实验性牙移动三叉神经节内神经生长因子受体mRNA的改变

目的:观察实验性牙移动时,NGF受体-TrkA mRNA在三叉神经节内的改变,方法:采用RT-PCR方法研究实验性牙移动后,三叉神经节内TrkA mRNA表达的改变。结果:实验性牙移动后6 h,实验侧TrkA mRNA的表达开始增加;24 h、3 d,1周实验组三叉神经节内TrkA mRNA的表达强于对照组;2周组,实验侧TrkA mRNA的表达恢复至正常水平。结论:实验性牙移动时,三叉神经节内TrkA的表达升高。     

实验性牙移动三叉神经节内降钙素基因相关肽改变

目的：观察实验性牙移动后,初级感觉神经元兴奋性递质降钙素基因相关肽（CGRP）的改变。分析正畸疼痛时,初级感觉神经元痛信号发生、传导及敏感化机制。方法：制备大鼠实验性牙移动动物模型,采用免疫荧光染色法和RT-PCR法分别观察不同时间点三叉神经节内CGRP免疫阳性结构的改变及CGRP mRNA表达的变化。结果：实验性牙移动后,实验侧三叉神经节（TG）内CGRP-ir节细胞以及CGRP mRNA的表达强于对侧。结论：实验性牙移动后,初级感觉神经元中痛感受兴奋性神经递质CGRP的合成、表达增加。表明实验性牙移动影响了初级感觉神经元痛信号的发生、传导,使之致敏。     

大鼠实验性牙移动过程中三叉神经节内甘丙肽表达的研究

目的：研究实验性牙移动过程中大鼠三叉神经节内甘丙肽表达的变化,探讨其与正畸疼痛缓解之间是否具有内在的联系。方法：选择雄性Wistar大鼠35只,建立正畸牙移动动物模型,将大鼠随机分为实验组与空白对照组。实验组左侧为加力侧,右侧为未加力侧,左右自身对照,分别于加力6h、12h、1、3、5、7d后处死动物,取大鼠三叉神经节,标本制备,进行免疫组织化学染色与图像分析。采用SPSSl6．0统计学软件进行统计学分析。结果：与空白对照组相比,实验组加力1d甘丙肽阳性细胞数增多,表达增强（P〈O．05）;加力3d阳性细胞数增多明显（P〈O．01）;加力5d甘丙肽免疫阳性细胞数达到高峰,神经节细胞中甘丙肽免疫阳性染色呈强阳性表达（P〈0．01）。实验组未加力侧各时间点与空白对照组之间甘丙肽表达无统计学差异。结论：GAL作为内源性镇痛物质与正畸牙移动所致牙体与牙周疼痛的缓解具有一定的内在联系。     

牙本质损伤后牙髓和三叉神经节内一氧化氮合酶的观察

目的 了解一氧化氮(NO)在牙髓神经感觉信息传递中的作用，观察牙本质损伤后三叉神经节内和牙髓内还原性辅酶Ⅱ硫辛酸脱氢酶(NADPH—D)的变化。方法 对大鼠实验性牙本质损伤后牙髓和三叉神经节内，以及人牙本质损伤后牙髓内一氧化氮合成酶(NOS)进行组织化学检测，计数统计每个大鼠三叉神经节和牙髓组织标本所有组织切片含NOS阳性细胞总数，结果 实验性大鼠牙本质损伤侧三叉神经节内NADPH—D阳性神经数明显多于对照侧(P＜0．05)，而阳性神经元细胞大小未见变化；人牙本质损伤牙髓组织内未发现NADPH—D阳性神经元细胞。结论 三叉神经节内的NO可能与牙髓神经痛信息传递和调控有关，而与牙髓内伤害性刺激的传递无关。     

