Department of Dentistry, Chang Gung Memorial Hospital, Taipei 105, Taiwan.
College of Oral Medicine, Taipei Medical University, Taipei 110, Taiwan.
Int J Mol Sci. 2020 Oct 30;21(21):8104. doi: 10.3390/ijms21218104.
Betel quid (BQ) chewing increased the risk of oral cancer and oral submucous fibrosis (OSMF), an oral premalignant disorder (OPMD) with malignant transformation potential. BQ components such as areca nut (AN), trauma by coarse AN fiber, catechin, copper, alkaloids, stimulated reactive oxygen species (ROS), inflammation and cytotoxicity are suggested to be the contributing factors. They may induce tissue inflammation, proliferation of fibroblasts and collagen deposition, myofibroblast differentiation and contraction, collagen cross-links and inhibit collagen phagocytosis, finally leading to the development of OSMF and oral cancer. These events are mediated by BQ components-induced changes of extracellular matrix (ECM) turnover via regulation of TGF-β1, plasminogen activator inhibitor-1 (PAI-1), cystatin, lysyl oxidase (LOX) and tissue inhibitors of metalloproteinases (TIMPs) and metalloproteinases (MMPs). Genetic susceptibility is also involved in these disease processes. Further understanding the molecular mechanisms of BQ-induced OSMF and oral cancer can be helpful for future disease prevention and treatment.
咀嚼槟榔会增加口腔癌和口腔黏膜下纤维性变（一种具有恶性转化潜能的口腔癌前病变）的风险。槟榔中的成分，如槟榔果（AN）、粗糙的 AN 纤维引起的创伤、儿茶素、铜、生物碱、活性氧（ROS）刺激、炎症和细胞毒性被认为是促成因素。它们可能引起组织炎症、成纤维细胞增殖和胶原沉积、肌成纤维细胞分化和收缩、胶原交联和抑制胶原吞噬，最终导致口腔黏膜下纤维性变和口腔癌的发展。这些事件是通过调节 TGF-β1、纤溶酶原激活物抑制剂-1（PAI-1）、组织蛋白酶、赖氨酰氧化酶（LOX）和金属蛋白酶抑制剂（TIMPs）和金属蛋白酶（MMPs）来介导的，由 BQ 成分诱导的细胞外基质（ECM）代谢变化所引起的。遗传易感性也参与了这些疾病过程。进一步了解 BQ 诱导的口腔黏膜下纤维性变和口腔癌的分子机制有助于未来的疾病预防和治疗。
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