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活性氧影响牙周炎发生发展及牙周组织再生 被引量:1

The role of reactive oxygen species in periodontitis and periodontal tissue regeneration
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摘要 背景:活性氧在牙周炎发生发展和牙周组织再生过程中发挥双刃剑作用,低浓度的活性氧诱导牙周膜成纤维细胞的分化,过量的活性氧会造成牙周组织损伤。炎症发生时,牙周组织中的活性氧聚集,通过多种细胞信号通路或通过氧化还原反应诱导细胞和组织的损伤。目的:对活性氧在牙周炎发生发展及牙周组织再生中的双刃剑效果进行综述,为临床治疗牙周炎及促进牙周组织再生提供潜在靶点及治疗思路。方法:通过检索1990年4月至2023年4月PubMed及中国知网数据库,英文检索词为“periodontal tissue engineering,periodontal defect,regeneration of periodontal tissue,chronic periodontitis,reactive oxygen species,oxidative stress,antioxidative stress,oxidative injuries,free radicals,reactive nitrogen species”,中文检索词为“牙周组织工程,牙周缺损,牙槽骨丧失,牙周组织再生,牙周炎,破骨细胞,氧化应激,抗氧化,活性氧”,经过对每条文献文题、摘要的筛选,排除与研究目的相关性差及内容陈旧、重复的文献,对最终符合标准的77篇文献进行综述。结果与结论:(1)活性氧是一种反应活性较高的自由基,在细菌入侵时活性氧经中性粒细胞的呼吸爆发作用大量释放,经其氧化还原反应或作为多效性生理信号传导剂在体内发挥双刃剑作用。(2)在牙周炎中,低浓度的活性氧可以杀灭入侵的病原菌,但高浓度的活性氧经JNK、RANK、Wnt/β-连环蛋白等通路促进炎症因子分泌,促进免疫损伤或通过氧化反应直接损伤组织等方式加重牙周炎症。(3)在牙周组织再生过程中,低浓度的活性氧可以经Nrf2等通路促进牙周膜干细胞的增殖与分化,并能促进血管内皮生长因子的分泌进而促进血管再生。这为牙周组织再生提供了种子及营养的环境,对促进牙周组织再生极为重要,而高浓度的活性氧则会降低牙周膜干细胞的活性,并损伤内皮细胞,不利于血管再生。这将影响伤口愈合,抑制牙周组织再生。(4)因此,探索活性氧在牙周炎发生发展和牙周组织再生中的作用并发现其作用的潜在机制,并探索其发挥减轻牙周炎症并促进牙周组织再生的适宜浓度,对未来临床牙周炎和牙周组织再生的治疗具有重要意义。以活性氧作为靶点,探索减轻牙周炎症并促进牙周膜干细胞活性及血管再生的方法,可能成为临床上有效治疗牙周炎并促进牙周组织再生的方法。 BACKGROUND:Reactive oxygen species is a double-edged sword in the development of periodontitis and the regeneration of periodontal tissue.Low concentration of reactive oxygen species induces the differentiation of periodontal fibroblasts,and excessive reactive oxygen species will cause damage to periodontal tissue.In the process of inflammation,the accumulation of reactive oxygen species in periodontal tissue induces damage to cells and tissues through a variety of signaling pathways or through redox reactions.OBJECTIVE:To review the double-edged sword effect of reactive oxygen species in periodontitis and periodontal tissue regeneration,thereby providing potential targets and treatment ideas for the clinical treatment of periodontitis and periodontal tissue regeneration.METHODS:Databases of CNKI and PubMed were searched for relevant articles published from April 1990 to April 2023 with the key words of“periodontal tissue engineering,periodontal defect,regeneration of periodontal tissue,chronic periodontitis,reactive oxygen species,oxidative stress,antioxidative stress,oxidative injuries,free radicals,reactive nitrogen species”in Chinese and English,respectively.By reading the titles and abstracts,repetitive studies or irrelevant literatures were excluded.Finally,77 articles were included for review.RESULTS AND CONCLUSION:Reactive oxygen species are a kind of free radicals with high reactivity.When bacteria invade,reactive oxygen species are released in large quantities by the respiratory explosion of neutrophils and play a double-edged sword role in the body through their redox reactions or as pleiotropic physiological signal transmitters.In periodontitis,low concentrations of reactive oxygen species can kill invading pathogenic bacteria,but high concentrations of reactive oxygen species promote the secretion of inflammatory factors through JNK,RANK,Wnt/β-Catenin and other pathways,promote immune damage or directly damage tissues through oxidative reactions or through other ways to aggravate periodontitis.In the process of periodontal tissue regeneration,low concentrations of reactive oxygen species can promote the proliferation and differentiation of periodontal ligament stem cells through Nrf2 and other pathways and can promote the secretion of vascular endothelial growth factor to promote vascular regeneration.This provides seeds and a nutrient environment for periodontal tissue regeneration,which is extremely important for promoting periodontal tissue regeneration.However,high concentrations of reactive oxygen species will reduce the activity of periodontal ligament stem cells and damage endothelial cells,which are not conducive to vascular regeneration.This will inhibit wound healing and periodontal tissue regeneration.Therefore,it is important to explore the role of reactive oxygen species in the development of periodontitis and periodontal tissue regeneration and to discover the potential mechanism of its action and to explore the appropriate concentration for its role in reducing periodontal inflammation and promoting periodontal tissue regeneration for the future treatment of periodontitis and periodontal tissue regeneration in clinical practice.Using reactive oxygen species as a target to explore ways to reduce periodontal inflammation and promote periodontal ligament stem cell activity and vascular regeneration may become a clinically effective method for treating periodontitis and promoting periodontal tissue regeneration.
