一氧化氮等气体信号分子与牙周疾病  

Nitric oxide and other gas signaling molecules and periodontal disease

作　　者：王艳芝[1,2] 李纾[1,2] 

机构地区：[1]山东大学口腔医院牙周科 [2]山东省口腔生物医学重点实验室,济南250012

出　　处：《国际口腔医学杂志》2014年第2期204-208,共5页International Journal of Stomatology

基　　金：国家自然科学基金(81271138)

摘　　要：一氧化氮在牙周病中可杀灭牙龈卟啉单胞菌,其机制可能是一氧化氮与微生物体内关键酶的结合,使其失活。高体积分数的一氧化氮可引起血管扩张和降低血小板的聚集,从而引起牙龈的出血。一氧化碳可抑制细胞间黏附分子-1和血管细胞黏附分子-1的表达,降低二者诱导的核因子(NF)-κB的活性,降低免疫活性细胞对血管内皮细胞和牙龈成纤维细胞的黏附,从而控制牙周炎病理性炎症反应。硫化氢通过增加牙龈上皮中白细胞介素(IL)-8的表达促进牙周炎症的发生,而IL-8的过度表达促进了中性粒细胞的积聚,进而造成牙周组织的损害。硫化氢可引起牙槽骨的吸收,原因在于硫化氢通过上调NF-κB受体活化因子配体(RANKL)的表达促进了破骨细胞的分化。硫化氢增大了黏膜的通透性,从而引发炎症。其原因在于硫化氢破坏了牙周组织屏障的完整性,导致黏膜的通透性增加。硫化氢不仅抑制胶原的合成,还促进胶原的降解。氢气可减轻牙周组织炎症,其机制可能为氢气降低了活性氧的体积分数,降低了组织中中性粒细胞的浸润和破骨细胞的分化,降低了促丝裂原激活蛋白激酶等炎症信号转导通路的活性。氢气通过消除活性氧来抑制RANKL与NF-κB受体活化因子的结合,通过减少破骨细胞内肌动蛋白的形成来降低骨的吸收。对一氧化氮、一氧化碳、硫化氢和氢气等气体信号分子的研究,或许可以为牙周病的防治打开一个新的窗口。In periodontal diseases, nitric oxide can kill Porphytomonas gingivalis, the mechanism of which may involve combination of nitric oxide with key enzymes of microorganisms and inactivating them. High volume fraction of nitric oxide can cause blood vessels to dilate and lower platelet aggregation, causing gum bleeding. Carbon monoxide can inhibit the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-l, reduce the activity of nuclear factor（NF）-r,B predominately induced by intercellular adhesion molecule-1 and vascular cell adhesion molecule, as well as lower immune active cells to vascular endothelial cells and gingival fibroblast adhesion, thus controlling periodontitis pathological inflammation. Hydrogen sulfide promotes the occurrence of periodontal disease by increasing the expression of interleukin（IL）-8 in gingival epithelium. Overexpression of IL-8 promotes accumulation of neutrophils, which causes periodontal tissue damage. Hydrogen sulfide can cause alveolar bone absorption because hydrogen sulfide can upregulate the expression of the receptor activator of nuclear factor-κB ligand（RANKL）, which promotes the differentiation of the osteoclast. Hydrogen sulfide increases the permeability of the mucosa, causing inflammation. The reason for this phenomenon is that hydrogen sulfide destroys the integrity of the periodontal tissue barrier, which increases mucous membrane permeability. Hydrogen sulfide inhibits synthesis of collagen and promotes its degradation. Hydrogen can relieve inflammation of periodontal tissue. The mechanism may reduce hydrogen and the volume fraction of reactiveoxygen species, reduce the infiltration of neutrophils in organization and osteoclast differentiation, or reduce the activity of inflammatory signal transduction pathways, such as the mitogen-activated protein kinase signaltransduction pathway. Hydrogen inhibits the combination of RANKL and NF-κB receptor activation factor by eliminating active oxygen, thus decreasing bone absorption b

关 键 词：牙周病 一氧化氮 一氧化碳 硫化氢 氢气 

分 类 号：R781.4[医药卫生—口腔医学]