大鼠眶下孔注射高渗盐水阿霉素后三叉神经节内的荧光表达

目的：观察大鼠眶下神经周围注射高渗盐水阿霉素（10：1）的混合溶液后,神经干及三叉神经节内阿霉素自体荧光的表达及其时相变化。方法：将含10%NaCl和1%阿霉素的混合溶液（A组）或单纯10%NaCl（B组）注入大鼠眶下孔后,分别于10h、20h、2d、4d、7d和10d观察眶下神经及神经节内阿霉素荧光的表达。给药后每天观察大鼠须垫部的感觉功能变化。结果：眶下孔内神经周围注射高渗盐水阿霉素溶液后10h、20h、48h时,眶下神经外膜呈现连续强阳性荧光表达,神经干和三叉神经节内荧光表达呈上升趋势,48h达高峰,10d消失。A组对照侧、B组三叉神经节及所有动物的下颌神经、眼神经前根纤维及后根均未见荧光表达。结论：大鼠眶下孔内注射高渗盐水阿霉素后,可在三叉神经节前外侧区见到神经节细胞内的荧光表达。神经节细胞的荧光表达是阿霉素破坏神经节细胞的必要条件,经皮穿刺注射高渗盐水阿霉素有望成为治疗三叉神经痛的可选方法。     

阿霉素眶下神经注射后对兔三叉神经节的影响

目的观察阿霉素对兔眶下神经及三叉神经节的作用。方法将不同浓度的阿霉素20μl注入眶下神经。从三叉神经复合动作电位、阿霉素自体荧光和形态学3个方面分不同时期对眶下神经、三叉神经节的病理生理改变予以观察。结果在适当浓度阿霉素作用下,阿霉素自体荧光于注射后10h出现,20h后达到高峰。复合动作电位振幅10h后开始降低,20h后基本消失。6个月后观察无恢复。术后15d始,可观察到病理改变,随时间延长而加重。6个月后无神经细胞再生表现。坏死神经和三叉神经节周围组织未见形态学改变。结论阿霉素可引起神经轴突和与其对应的神经元的永久损害。其作用有高度的选择性和自限性。     

脂质体阿霉素对大鼠三叉神经形态与功能影响的实验研究

目的 :观察脂质体阿霉素对大鼠三叉神经形态与功能的影响。方法 :3 3g/L脂质体阿霉素直接注射于大鼠一侧眶下神经束 ,对侧以生理盐水对照。神经电生理检查给药后大鼠的二腹肌肌电的变化 ,光镜下观察实验侧三叉神经节细胞的形态学变化 ,透射电镜观察三叉神经节细胞的超微形态结构变化。结果 :神经电生理结果显示动物对针刺反应不敏感 ,并显示不同时间左右两侧潜伏期 (ms)及痛阈 (mA)的变化都有显著性差异 (P <0 .0 5 ) ;实验侧光镜下可见大量细胞皱缩 ,形态不规则 ,细胞周围出现空隙 ;电镜下可见胞质中出现不规则的电子致密物质 ,线粒体、高尔基体、粗面内质网、核膜、有髓神经纤维髓鞘和无髓神经纤维病理性改变。结论 :脂质体阿霉素注入神经干后 ,可以选择性破坏相应的节细胞 ,引起神经功能上的变化。     

眶下神经束注射阿霉素对大鼠三叉神经脊束尾侧核内P物质的影响

通过动物实验观测阿霉素轴浆逆行传递对三叉神经脊束核内SP表达的影响，探讨阿霉素神经干注射治疗三叉神经痛(trigeminal neuralgia，TN)的作用机制以及神经肽与TN的发病关系。     

阿霉素神经干注射治疗原发性三叉神经病的复发原因分析

目的 探讨阿霉素神经干注射治疗原发性三叉神经痛的复发原因。方法 研究68例采用该技术治疗的患者术后复发与临床因素及术后疾病消失时间的关系。结果 复发与患者的性别、年龄、病程及板机点无关（P＞0．05）。而与三叉神经的分支及术后疾病消失时间有关（P＜0．05）。第Ⅱ支得发率高于其它两支;术后疼痛消失时间越长,复发率越高。结论 三叉神经细胞体的破坏不全可能是该技术治疗原发性三叉神经痛复发的主要原因。     

阿霉素注射治疗老年三叉神经痛的临床观察

目的:探讨阿霉素外周神经分支注射治疗老年原发性三叉神经痛的疗效。方法:对56例老年原发性三叉神经痛患者进行外周神经分支注射阿霉素治疗,1年后观察疗效。结果:随访到54例,其中48例疼痛缓解,疼痛缓解率为88.89%。结论:阿霉素外周神经分支注射治疗老年原发性三叉神经痛创伤小、并发症少,效果可靠。     