单侧咀嚼大鼠三叉神经节内PPTAmRNA及其相应蛋白的表达研究

目的:观察磨除单侧后牙造成单侧咀嚼的大鼠三叉神经节内P物质(substance P,SP)及编码 SP 的前速激肽原 A(PPTA)mRNA 的表达情况,进一步探讨颞颌关节病的发病机制.方法:Wistar 雄性大鼠48只,随机分为6组,包括3个实验组及相应对照组,每组8只.实验组动物磨除右侧上、下颌磨牙,人为造成单侧咀嚼.双侧三叉神经节切片行 SP 免疫组化(SABC法)和原位杂交反应.光镜观察拍片,并用 Image Pro Plus 5.1 图像分析软件进行测定.结果与对照组比较,用SPSS10.0软件进行统计分析.结果:每一实验组咀嚼侧和非咀嚼侧三叉神经节内 SP 免疫阳性神经元百分比与各自对照组比较显著降低(p<0.01,p<0.05),非咀嚼侧明显低于咀嚼侧(P<0.01,p<0.05).原位杂交结果显示,每一实验组咀嚼侧与非咀嚼侧三叉神经节中 PPTAmRNA 阳性神经元的数量较各自对照组明显增高(p<0.01),非咀嚼侧明显高于咀嚼侧(p<0.01,p<0.05).结论:三叉神经节内 SP 和 PPTAmRNA 参与了单侧咀嚼引起的颞颌关节病的病理过程,且两侧三叉神经节内SP释放量、PPTAmRNA 合成量不同.     

蟾酥制剂对大鼠三叉神经节及三叉神经脊束核尾侧亚核中P物质的影响

目的：比较分析蟾酥制剂作用于牙髓后，三叉神经节(TG)和三叉神经脊束核尾侧亚核(Vc)内P物质(SP)的变化。方法：利用免疫组织化学染色方法，观察大鼠牙齿开髓封药0、1、2、4、6、24h后TG和Vc内sP的变化。结果：开髓1h时TG内阳性神经元的数目少于对照侧，4h后阳性神经元数量逐渐增多，接近正常。封药1h后Vc内密度低于对照侧，4h时密度明显高于对照侧，随后逐渐减低，至24h后已与对照侧密度一致。结论：蟾酥制剂可抑制TG内SP的合成和释放，Vc内三叉神经末梢释放SP减少。     

实验性牙移动牙周膜内降钙素基因相关肽样神经纤维的改变

目的：研究实验性牙移动过程中，牙周膜内降钙素基因相关肽（CGRP）样神经纤维的改变。方法：在大鼠左侧第一、二磨牙间塞入一弹性橡皮圈模拟临床正畸加力状态，对牙周膜内神经进行CGRP免疫组化染色。结果：加力6h后，牙周膜和牙髓内CGRP样神经纤维明显减少；施力3d后表达开始增加，1周时表达最强，2周时趋于恢复正常。结论：实验性牙移动引起牙周膜内CGRP样神经纤维规律性的改变，提示CGRP免疫阳性感觉神经可能参与实验性牙移动中的骨组织改建和局部的炎性反应。     

口腔颌面部神经疾病

下牙槽神经、舌神经干注射阿霉素联合颊神经撕脱治疗第Ⅲ支三叉神经痛的疗效观察，变速牵引与常速牵引成骨对下牙槽神经影响的比较研究，上颌窦径路上颌神经撕脱术12例临床报告，实验性牙移动三叉神经节内神经生长因子受体mRNA的改变……     

减阻牵张正畸牙移动过程中牙周组织超微结构变化的研究

目的：研究减阻牵张正畸牙移动过程中牙周组织超微结构的变化，为此方法矫治正畸牙提供理论依据。方法：将6只杂种犬随机分为2周、3周、6周二组，拔除下颌两侧第二前磨牙，随机选择一侧为实验侧，实施减阻牵张措施加快牙齿移动速度，另一侧为空白对照侧，实验侧加力2周、固定保持1周、4周时，制备移动牙标本，进行透射电镜观察。结果：对照侧无明显成骨及破骨迹象；加力2周组张力侧成骨细胞、成纤维细胞的胞浆内高尔基体、内质网等细胞器非常丰富，分泌功能旺盛；压力侧破骨细胞增多，高尔基体发达，线粒体、溶酶体增多，成纤维细胞细胞器发达，间充质细胞、活跃的巨噬细胞增多；随着固定保持时间的延长，实验侧与对照侧超微结构的差异变小。结论：正畸牙压力侧减阻后，在强、高频率加力方式作片用下，牙周组织细胞功能旺盛、改建活跃，无不可逆的细胞变性坏死变化。     

