活性氧在牙周炎中病理作用的研究进展
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摘要
牙周炎是一种常见的慢性炎症疾病,引起牙周组织的损伤,受损部位包括牙龈、牙周韧带和牙槽骨。引发牙周炎的主要原因是人体对口腔微生物及其代谢产物的免疫反应,其中活性氧(ROS)的稳态失衡和抗氧化防御系统在牙周炎的发病进程中扮演了重要的促进角色。升高的ROS引发病灶组织细胞的自噬,导致相应的组织细胞凋亡,进一步阐明牙周炎自噬过程中氧还原调控的作用和机制,对牙周病治疗策略的研究具有一定的临床指导意义。笔者对ROS在牙周炎中的相关病理作用做了简要综述。
Periodontitis is a chronic inflammatory disease that causes injury in periodontal tissues,including gum,periodontal ligament and alveolar bone. The main cause of periodontal tissue destruction is the host immune response to oral microbes and their metabolites,in which the steady-state imbalance of reactive oxygen species and the antioxidant defense system play an important role. Increased reactive oxygen species induce autophagy,leading to apoptosis of the corresponding tissue. To further elucidate the role and mechanism of oxygen reduction in autophagy of periodontitis,and to study the therapeutic strategies of periodontal disease has certain clinical significance. In this article,we briefly reviewed the related pathological effects of ROS on periodontitis.
Periodontitis is a chronic inflammatory disease that causes injury in periodontal tissues,including gum,periodontal ligament and alveolar bone. The main cause of periodontal tissue destruction is the host immune response to oral microbes and their metabolites,in which the steady-state imbalance of reactive oxygen species and the antioxidant defense system play an important role. Increased reactive oxygen species induce autophagy,leading to apoptosis of the corresponding tissue. To further elucidate the role and mechanism of oxygen reduction in autophagy of periodontitis,and to study the therapeutic strategies of periodontal disease has certain clinical significance. In this article,we briefly reviewed the related pathological effects of ROS on periodontitis.
引文
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[27] PATIL VS,PATIL VP,GOKHALE N,et al. Chronic Periodontitis in Type 2 Diabetes Mellitus:Oxidative Stress as a Common Factor in Periodontal Tissue Injury[J]. Journal of Clinical&Diagnostic Research Jcdr,2016,10(4):BC12.
[2] MARQUIS RE. Oxygen metabolism,oxidative stress and acid-base physiology of dental plaque biofilms[J]. Journal of Industrial Microbiology,1995,15(3):198-207.
[3] DUMITRESCU AL. Depression and inflammatory periodontal Disease considerations—an interdisciplinary approach[J]. Frontiers in Psychology,2016,7:347.
[4] NAYAR G,GAUNA A,CHUKKAPALLI S,et al.,Polymicrobial infection alter inflammatory microRNA in rat salivary glands during periodontal disease[J]. Anaerobe,2016,38:70-75.
[5] DI MEO S,REED TT,VENDITTI P,et al. Role of ROS and RNS Sources in Physiological and Pathological Conditions[J]. Oxid Med Cell Longev,2016,2016:1245049. DOI:10. 1155/2016/1245049.
[6] TAMAKI N,HAYASHIDA H,FUKUI M,et al. Oxidative stress and antibody levels to periodontal bacteria in adults:the Nagasaki Islands study[J]. Oral Diseases,2014,20(3):e49-e56. DOI:10.1111/odi. 12127.
[7] GALLI C,PASSERI G,MACALUSO GM. Fox Os,Wnts and oxidative stress-induced bone loss:new players in the periodontitis arena?[J]. Journal of Periodontal Research,2011,46(4):397.
[8] LAMONT RJ,HAJISHENGALLIS G. Polymicrobial synergy and dysbiosis in inflammatory disease[J]. Trends in Molecular Medicine,2015,21(3):172-183.
[9] ZHANG L,WANG K,LEI Y,et al. Redox signaling:Potential arbitrator of autophagy and apoptosis in therapeutic response[J]. Free Radical Biology&Medicine,2015,89:452-465.
[10] FILOMENI G,DE ZD,CECCONI F. Oxidative stress and autophagy:the clash between damage and metabolic needs[J]. Cell Death&Differentiation,2015,22(3):377.
