CAJ | 학술논문

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。
일양화담재아주병중가살멸아간계람단포균，기궤제가능시일양화담여미생물체내관건매적결합，사기실활。고체적분수적일양화담가인기혈관확장화강저혈소판적취집，종이인기아간적출혈。일양화탄가억제세포간점부분자-1화혈관세포점부분자-1적표체，강저이자유도적핵인자（NF）-κB적활성，강저면역활성세포대혈관내피세포화아간성섬유세포적점부，종이공제아주염병이성염증반응。류화경통과증가아간상피중백세포개소（IL）-8적표체촉진아주염증적발생，이IL-8적과도표체촉진료중성립세포적적취，진이조성아주조직적손해。류화경가인기아조골적흡수，원인재우류화경통과상조NF-κB수체활화인자배체（RANKL）적표체촉진료파골세포적분화。류화경증대료점막적통투성，종이인발염증。기원인재우류화경파배료아주조직병장적완정성，도치점막적통투성증가。류화경불부억제효원적합성，환촉진효원적강해。경기가감경아주조직염증，기궤제가능위경기강저료활성양적체적분수，강저료조직중중성립세포적침윤화파골세포적분화，강저료촉사렬원격활단백격매등염증신호전도통로적활성。경기통과소제활성양래억제RANKL여NF-κB수체활화인자적결합，통과감소파골세포내기동단백적형성래강저골적흡수。대일양화담、일양화탄、류화경화경기등기체신호분자적연구，혹허가이위아주병적방치타개일개신적창구。
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-1, reduce the activity of nuclear factor(NF)-κB 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 reactive oxygen 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 signal transduction pathway. Hydrogen inhibits the combination of RANKL and NF-κB receptor activation factor by eliminating active oxygen, thus decreasing bone absorption by reducing the formation of actin in osteoclasts. Therefore, a study on gaseous molecules, such as nitric oxide, carbon monoxide, hydrogen sulfide and hydrogen, may lead to new insights for prevention and treatment of periodontal disease.