大鼠正畸牙移动过程中TRPV1和CGRP在三叉神经节中的表达变化

目的建立SD大鼠正畸牙移动模型,研究牙移动过程中,三叉神经节(trigeminal ganglion,TG)中瞬时受体电位香草酸亚型1（transient receptor potential vanilloid 1,TRPV1）及降钙素基因相关肽(calcitonin gene related peptide,CGRP)的表达位置及表达量的变化规律,进而探讨其在正畸疼痛中的作用机制。方法将66只SD大鼠随机分为空白对照组（6只）、假手术组（6只）和实验组（54只）。建立正畸牙移动模型,实验组大鼠施加50 g力后,分别于4、8 h、1 d（1 d组按力值大小分为1 d-30 g、1 d-50 g、1 d-80 g 3个亚组）、3、5、7、14 d,随机处死6只,切取三叉神经节,采用免疫荧光技术分别检测大鼠三叉神经节中TRPV1及CGRP的表达位置及表达量变化。采用SPSS16.0软件包对数据进行统计学分析。结果免疫荧光染色显示,TRPV1及CGRP主要表达于小型及中型神经元。随着加力时间的延长,三叉神经节中TRPV1免疫反应阳性（TRPV1-IR）神经元百分比及CGRP免疫反应阳性（CGRP-IR）神经元百分比增加,1~3 d相继达到高峰,之后逐渐降低,回落至初始水平,且两者随加力力值增大而呈现增高趋势。结论大鼠正畸牙移动过程中,三叉神经节内TRPV1及CGRP的表达随加力时间及加力力值改变呈现规律性变化,提示TRPV1及CGRP可能在正畸疼痛的发生机制中具有重要作用。     

Increased expression of TRPV1 in the trigeminal ganglion is involved in orofacial pain during experimental tooth movement in rats

To investigate whether transient receptor potential vanilloid type 1 (TRPV1) is involved in pain induced by experimental tooth movement, experiments were performed in male Sprague‐Dawley rats weighing 200–250 g. Directed face‐grooming behavior was used to evaluate nocifensive behavior in rats during experimental tooth movement. The distribution of TRPV1 in the trigeminal ganglion (TG) was evaluated by immunohistochemistry, and its expression was detected by western blotting at several time points following the application of various magnitudes of force during tooth movement. Immunohistochemical analysis revealed that TRPV1 was expressed in TG, and its expression was increased after experimental tooth movement. Western blot results also showed that experimental tooth movement led to a statistically significant increase in expression of TRPV1 protein in TG. Meanwhile, the time spent on directed face‐grooming peaked on day 1 and thereafter showed a gradual decrease. In addition, both the change in TRPV1 expression in the TG and directed face‐grooming behavior were modulated in a force‐dependent manner and in concert with initial orthodontic pain responses. Our results reveal that TRPV1 expression is modulated by experimental tooth movement and is involved in tooth‐movement pain.     

Chemokine ligand 2 in the trigeminal ganglion regulates pain induced by experimental tooth movement

Objective:To test the hypothesis that the chemokine ligand 2/chemokine receptor 2 (CCL2/CCR2) signaling pathway plays an important role in pain induced by experimental tooth movement.Materials and Methods:Expression of CCL2/CCR2 in the trigeminal ganglion (TG) was determined by Western blotting 0 hours, 4 hours, 1 day, 3 days, 5 days, and 7 days after tooth movement. CCL2 localization and cell size distribution were revealed by immunohistochemistry. The effects of increasing force on CCL2 expression and behavioral changes were investigated. Furthermore, the effects of CCL2/CCR2 antagonists on these changes in pain behaviors were all evaluated. Exogenous CCL2 was injected into periodontal tissues and cultured TG neurons with different concentrations, and then the pain responses or c-fos expression were assessed.Results:Experimental tooth movement led to a statistically significant increase in CCL2/CCR2 expression from day 3 to day 7, especially in small to medium-sized TG neurons. It also triggered an increase in the time spent on directed face-grooming behaviors in a force magnitude–dependent and CCL2 dose–dependent manner. Pain induced by experimental tooth movement was effectively blocked by a CCR2 antagonist and by CCL2 neutralizing antibody. Also, exogenous CCL2 led to an increase in c-fos expression in cultured TG neurons, which was blocked by CCL2 neutralizing antibody.Conclusions:The peripheral CCL2/CCR2 axis is modulated by experimental tooth movement and involved in the development of tooth movement pain.     

