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

口腔异味是由挥发性硫化合物（VSCs）引起的，包括甲基硫化物。几项研究表明，甲基硫化物的数量与更深的口袋有关。此外，最近的研究表明牙周病细菌产生VSC。因此，我们认为甲基硫醇作为病原菌因子在牙周病的诱导和发展中起着功能性作用。最近的研究表明，在较深的或出血的口袋区域检测到许多死亡的上皮细胞。然而，细胞的细胞毒性机制尚不完全清楚。因此，我们以口腔上皮细胞系KB细胞为研究对象，探讨甲基巯基顿诱导细胞死亡的可能性，并观察到VSC通过坏死方式对KB细胞表现出细胞毒性作用。牙周病是一种以牙龈炎症和牙周组织牙槽骨吸收为特征的慢性疾病。最近的研究表明，更多的病原菌的毒力因子，如脂多糖（LPS），能够刺激炎症细胞因子（IL-1、tnf - α和IL-6），这些细胞因子也是骨吸收的诱导剂，并且这些细胞因子与牙周病的进展密切相关。研究表明，高迁移率组蛋白1 （HMGB1）是一种结构染色质结合因子，可从坏死细胞而非凋亡细胞中释放，HMGB1可刺激单核细胞和巨噬细胞中IL-1和tnf - α的表达。然后，有人认为HMGB1是一种DNA结合细胞因子，也促进坏死诱导的炎症。有趣的是，HMGB1是由甲基巯基顿破坏的坏死KB细胞分泌的，我们检测了死亡细胞的上清是否能够诱导小鼠巨噬细胞样细胞系RAW264.7细胞中tnf - α的表达。然后用上清刺激tnf - α的表达，用抗hmgb1抗体处理使其生物活性消失。因此，提示在成人牙周病中，甲基巯基酮可能诱导口腔上皮细胞坏死，而坏死可通过从坏死细胞中释放HMGB1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