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疼痛性人牙髓和灼口综合征中钠离子通道 Na v 1.7 的免疫反应性。

Sodium channel Na v 1.7 immunoreactivity in painful human dental pulp and burning mouth syndrome.

机构信息

Dental Institute, King's College London, Guy's Hospital, Oral Surgery Department, Great Maze Pond, London, UK.

出版信息

BMC Neurosci. 2010 Jun 8;11:71. doi: 10.1186/1471-2202-11-71.

Abstract

BACKGROUND

Voltage gated sodium channels Na v 1.7 are involved in nociceptor nerve action potentials and are known to affect pain sensitivity in clinical genetic disorders.

AIMS AND OBJECTIVES

To study Na v 1.7 levels in dental pulpitis pain, an inflammatory condition, and burning mouth syndrome (BMS), considered a neuropathic orofacial pain disorder.

METHODS

Two groups of patients were recruited for this study. One group consisted of patients with dental pulpitis pain (n = 5) and controls (n = 12), and the other patients with BMS (n = 7) and controls (n = 10). BMS patients were diagnosed according to the International Association for the Study of Pain criteria; a pain history was collected, including the visual analogue scale (VAS). Immunohistochemistry with visual intensity and computer image analysis were used to evaluate levels of Na v 1.7 in dental pulp tissue samples from the dental pulpitis group, and tongue biopsies from the BMS group.

RESULTS

There was a significantly increased visual intensity score for Na v 1.7 in nerve fibres in the painful dental pulp specimens, compared to controls. Image analysis showed a trend for an increase of the Na v 1.7 immunoreactive % area in the painful pulp group, but this was not statistically significant. When expressed as a ratio of the neurofilament % area, there was a strong trend for an increase of Na v 1.7 in the painful pulp group. Na v 1.7 immunoreactive fibres were seen in abundance in the sub-mucosal layer of tongue biopsies, with no significant difference between BMS and controls.

CONCLUSION

Na v 1.7 sodium channel may play a significant role in inflammatory dental pain. Clinical trials with selective Na v 1.7 channel blockers should prioritize dental pulp pain rather than BMS.

摘要

背景

电压门控钠离子通道 Na v 1.7 参与伤害感受器神经动作电位,已知其会影响临床遗传疾病中的疼痛敏感性。

目的和目标

研究牙髓痛(一种炎症性疾病)和灼口综合征(BMS)中 Na v 1.7 的水平,BMS 被认为是一种神经性口面疼痛障碍。

方法

本研究招募了两组患者。一组包括牙髓痛患者(n = 5)和对照组(n = 12),另一组为 BMS 患者(n = 7)和对照组(n = 10)。BMS 患者根据国际疼痛研究协会的标准进行诊断;收集疼痛病史,包括视觉模拟评分(VAS)。使用免疫组织化学的视觉强度和计算机图像分析评估牙髓痛组的牙髓组织样本和 BMS 组的舌活检中 Na v 1.7 的水平。

结果

与对照组相比,疼痛牙髓标本中神经纤维的 Na v 1.7 视觉强度评分显著增加。图像分析显示疼痛牙髓组 Na v 1.7 免疫反应阳性%面积有增加的趋势,但无统计学意义。当以神经丝%面积的比值表示时,疼痛牙髓组 Na v 1.7 的增加有强烈的趋势。在舌活检的黏膜下层中可以看到大量的 Na v 1.7 免疫反应纤维,BMS 组和对照组之间没有显著差异。

结论

Na v 1.7 钠离子通道可能在炎症性牙痛中起重要作用。具有选择性 Na v 1.7 通道阻滞剂的临床试验应优先考虑牙髓痛,而不是 BMS。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6d1/2890014/e6bd6df1b89b/1471-2202-11-71-1.jpg

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