Importance and functional roles of methylmercaptan, one of the main causes of oral malodar, in progression of

口腔恶臭是由挥发性硫化合物（VSC），包括甲硫醇。几项研究表明，甲硫醇的量与更深的口袋有关。另外，最近的研究表明，牙周病细菌产生的VSC。近年来的研究发现，在牙周病的深部或出血区，有大量死亡的上皮细胞，这些细胞在牙周病的发生、发展过程中起着重要的作用。然而，它是不知道的细胞毒性机制，完全。因此，我们通过使用口腔上皮细胞系KB细胞来研究甲硫醇诱导细胞死亡的可能性，并观察到VSC通过坏死的方式对KB细胞产生细胞毒性作用。牙周病是一种以牙龈炎症和牙周组织中牙槽骨吸收为特征的慢性疾病。近年来的研究表明， ...更多信息 致病菌如脂多糖（LPS）能够刺激炎性细胞因子（IL-1、TNF-α和IL-6），这些细胞因子也是骨吸收的诱导物，然后，这些细胞因子密切地促进牙周病的进展。研究表明，高迁移率族蛋白1（HMGB 1）是一种结构性染色质结合因子，其从坏死细胞而不是凋亡细胞中释放，并且HMGB 1能够刺激单核细胞和巨噬细胞中IL-1和TNF-α的表达。然后，已经表明HMGB 1是DNA结合细胞因子，并且也促进坏死诱导的炎症。有趣的是，证明HMGB 1是由甲硫醇破坏的坏死KB细胞分泌的，并且我们检查了死亡细胞的上清液是否能够诱导小鼠巨噬细胞样细胞系RAW 264.7细胞中TNF-α的表达。结果表明，在成人牙周病中，甲硫醇诱导口腔上皮细胞坏死，坏死细胞通过释放HMGB 1刺激炎症细胞因子的表达。少

Oral malodor is caused by volatile sulfur compounds (VSCs) including methylmercapton. Several studies showed that amount of methylmercapton are correlated with deeper pockets. In addition, resent studies show that periodontopathic bacteria produce the VSC. Therefore, it is proposed us that methylmercaptan plays a functional role (s) as pathogen factor for induction and progression of periodontal disease.Resent studies have investigated that many dead epithelial cells are detected in the area of deeper or bleeding pockets. However, it is not known the cytotoxic mechanisms of the cells, completely. And so, we examine a possibility that methylmercapton induces the cell death via using oral epithelial cell line KB cells and observed that the VSC exhibits cytotoxic effect on KB cells via necrosis manner.Periodontal disease is a chronic disease characterized by inflammation of gingival and resorption of alveolar bone in periodontal tissues. Resent studies indicated that virulence factors of … More pathogenic bacteria, such as lipopolysacchaaride (LPS), are able to stimulate inflammatory cytokines (IL-1, TNF-alpha, and IL-6), which are also inducers of bone resorption, and then, these cytokines closely contribute to progression of periodontal disease. It has been showed that hight mobility group protein 1 (HMGB1), an architectural chromatin-binding factor, is released from necrotic cells but not apoptotic cells and that HMGB1 is able to stimulate expression of IL-1 and TNF-alpha in monocyte and macrophage. Then, it has been suggested that HMGB1 is a DNA binding cytokine and also promote necrosis-induced inflammation. It is interesting to demonstrate that HMGB1 is secreted from necrotic KB cells destroyed by methylmercapton, and we examined whether the supernatant of the death cells is able to induce expression of TNF-alpha in mouse macrophage like cell line RAW264.7 cells. Then the supernatant stimulated the expression of TNF-alpha and the biological activity was abolished by treatment of anti-HMGB1 antibody.Therefore, it was suggested a possibility that methylmercapton induces the necrosis of oral epithelial cell and the necrosis is able to stimulate the expression of inflammation cytokines through the release of HMGB1 from the necrosis cells, in adult periodontal disease. Less