Carina Domaneschi, Vanessa Juliana Gomes Carvalho, Bruno Munhoz Marotta, Norberto Nobuo Sugaya, Fábio Daumas Nunes, Camila de Barros Gallo
{"title":"电压门控钠通道基因表达在灼口综合征:一项病例对照研究。","authors":"Carina Domaneschi, Vanessa Juliana Gomes Carvalho, Bruno Munhoz Marotta, Norberto Nobuo Sugaya, Fábio Daumas Nunes, Camila de Barros Gallo","doi":"10.1590/1807-3107bor-2023.vol37.0005","DOIUrl":null,"url":null,"abstract":"<p><p>Burning mouth syndrome (BMS) is a condition characterized by painful symptoms of the oral mucosa, despite the absence of any clinical signs. Its etiology is unknown, and there is still no effective treatment to date. Current evidence has shown neuropathic impairment in BMS patients. Neuropathic pain can be related to the dysfunction of voltage-gated sodium channels, considering that these receptors regulate the induction of action potentials in nociceptive neurons. This study evaluated the gene expression of voltage-gated sodium channels Na v 1.7, Na v 1.8 and Na v 1.9 in these patients. The gene expressions of these channels were assessed by real time RT-PCR analysis of fresh-frozen tongue biopsies in a case-control study composed of 12 patients with BMS, and 5 healthy control patients, proportionally matched by sex and age, and analyzed using the 2^(-Delta Delta CT) method. There was no statistically significant difference between the analyzed groups, despite the increase in Na v 1.7 (fold-change = 3.13, p = 0.52) and decrease in Na v 1.9 (fold-change = 0.45, p = 0.36) gene expression in the BMS group. The Na v 1.8 gene was not expressed in any of the samples analyzed. Although the gene expression in the voltage-gated sodium channels in BMS under study seems to be comparable with that of the normal oral mucosa, the functionality of these channels in BMS has not yet been identified, thus suggesting that further research is needed to better understand these voltage-gated sodium channels.</p>","PeriodicalId":48942,"journal":{"name":"Brazilian Oral Research","volume":null,"pages":null},"PeriodicalIF":2.5000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Voltage-gated sodium channels gene expression in Burning Mouth Syndrome: a case-control study.\",\"authors\":\"Carina Domaneschi, Vanessa Juliana Gomes Carvalho, Bruno Munhoz Marotta, Norberto Nobuo Sugaya, Fábio Daumas Nunes, Camila de Barros Gallo\",\"doi\":\"10.1590/1807-3107bor-2023.vol37.0005\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Burning mouth syndrome (BMS) is a condition characterized by painful symptoms of the oral mucosa, despite the absence of any clinical signs. Its etiology is unknown, and there is still no effective treatment to date. Current evidence has shown neuropathic impairment in BMS patients. Neuropathic pain can be related to the dysfunction of voltage-gated sodium channels, considering that these receptors regulate the induction of action potentials in nociceptive neurons. This study evaluated the gene expression of voltage-gated sodium channels Na v 1.7, Na v 1.8 and Na v 1.9 in these patients. The gene expressions of these channels were assessed by real time RT-PCR analysis of fresh-frozen tongue biopsies in a case-control study composed of 12 patients with BMS, and 5 healthy control patients, proportionally matched by sex and age, and analyzed using the 2^(-Delta Delta CT) method. There was no statistically significant difference between the analyzed groups, despite the increase in Na v 1.7 (fold-change = 3.13, p = 0.52) and decrease in Na v 1.9 (fold-change = 0.45, p = 0.36) gene expression in the BMS group. The Na v 1.8 gene was not expressed in any of the samples analyzed. Although the gene expression in the voltage-gated sodium channels in BMS under study seems to be comparable with that of the normal oral mucosa, the functionality of these channels in BMS has not yet been identified, thus suggesting that further research is needed to better understand these voltage-gated sodium channels.</p>\",\"PeriodicalId\":48942,\"journal\":{\"name\":\"Brazilian Oral Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Brazilian Oral Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1590/1807-3107bor-2023.vol37.0005\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Dentistry\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brazilian Oral Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1590/1807-3107bor-2023.vol37.0005","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Dentistry","Score":null,"Total":0}
引用次数: 0
摘要
灼口综合征(BMS)是一种以口腔黏膜疼痛症状为特征的疾病,尽管没有任何临床体征。其病因不明,至今仍没有有效的治疗方法。目前的证据显示BMS患者存在神经性损伤。神经性疼痛可能与电压门控钠通道功能障碍有关,考虑到这些受体调节伤害性神经元的动作电位诱导。本研究评估了这些患者电压门控钠通道Na v 1.7、Na v 1.8和Na v 1.9的基因表达。对12例BMS患者和5例按性别和年龄比例匹配的健康对照患者进行病例对照研究,采用实时RT-PCR分析新鲜冷冻舌组织切片中这些通道的基因表达,并采用2^(-Delta -Delta CT)方法进行分析。BMS组Na v 1.7基因表达增加(fold-change = 3.13, p = 0.52), Na v 1.9基因表达减少(fold-change = 0.45, p = 0.36),各组间差异无统计学意义。Na v1.8基因在分析的所有样品中均未表达。虽然所研究的BMS中电压门控钠通道的基因表达似乎与正常口腔黏膜相当,但这些通道在BMS中的功能尚未确定,因此需要进一步研究以更好地了解这些电压门控钠通道。
Voltage-gated sodium channels gene expression in Burning Mouth Syndrome: a case-control study.
Burning mouth syndrome (BMS) is a condition characterized by painful symptoms of the oral mucosa, despite the absence of any clinical signs. Its etiology is unknown, and there is still no effective treatment to date. Current evidence has shown neuropathic impairment in BMS patients. Neuropathic pain can be related to the dysfunction of voltage-gated sodium channels, considering that these receptors regulate the induction of action potentials in nociceptive neurons. This study evaluated the gene expression of voltage-gated sodium channels Na v 1.7, Na v 1.8 and Na v 1.9 in these patients. The gene expressions of these channels were assessed by real time RT-PCR analysis of fresh-frozen tongue biopsies in a case-control study composed of 12 patients with BMS, and 5 healthy control patients, proportionally matched by sex and age, and analyzed using the 2^(-Delta Delta CT) method. There was no statistically significant difference between the analyzed groups, despite the increase in Na v 1.7 (fold-change = 3.13, p = 0.52) and decrease in Na v 1.9 (fold-change = 0.45, p = 0.36) gene expression in the BMS group. The Na v 1.8 gene was not expressed in any of the samples analyzed. Although the gene expression in the voltage-gated sodium channels in BMS under study seems to be comparable with that of the normal oral mucosa, the functionality of these channels in BMS has not yet been identified, thus suggesting that further research is needed to better understand these voltage-gated sodium channels.