Horinuki E, Yamamoto K, Shimizu N, Koshikawa N, Kobayashi M
Department of Pharmacology, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan Department of Orthodontics, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan.
Department of Pharmacology, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan Division of Oral and Craniomaxillofacial Research, Dental Research Center, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan.
J Dent Res. 2016 Jul;95(8):897-905. doi: 10.1177/0022034516641276. Epub 2016 Mar 28.
Cortical excitation responding to periodontal ligament (PDL) stimulation is observed in the rat primary somatosensory (S1), secondary somatosensory, and insular oral region of the cortex (S2/IOR), which are considered to process somatosensation, including nociception. Our previous studies have demonstrated that excitatory propagation induced by PDL stimulation is facilitated in S1 and S2/IOR 1 d after experimental tooth movement (ETM), and tetanic stimulation of IOR induces long-term potentiation of cortical excitatory propagation consistently. These findings raise the possibility that ETM induces neuroplastic changes, and as a result, facilitation of cortical excitation would be sustained for weeks. However, no information is available about the temporal profiles of the facilitated cortical responses. We estimated PDL stimulation-induced cortical excitatory propagation in S1 and S2/IOR of rats by optical imaging 1 to 7 d after ETM of the maxillary first molar. ETM models showed facilitated cortical excitatory propagation in comparison with controls and sham groups 1 d after ETM, but the facilitation gradually recovered to the control level 3 to 7 d after ETM. Sham groups that received wire fixation without orthodontic force tended to enhance cortical responses, although the differences between controls and sham groups were almost insignificant. We also examined the relationship between cortical responses and expression of inflammatory cytokines, interleukin (IL)-1β and tumor necrosis factor (TNF)-α, in PDL of the first molar. The peak amplitude of optical signals responding to PDL stimulation tended to be increased in parallel to the number of IL-1β and TNF-α immunopositive cells, suggesting that, at least in part, the enhancement of cortical responses is induced by PDL inflammation. These findings suggest that ETM-induced facilitation of cortical excitatory propagation responding to PDL stimulation 1 d after ETM recovers to the control level within a week. The time course of the facilitated cortical responses is comparable to that of pain and discomfort induced by clinical orthodontic treatments.
在大鼠初级体感皮层（S1）、次级体感皮层以及皮层的岛叶口腔区域（S2/IOR）中观察到了对牙周韧带（PDL）刺激产生反应的皮层兴奋，这些区域被认为负责处理包括伤害感受在内的躯体感觉。我们之前的研究表明，实验性牙齿移动（ETM）后1天，PDL刺激诱导的兴奋性传播在S1和S2/IOR中得到促进，并且对IOR的强直刺激持续诱导皮层兴奋性传播的长时程增强。这些发现增加了ETM诱导神经可塑性变化的可能性，结果是皮层兴奋的促进作用会持续数周。然而，关于皮层反应促进作用的时间进程尚无相关信息。我们通过光学成像评估了上颌第一磨牙ETM后1至7天，大鼠S1和S2/IOR中PDL刺激诱导的皮层兴奋性传播。ETM模型在ETM后1天与对照组和假手术组相比，显示出皮层兴奋性传播得到促进，但这种促进作用在ETM后3至7天逐渐恢复到对照水平。接受无正畸力钢丝固定的假手术组倾向于增强皮层反应，尽管对照组和假手术组之间的差异几乎不显著。我们还研究了皮层反应与第一磨牙PDL中炎性细胞因子白细胞介素（IL）-1β和肿瘤坏死因子（TNF）-α表达之间的关系。对PDL刺激产生反应的光信号峰值幅度倾向于与IL-1β和TNF-α免疫阳性细胞的数量平行增加，这表明至少部分皮层反应的增强是由PDL炎症诱导的。这些发现表明，ETM后1天ETM诱导的对PDL刺激的皮层兴奋性传播促进作用在一周内恢复到对照水平。皮层反应促进作用的时间进程与临床正畸治疗引起的疼痛和不适的时间进程相当。
