in today's society at high, unphysiological quantities as a dietary supplement (for example in finished products). They can therefore exert pharmacological-immunological effects via the electrolyte balance and their local tissue concentration. In our own preliminary work we could show that Na+-rich nutrition leads to Na+ deposition in the skin, which is accompanied by macrophage infiltration. These increasingly express the transcription factor NFAT5 (increased transcription of osmoprotective genes). In preliminary experiments, an increased Na+ concentration in hPDL fibroblasts led to an induction of NFAT5 and genes regarding the remodeling of the extracellular matrix and the RANKL / OPG system. Due to the direct influence of Na+ on the activity of immune cells such as macrophages and hPDL fibroblasts, it can be assumed that the local NaCl concentration in the periodontium could also have an influence on the sterile inflammatory reaction induced by orthodontic tooth movement. However, the role of immunomodulatory properties of electrolytes in this regard has not been studied to date. NaCl could therefore cause an unexpected acceleration or inhibition of orthodontic tooth movement, but also an increase or decrease of undesired associated tooth root resorption, periodontal bone loss or early relapse of the moved teeth towards the initial position. In addition to formulating first preventive recommendations for salt consumption during orthodontic therapy, the exploration of these relationships may also allow targeted use of NaCl as an adjuvant therapeutic. The aim of the proposed project is therefore to investigate the effects of a NaCl-rich / poor diet on orthodontic tooth movement and associated side effects as well as the underlying molecular processes, in particular a possible regulation via NFAT5.