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氧化应激损伤与口腔疾病相关性的研究进展
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  • 英文篇名:Research progress on the association between oxidative stress injury and certain oral diseases
  • 作者:吴东蕾 ; 刘静
  • 英文作者:Wu Donglei;Liu Jing;School of Stomatology,Jinan University;
  • 关键词:口腔疾病 ; 氧化应激 ; 抗氧化物 ; 活性氧
  • 英文关键词:oral diseases;;oxidative stress;;antioxidant;;reactive oxygen species
  • 中文刊名:GWKQ
  • 英文刊名:International Journal of Stomatology
  • 机构:暨南大学口腔医学院;
  • 出版日期:2019-01-01
  • 出版单位:国际口腔医学杂志
  • 年:2019
  • 期:v.46
  • 基金:暨南大学优秀人才基金(51025036)~~
  • 语种:中文;
  • 页:GWKQ201901013
  • 页数:6
  • CN:01
  • ISSN:51-1698/R
  • 分类号:68-73
摘要
氧化应激指由于细胞内源性抗氧化系统不能有效清除堆积在体内的大量自由基,导致机体内氧化和抗氧化系统处于失衡的一种状态,其参与各种疾病的发生、发展。口腔颌面部组织在各种内、外源性因素的刺激下,可引发氧化应激并导致相关组织损伤。本文就各种外周刺激引发口腔颌面部氧化应激损伤及其与口腔疾病(包括颞下颌关节紊乱病、咀嚼肌疾病、牙周病、口腔癌及癌前病变)相关性的研究进行综述,从氧化应激角度为相关口腔颌面部疾病的发病机制研究、诊断及治疗提供新思路。
        Oxidative stress is a state in which oxidation exceeds the antioxidant systems when the endogenous antioxidant system cannot effectively remove the large amount of free radicals accumulated in the body. It participates in the development of various diseases. The oral cavity is usually attacked by multiple endogenous or exogenous stimulations,which can lead to stress injury. This article reviews the research progress of oxidative stress in oral and maxillofacial regions induced by various peripheral stimuli and its correlation with related diseases, including temporomandibular disorders, masticatory muscle diseases, periodontal diseases, oral cancer and precancerous lesions. It also provides a new idea for the etiologic investigation, diagnosis and treatment of oral diseases from the perspective of oxidative stress.Moreover, it provides an update of the literature concerning the association of oxidative stress with pathological conditions related to oral cavity, focusing on the diagnostic and therapeutic importance of the tests based on saliva specimens in a preventive perspective.
引文
[1] Poprac P, Jomova K, Simunkova M, et al. Targeting free radicals in oxidative stress-related human diseases[J]. Trends Pharmacol Sci, 2017, 38(7):592-607.
    [2] Valko M,Leibfritz D, Moncol J, et al. Free radicals and antioxidants in normal physiological functions and human disease[J]. Int J Biochem Cell Biol, 2007,39(1):44-84.
    [3] Moloney JN, Cotter TG. ROS signalling in the biology of cancer[J]. Semin Cell Dev Biol, 2018, 80:50-64.
    [4] Kawai Y, Kubota E, Okabe E. Reactive oxygen species participation in experimentally induced arthritis of the temporomandibular joint in rats[J]. J Dent Res,2000, 79(7):1489-1495.
    [5] Lee MC, Kawai Y, Shoji H, et al. Evidence of reactive oxygen species generation in synovial fluid from patients with temporomandibular disease by electron spin resonance spectroscopy[J]. Redox Rep,2004, 9(6):331-336.
    [6] Etoz OA, Akcay H, Neselioglu S, et al. Total antioxidant capacity and total oxidant status of synovialfluids in patients with temporomandibular joint pain and dysfunction[J]. Clin Oral Investig, 2012, 16(6):1557-1561.
    [7] Ishimaru K,Ohba S, Yoshimura H, et al. Antioxidant capacity of synovial fluid in the temporomandibular joint correlated with radiological morphology of temporomandibular disorders[J]. Br J Oral Maxillofac Surg, 2015, 53(2):114-120.
    [8] Nitzan DW, Goldfarb A, Gati I, et al. Changes in the reducing power of synovial fluid from temporomandibular joints with'anchored disc phenomenon'[J]. J Oral Maxillofac Surg, 2002, 60(7):735-740.
    [9] Rodriguez de Sotillo D, Velly AM, Hadley M, et al.Evidence of oxidative stress in temporomandibular disorders:a pilot study[J]. J Oral Rehabil, 2011, 38(10):722-728.
    [10] Yamaza T, Masuda KF, Atsuta I, et al. Oxidative stress-induced DNA damage in the synovial cells of the temporomandibular joint in the rat[J]. J Dent Res,2004, 83(8):619-624.
    [11] Ueno T, Yamada M, Sugita Y,et al. N-acetyl cysteine protects TMJ chondrocytes from oxidative stress[J].J Dent Res, 2011, 90(3):353-359.
    [12] Lecarpentier Y. Physiological role of free radicals in skeletal muscles[J]. J Appl Physiol(1985),2007, 103(6):1917-1918.
    [13] Magalhaes J,Ascensao A,Soares JM, et al. Acute and severe hypobaric hypoxia increases oxidative stress and impairs mitochondrial function in mouse skeletal muscle[J]. J Appl Physiol(1985), 2005, 99(4):1247-1253.
    [14] Cui M,Li Q,Zhang M,et al. Long-term curcumin treatment antagonizes masseter muscle alterations induced by chronic unpredictable mild stress in rats[J]. Arch Oral Biol, 2014, 59(3):258-267.