射频热凝术联合注射阿霉素治疗三叉神经下颌支痛的临床研究

目的 评价3D打印模板引导射频热凝术联合注射阿霉素治疗三叉神经下颌支痛的临床应用价值。方法将2019年1月—2020年9月在郑州市口腔医院接受射频热凝治疗的50例原发性三叉神经下颌支痛患者随机分为2组,以3D打印模板引导射频热凝术联合注射阿霉素为研究组（n=25）,以3D打印模板单纯辅助射频热凝术为对照组（n=25）,对比分析2组患者术前,术后即刻及术后1、3、6、12个月时的疼痛情况,即视觉模拟评分（VAS）。采用Brisman三叉神经疼痛疗效评定标准对术后各随访时间段的治疗效果进行评估,并记录术后并发症的情况。结果 2组患者术后即刻VAS及术后1、3、6、12个月时的VAS与术前比较均明显下降,差异均有统计学意义（P<0.05）;根据Brisman三叉神经痛疗效评定标准,2组患者在术后1和3个月时的有效性差异无统计学意义（P>0.05）;术后6和12个月时,研究组的有效性高于对照组,差异均有统计学意义（P<0.05）。研究组患者在随访期间无复发病例,对照组患者在术后3个月时复发1例,术后6个月时复发2例,术后12个月时复发4例;2组患者均未出现明显并发症。结论 3...     

鞘内注射阿霉素后离断三叉神经治疗带状疱疹后疼痛

目的观察阿霉素对三叉神经分布区带状疱疹后疼痛(PHN)的镇痛效果。方法对24患者用1%阿霉素直接注射至PHN相应分支的神经干,观察皮肤症状和异常性疼痛,于术后3d、7d、3个月进行评价。结果术后取得了95.8%的疗效,术后3d有效17例,缓解5例,无改善1例;术后7d有效23例,无效1例;术后3月有效23例,无效病例失访。有效病例在3～24个月内均无复发。结论阿霉素神经鞘内注射后,能有效的消除三叉神经分布区PHN,近期疗效较好。     

眶下孔周围注射滑石粉制作新型大鼠三叉神经痛动物模型的实验研究

目的: 应用滑石粉悬液进行眶下孔周围注射,建立一种新型大鼠三叉神经痛（trigeminal neuralgia,TN）动物模型。方法: 选取Wistar雄性大鼠30只,随机分为2组,一组在眶下神经孔周围注射30%滑石粉混悬液0.3 mL,另一组注射同等剂量的生理盐水,于术前3 d、术后3 d及术后1、2、3、4、6、8、12周分别进行行为学观察,Von Frey纤维测定大鼠机械性刺激反应阈值,利用方差分析对机械刺激阈值进行统计学分析。于术后3 d及术后4、8、12周取眶下孔周围组织作组织病理学观察,应用免疫组织化学的方法检测眶下区组织肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)的表达,采用SPSS16.0软件包对各检测值进行分组t检验。结果: 实验组大鼠术后3 d眶下神经支配区域机械痛反应阈值与术前及对照组相比显著降低（P<0.01),大鼠易激惹,具有搔抓面部或攻击行为。直到术后12周,机械痛阈值仍然显著低于对照组。实验组术后3 d组织病理学观察主要呈炎症表现,炎性因子表达减少;术后1周炎症更剧烈,炎性因子表达。术后4周,局部出现炎性肉芽组织增生,炎性因子表达最高;4~12周炎性反应逐渐减轻,炎性因子表达逐渐减少,局部瘢痕形成并逐渐加重,可见瘢痕压迫眶下神经。结论: 眶下孔周围注射滑石粉悬液可以建立稳定的TN动物模型,该造模方法简单易行,为进一步研究TN发病机制和模拟临床治疗提供了一种可靠、有效的动物模型。     

阿霉素神经干注射治疗原发性三叉神经痛的复发原因分析

目的 探讨阿霉素神经干注射治疗原发性三叉神经痛的复发原因。方法 研究６８例采用该技术治疗的患者术后复发与临床因素及术后疼痛消失时间的关系。结果 复发与患者的性别、年龄、病程及板机点无关（Ｐ＞０．０５）;而与三叉神经的分支及术后疼痛消失时间有关（Ｐ＜０．０５）。第ＩＩ支复发率高于其它两支;术后疼痛消失时间越长,复发率越高。结论 三叉神经细胞体的破坏不全可能是该技术治疗原发性三叉神经痛复发的主要原因。     

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。     

Interaction between calcitonin gene‐related peptide‐immunoreactive neurons and satellite cells via P2Y12R in the trigeminal ganglion is involved in neuropathic tongue pain in rats