作者 翟浩嫣 赵圆 范登莹 刘春艳 Zhai Haoyan;Zhao Yuan;Fan Dengying;Liu Chunyan(Department of Orthodontics,School and Hospital of Stomatology,Hebei Medical University,Hebei Key Laboratory of Stomatology,Hebei Clinical Research Center for Oral Diseases,Shijiazhuang 050017,Hebei Province,China)
出处 《中国组织工程研究》 CAS 北大核心 2024年第14期2254-2260,共7页 Chinese Journal of Tissue Engineering Research
基金 2021年政府资助省级医学优秀人才项目(361029),项目负责人:刘春艳 2022年引进留学人员资助项目(C20220353),项目负责人:刘春艳。
关键词 氧化应激 破骨细胞 牙周组织再生 ROS 牙周炎 活性氧 血管生成 牙周膜干细胞 oxidative stress osteoclast periodontal tissue regeneration ROS periodontitis reactive oxygen species angiogenesis periodontal ligament stem cells
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  • 1Ito K, Lim S, Caramori G, et al. Cigarette smoking reduces histone deacetylase 2 expression, enhances cytokine expression, and inhibitsglucocorticoid actions in alveolar macrophages[J]. FASEB J, 2001, 15(6):1110-1112.
  • 2Schubert S Y, Neeman I, Resnick N. A novel mechanism for the inhibition of NF-kappaB activation in vascular endothelial cells by natural antioxidants[J]. FASEB J, 2002,16(14):1931-1933.
  • 3Levrand S, Pesse B, Feihl F, et al. Peroxynitrite is a potent inhibitor of NF-kappaB activation triggered by inflammatory stimuli in cardiac and endothelial cell lines[J]. Biol Chem, 2005,280(41): 34878-34887.
  • 4Park S W, Huq M D, Hu X, et al. Tyrosine nitration on p65: a novel mechanism to rapidly inactivate nuclear factor-kappaB[J]. Mol Cell Proteomics, 2005,4(3):300-309.
  • 5Sakon S, Xue X, Takekawa M, et al. NF-KB inhibits TNF-induced accumulation of ROS that mediate prolonged MAPK activation and necrotic cell death[J]. EMBO J, 2003,22:3898-3909.
  • 6Pham C G, Bubici C, Zazzeroni F, et al. Ferrhin heavy chain upregulation by NF-KB inhibits TNFa-induced apoptosis by suppressing reactive oxygen species[J]. Cell, 2004,119:529-542.
  • 7Torti F M, Torti S V. Regulation of ferritin genes and protein[J]. Blood, 2002,99:3505-3516.
  • 8Makarov S S. NF-KB as a therapeutic target in Chronic inflammaion: recent advances[J]. MOI Med Today, 2000,6:441-448.
  • 9Bernard D, Quatannens B, Begue A, et al. Antiproliferative and antiapoptotic effects of crel may occur within the same cells via the up -regulation of manganese superoxide dismutase [J]. Cancer Res, 2001,61:2656-2664.
  • 10Delhalle S, Deregowski V, Benoit V, et al. NF-KB-dependent MnSOD expression protects adenocarcinoma cells from TNFa-induced apoptosis[J]. Oncogene, 2002,21:3917-3924.

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