Smokeless tobacco (paan and gutkha) consumption, prevalence, and contribution to oral cancer.
Smokeless tobacco (paan and gutkha) consumption, prevalence, and contribution to oral cancer.
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DOI：
10.4178/epih.e2017009
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发表时间：
2017
影响因子：
3.8
通讯作者：
Abdollahi M
中科院分区：
文献类型：
--
作者：
Niaz K;Maqbool F;Khan F;Bahadar H;Ismail Hassan F;Abdollahi M
无烟烟草的消费在世界各地普遍存在，会导致口腔粘膜下纤维化(OSMF)，这是一种具有恶性潜能的长期破坏性口腔疾病。在这篇综述中，我们主要关注无烟烟草的消费，如PAAN和GUTKHA，以及这些物质在OSMF和最终口腔癌诱导中的作用。要检查的文章列表是使用PubMed、Scope和Google Scholar提供的引文发现工具建立的。持续咀嚼PAAN和吞咽牙胶会引发黏膜下组织进行性纤维化。一般来说，OSMF的发生是由多种风险因素造成的，特别是无烟烟草及其成分，如槟榔、槟榔和熟石灰，这些成分用于帕恩和古特卡。在南亚国家，口腔癌的发病率女性高于男性。无论有没有槟榔，人类口腔上皮细胞都会受到槟榔中熟石灰的致癌和遗传毒性影响。3-(甲基亚硝氨基)-丁腈、亚硝胺和尼古丁等产品会在无烟烟草中引发活性氧的产生，最终导致烟草消费者口腔中具有致癌作用的成纤维细胞、DNA和RNA损伤。细胞色素P450酶对烟草中亚硝胺的代谢激活可能导致主要致癌物N-亚硝基烟碱和微核的形成，这些都是遗传毒性的指标。这些影响会导致进一步的DNA损伤，最终导致口腔癌。
Smokeless tobacco consumption, which is widespread throughout the world, leads to oral submucous fibrosis (OSMF), which is a long-lasting and devastating condition of the oral cavity with the potential for malignancy. In this review, we mainly focus on the consumption of smokeless tobacco, such as paan and gutkha, and the role of these substances in the induction of OSMF and ultimately oral cancer. The list of articles to be examined was established using citation discovery tools provided by PubMed, Scopus, and Google Scholar. The continuous chewing of paan and swallowing of gutkha trigger progressive fibrosis in submucosal tissue. Generally, OSMF occurs due to multiple risk factors, especially smokeless tobacco and its components, such as betel quid, areca nuts, and slaked lime, which are used in paan and gutkha. The incidence of oral cancer is higher in women than in men in South Asian countries. Human oral epithelium cells experience carcinogenic and genotoxic effects from the slaked lime present in the betel quid, with or without areca nut. Products such as 3-(methylnitrosamino)-proprionitrile, nitrosamines, and nicotine initiate the production of reactive oxygen species in smokeless tobacco, eventually leading to fibroblast, DNA, and RNA damage with carcinogenic effects in the mouth of tobacco consumers. The metabolic activation of nitrosamine in tobacco by cytochrome P450 enzymes may lead to the formation of N-nitrosonornicotine, a major carcinogen, and micronuclei, which are an indicator of genotoxicity. These effects lead to further DNA damage and, eventually, oral cancer.