[11] AKALIN FA,BALTACIOG LU E,ALVER A,et al. Lipid peroxidation levels and total oxidant status in serum,saliva and gingival crevicular fluid in patients with chronic periodontitis[J]. Journal of Clinical Periodontology,2007,34(7):558-565.
[12] BALTACOG LU E,KEHRIBAR MA,YUVA P,et al. Total Oxidant status and bone resorption biomarkers in serum and gingival crevicular fluid of patients with periodontitis[J]. Journal of Periodontology,2013,85(2):317-326.
[13] KANZAKI H,SHINOHARA F,KAJIYA M,et al. The Keap1/Nrf2protein axis plays a role in osteoclast differentiation by regulating intracellular reactive oxygen species signaling[J]. Journal of Biological Chemistry,2013,288(32):23009-23020.
[14] THUMMURI D,JEENGAR MK,SHRIVASTAVA S,et al. Thymoquinone prevents RANKL-induced osteoclastogenesis activation and osteolysis in an in vivo model of inflammation by suppressing NFKB and MAPK Signalling[J]. Pharmacological Research,2015,99:63-73.
[15] LIU W,GU J,QI J,et al. Lentinan exerts synergistic apoptotic effects with paclitaxel in A549 cells via activating ROS-TXNIP-NLRP3 inflammasome[J]. Journal of Cellular and Molecular Medicine,2015,19(8):1949-1955.
[16] PRADEEP AR,RAO NS,BAJAJ P,et al. 8-Isoprostane:a lipid peroxidation product in gingival crevicular fluid in healthy,gingivitis and chronic periodontitis subjects[J]. Archives of Oral Biology,2013,58(5):500-504.
[17] KABAT AM,POTT J,MALOY KJ. The mucosal immune system and its regulation by autophagy[J]. Frontiers in Immunology,2016,7:240.
[18] LEVINE B,KLIONSKY DJ. Autophagy wins the 2016 Nobel Prize in Physiology or Medicine:Breakthroughs in baker's yeast fuel advances in biomedical research[J]. Proceedings of the National Academy of Sciences,2017,114(2):201-205.
[19] BULLON P,CORDERO MD,QUILES JL,et al. Autophagy in periodontitis patients and gingival fibroblasts:unraveling the link between chronic diseases and inflammation[J]. BMC Medicine,2012,10(1):122.
[20] GOLZ L,MEMMERT S,RATH-DESCHNER B,et al. LPS from P.gingivalis and Hypoxia increases oxidative stress in periodontal ligament fibroblasts and contributes to periodontitis[J]. Mediators of Inflammation,2014,2014:13.
[21] YANG Z,KLIONSKY DJ. Eaten alive:a history of macroautophagy[J]. Nature Cell Biology,2010,12:814.
[22] WANG G,ZHANG T,SUN W,et al. Arsenic sulfide induces apoptosis and autophagy through the activation of ROS/JNK and suppression of Akt/m TOR signaling pathways in osteosarcoma[J].Free Radical Biology and Medicine,2017,106:24-37.
[23] ZHAO Y,QU T,WANG P,et al. Unravelling the relationship between macroautophagy and mitochondrial ROS in cancer therapy[J]. Apoptosis,2016,21(5):517-531.
[24]李柄辉,孟继明,王朝阳,等.牙周病和胃癌发生风险相关性的Meta分析[J].中国循证医学杂志,2017(10):1183-1187.
[25] ZHONG Z,SANCHEZ-LOPEZ E,KARIN M. Autophagy,Inflammation,and Immunity:A Troika Governing Cancer and Its Treatment[J]. Cell,2016,166(2):288-298.
[26] AN Y,LIU W,XUE P,et al. Increased autophagy is required to protect periodontal ligament stem cells from apoptosis in inflammatory microenvironment[J]. Journal of Clinical Periodontology,2016,43(7):618.
[27] PATIL VS,PATIL VP,GOKHALE N,et al. Chronic Periodontitis in Type 2 Diabetes Mellitus:Oxidative Stress as a Common Factor in Periodontal Tissue Injury[J]. Journal of Clinical&Diagnostic Research Jcdr,2016,10(4):BC12.