The P2Y₁₂ receptor expressed in satellite cells of the trigeminal ganglion is thought to contribute to neuropathic pain. The functional interaction between neurons and satellite cells via P2Y₁₂ receptors and phosphorylated extracellular signal‐regulated kinase 1/2 (pERK1/2) underlying neuropathic pain in the tongue was evaluated in this study. Expression of P2Y₁₂ receptor was enhanced in pERK1/2‐immunoreactive cells encircling trigeminal ganglion neurons after lingual nerve crush. The administration to lingual nerve crush rats of a selective P2Y₁₂ receptor antagonist, MRS2395, attenuated tongue hypersensitivity to mechanical and heat stimulation and suppressed the increase in the relative numbers of calcitonin gene‐related peptide (CGRP)‐immunoreactive neurons and neurons encircled by pERK1/2‐immunoreactive cells. Administration of the P2Y_1,12,13 receptor agonist, 2‐(methylthio)adenosine 5′‐diphosphate trisodium salt hydrate (2‐MeSADP), to naïve rats induced neuropathic pain in the tongue, as in lingual nerve crush rats. Co‐administration of 2‐MeSADP + MRS2395 to naïve rats did not result in hypersensitivity of the tongue. The relative number of CGRP‐immunoreactive neurons increased following this co‐administration, but to a lesser degree than observed in 2‐MeSADP‐administrated naïve rats, and the relative number of neurons encircled by pERK1/2‐immunoreactive cells did not change. These results suggest that the interaction between activated satellite cells and CGRP‐immunoreactive neurons via P2Y₁₂ receptors contributes to neuropathic pain in the tongue associated with lingual nerve injury.     

Palmatine alleviates hyperalgesia by inhibiting the expression of calcitonin gene-related peptide in the trigeminal ganglion of rats with chronic constriction injury of the infraorbital nerve

Trigeminal neuralgia is one of the most common of the neuropathic pains, and it can seriously influence patients’ quality of life. Calcitonin gene-related peptide (CGRP) is a type of nociceptive neurotransmitter that is expressed in neurons of the trigeminal ganglion and plays a major part in transmitting pain. The rat model of trigeminal neuralgia was established by causing a chronic constriction injury of the infraorbital nerve (CCI-ION). Male Sprague-Dawley rats (n = 24) were randomly divided into a sham control group (sham, n = 6), sham-treated with palmatine group (sham + palmatine, n = 6), trigeminal nerve model group (TN, n = 6), and trigeminal nerve treated with palmatine group (TN + palmatine, n = 6). Fifteen days after the operation the mechanical response threshold was decreased in the TN group compared with the sham group. From postoperative day 7 to day 15, the mechanical response threshold in the TN + palmatine group significantly increased compared with the TN group. On postoperative day 15 the results of quantitative polymerase chain reaction (qPCR), immunohistochemical staining, and western blotting showed an obvious increase in expression of CGRP and its receptors, serum concentrations of interleukin-1β (IL-1β), and tumour necrosis factor-α (TNF-α), and phosphorylation of protein kinase C (PKC) in the trigeminal ganglia of the TN group compared with the sham group, but these increases could be down-regulated by treatment with palmatine. Palmatine might therefore have therapeutic potential for the treatment of trigeminal neuralgia by inhibiting the expression of CGRP and its receptors in trigeminal ganglia, suppressing the serum concentrations of IL-1β and TNF-α, and decreasing the phosphorylation of PKC in the trigeminal ganglia of affected rats.     

Changes in pituitary and prolactin cells of Wistar rats after two dental fillings with bisphenolic resins

Bisphenol-A (BPA) is used to manufacture dental materials such as sealants, fillings and cements. There is evidence of its estrogenic effects on recipients after the placement of dental sealants. Pituitary and especially prolactin (PRL) cells are targets for estrogens.

Objectives

The aim of this research was to determine if BPA eluted from dental resins can alter the proliferation of pituitary cells and PRL cells in the short, medium and long term in a case-control assay.

Methods

Two dental fillings were inserted in the lower incisors of Wistar rats divided into groups sacrificed after one, three, five and seven months. Immunocytochemical treatment was carried out in order to determine proliferating cell nuclear antigen (PCNA) positive cells, PRL-positive cells, PRL- and PCNA-positive cells.

Results

A significant increase of PCNA-positive cells after one (p < 0.05), three (p < 0.01) and five months (p < 0.01) was recorded. PRL-positive cells showed no statistically significant difference between intervened animals and controls. PRL- and PCNA-positive cells manifested a significant increase after five months (p < 0.05). A significant decrease in proliferating cells was observed after seven months (p < 0.05) for PCNA-positive cells and (p < 0.01) for PRL- and PCNA-positive cells.

Conclusion

Low quantities of BPA eluted during mastication can affect immunocytochemical patterns of pituitary cells, increasing cellular proliferation in the short, medium and long term although PRL cell population remained unaffected after dental fillings.