Increase of galanin in trigeminal ganglion during tooth movement

It is known that nerve fibers containing neuropeptides such as galanin increase in the periodontal ligament during experimental tooth movement. However, the origin of galanin-containing nerve fibers in the periodontal ligament remains unclear. This study was conducted to examine our hypothesis that the increased galanin nerve fibers have a sensory neuronal origin, and that the peptide is associated with pain transmission and/or periodontal ligament remodeling during experimental tooth movement. In control rats, galanin-immunoreactive trigeminal ganglion cells were very rare and were observed predominantly in small ganglion cells. After 3 days of experimental tooth movement, galanin-immunoreactive trigeminal ganglion cells significantly increased, and the most marked increase was observed at 5 days after experimental tooth movement. Furthermore, their cell size spectrum also significantly changed after 3 and 5 days of movement: Medium-sized and large trigeminal ganglion cells began expressing, and continued to express, galanin until 14 days after experimental tooth movement. These findings suggest that the increase of galanin in the periodontal ligament during experimental tooth movement at least partially originates from trigeminal ganglion neurons and may play a role in pain transmission and/or periodontal remodeling.     

Effect of resveratrol on the hyperexcitability of nociceptive neurons associated with ectopic hyperalgesia induced by experimental tooth movement

The present study investigated whether, under in vivo conditions, systemic administration of resveratrol attenuates the experimental tooth movement-induced ectopic hyperalgesia associated with hyperexcitability of nociceptive trigeminal spinal nucleus caudalis (SpVc) neurons. The threshold of escape from mechanical stimulation applied to the ipsilateral whisker pad in rats exposed to experimental tooth movement was significantly lower than seen in control rats from day 1 to 3 following movement of the right maxillary first molar tooth. The lowered mechanical threshold in the rats exposed to experimental tooth movement had almost returned to the level of sham-treated naïve rats at day 3 following administration of resveratrol. The mean mechanical threshold of nociceptive SpVc neurons was significantly lower after experimental tooth movement but the lower threshold could be reversed by administration of resveratrol. The higher discharge frequency of nociceptive SpVc neurons for noxious mechanical stimuli observed in rats exposed to experimental tooth movement was statistically significantly lower following resveratrol administration. These results suggest that resveratrol attenuates experimental tooth movement-induced mechanical ectopic hyperalgesia via suppression of peripheral and/or central sensitization. These findings support the idea that resveratrol, a complementary alternative medicine, is a potential therapeutic agent for the prevention of experimental tooth movement-induced ectopic hyperalgesia.     

静磁场对大鼠三叉神经节中SP-mRNA作用的实验研究

目的　探讨静磁场对大鼠三叉神经节中SP-mRNA的影响。方法　将 4 4只 6～ 7周的大鼠置于静磁场中 ,在 1、2、6、1 2和 2 4h时分别将动物处死 ,取其三叉神经节 ,用原位杂交方法研究SP-mRNA在各时间点的变化。结果　在静磁场作用下三叉神经节中SP-mRNA的表达呈上调变化 ,2h时达峰值 ,各时间点与正常对照组间均存在显著性差异 (P <0 0 1 )。结论　静磁场可以使三叉神经节中的SP-mRNA呈现上调性变化。     

正畸牙齿移动刺激信息传导通路的动物实验研究

研究丘脑腹后内侧核（ＶＰＭ）是否接受来自三叉神经脊核尾业核传入的牙齿移动性刺激信息,从而探讨牙齿动引起的伤害性刺激信息在中枢神经系统内的感觉传导通路。方法：用微量注射器将２％荧光金ＦＧ）注入大鼠ＶＰＭ４－６ｄ后,进行对侧的实验性牙齿移动２ｈ,用ＦＯＳ蛋白免疫化方法观察Ｖｃ内神经元对ｃ－ｆｏｓ的表达以及是否存在ＦＧ与ＦＯＳ双重阳性的神经元。结果ＦＯＳ阳性神经元密集分布于同侧Ｖｃ浅层,呈带状,背外侧居