    [15] Iyomasa MM, Fernandes FS, Iyomasa DM, et al.Metabolic changes in masseter muscle of rats submitted to acute stress associated with exodontia[J].PLoS One, 2015, 10(6):e0128397.
    [16] Loyola BM, Nascimento GC, Fernandez RA, et al.Chronic stress effects in contralateral medial pterygoid muscle of rats with occlusion alteration[J].Physiol Behav, 2016, 164(PtA):369-375.
    [17] Powers SK,Smuder AJ,Judge AR. Oxidative stressand disuse muscle atrophy:cause or consequence[J].Curr Opin Clin Nutr Metab Care, 2012, 15(3):240-245.
    [18] Spassov A, Gredes T, Gedrange T, et al. Increased oxidative stress in dystrophin deficient(mdx)mice masticatory muscles[J]. Exp Toxicol Pathol, 2011,63(6):549-552.
    [19] Gedrange T, Lupp A, Walter B, et al. Oxidative state and histological changes in muscles of mastication after conditioning training[J]. Exp Toxicol Pathol,2001,53(1):89-96.
    [20] Steinbacher P, Eckl P. Impact of oxidative stress on exercising skeletal muscle[J]. Biomolecules, 2015,5(2):356-377.
    [21] Debold EP. Potential molecular mechanisms underlying muscle fatigue mediated by reactive oxygen and nitrogen species[J]. Front Physiol, 2015, 6:239.
    [22]沈妍欣,郭淑娟,吴亚菲.慢性牙周炎的氧化应激及抗氧化治疗研究进[J].中华口腔医学杂志,2016, 51(7):442-446.Shen YX, Guo SJ, Wu YF. Oxidative stress and antioxitant therapy of chronic periodontitis[J]. Chin J Stomatol,2016, 51(7):442-446.
    [23] Liu Z, Liu Y, Song Y, et al. Systemic oxidative stress biomarkers in chronic periodontitis:a meta-analysis[J]. Dis Markers, 2014, 2014:931083.
    [24] Biju T, Shabeer MM, Amitha R, et al. Comparative evaluation of serum superoxide dismutase and glutathione levels in periodontally diseased patients:an interventional study[J]. Indian J Dent Res, 2014, 25(5):613-616.
    [25] Oktay S, Chukkapalli SS, Rivera-Kweh MF, et al.Periodontitis in rats induces systemic oxidative stress that is controlled by bone-targeted antiresorptives[J].J Periodontol, 2015, 86(1):137-145.
    [26] Wu W,Yang N,Feng X,et al. Effect of vitamin C administration on hydrogen peroxide-induced cytotoxicity in periodontal ligament cells[J]. Mol Med Rep, 2015, 11(1):242-248.
    [27] Waddington RJ,Moseley R,Embery G. Reactive oxygen species:a potential role in the pathogenesis of periodontal diseases[J]. Oral Dis, 2000, 6(3):138-151.
    [28] Golz L, Memmert S, Rath-Deschner B, et al. LPSfrom P. gingivalis and hypoxia increases oxidative stress in periodontal ligament fibroblasts and contributes to periodontitis[J]. Mediators Inflamm, 2014,2014:986264.
    [29] Korde SD, Basak A, Chaudhary M, et al. Enhanced nitrosative and oxidative stress with decreased total antioxidant capacity in patients with oral precancer and oral squamous cell carcinoma[J]. Oncology, 2011,80(5/6):382-389.
    [30] Choudhari SK, Chaudhary M, Gadbail AR, et al.Oxidative and antioxidative mechanisms in oral cancer and precancer:a review[J]. Oral Oncol, 2014,50(1):10-18.
    [31] Agha-Hosseini F, Mirzaii-Dizgah I, Farmanbar N, et al. Oxidative stress status and DNA damage in saliva of human subjects with oral lichen planus and oral squamous cell carcinoma[J]. J Oral Pathol Med,2012,41(10):736-740.
    [32] Bose KS, Vyas P, Singh M. Plasma non-enzymatic antioxidants-vitamin C, E,β-carotenes, reduced glutathione levels and total antioxidant activity in oral sub mucous fibrosis[J]. Eur Rev Med Pharmacol Sci,2012, 16(4):530-532.
    [33] Chitra S, Balasubramaniam M, Hazra J. Effect ofa-tocopherol on salivary reactive oxygen species and trace elements in oral submucous fibrosis[J]. Ann Clin Biochem, 2012, 49(Pt 3):262-265.
    [34] Li B, Lu M, Jiang XX, et al. Inhibiting reactive oxygen species-dependent autophagy enhanced baicaleininduced apoptosis in oral squamous cell carcinoma[J]. J Nat Med, 2017, 71(2):433-441.
    [35] Qin X,Kuang H, Chen L, et al. Coexpression of growth differentiation factor 11 and reactive oxygen species in metastatic oral cancer and its role in inducing the epithelial to mesenchymal transition[J].Oral Surg Oral Med Oral Pathol Oral Radiol, 2017,123(6):697-706.
    [36] Lee SS, Tsai CH, Tsai LL, et al.β-catenin expression in areca quid chewing-associated oral squamous cell carcinomas and upregulated by arecoline in human oral epithelial cells[J]. J Formos Med Assoc, 2012,111(4):194-200.
    [37] Lee SS, Tsai CH, Yang SF, et al. Hypoxia inducible factor-la expression in areca quid chewing-associated oral squamous cell carcinomas[J]. Oral Dis,2010, 16(7):696-701.

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