国际口腔医学杂志 ›› 2017, Vol. 44 ›› Issue (6): 664-668.doi: 10.7518/gjkq.2017.06.008

• 牙周专栏 • 上一篇    下一篇

炎性衰老在糖尿病牙周炎中的作用机制及研究现状

张鹏1, 丁一2, 王琪1   

  1. 1.口腔疾病研究国家重点实验室 国家口腔疾病临床医学研究中心,四川大学华西口腔医院修复科 成都 610041;
    2.口腔疾病研究国家重点实验室 国家口腔疾病临床医学研究中心,四川大学华西口腔医院牙周病科 成都 610041
  • 收稿日期:2017-04-10 修回日期:2017-08-15 出版日期:2017-11-01 发布日期:2017-11-01
  • 通讯作者: 王琪,副教授,博士,Email:wqinno8751@gmail.com
  • 作者简介:张鹏,硕士,Email:pengno1@qq.com
  • 基金资助:
    国家自然科学基金(81200794); 成都市国际科技合作项目(2015-GH02-00035-HZ)

Research on the role of inflammaging in diabetes mellitus-associated periodontitis

Zhang Peng1, Ding Yi2, Wang Qi1   

  1. 1. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Dept. of Prosthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China;
    2. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Dept. of Periodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
  • Received:2017-04-10 Revised:2017-08-15 Online:2017-11-01 Published:2017-11-01
  • Supported by:
    This study was supported by National Natural Science Foundation of China(81200794) and International Cooperation Project of Chengdu Municipal Science and Technology Bureau(2015-GH02-00035-HZ).

摘要: 糖尿病牙周炎近来被认为是一种衰老相关疾病,其预防和控制是临床治疗的难点。炎性衰老目前被发现是糖尿病并发症发生和发展的重要因素。本文就炎性衰老及其在糖尿病牙周炎中潜在作用机制进行综述,为研究糖尿病患者牙周炎发生发展的机制和治疗方法提供新的思路。

关键词: 糖尿病牙周炎, 炎性衰老, 氧化应激, 炎性细胞因子, DNA损伤, 自噬

Abstract: Diabetes mellitus-associated periodontitis is a common age-related disease. However, methods for the prevention and treatment of this disease need further development. Inflammaging has been recently raised as an important factor in the occurrence and development of diabetic complications. This paper reviewed the relevant literature about the research and mechanism on the role of inflammaging in diabetes mellitus-associated periodontitis and provided the new approach for pathogenesis and treatment of periodontitis inpatients with diabetes.

Key words: diabetes mellitus-associated periodontitis, inflammaging, oxidative stress, inflammatory cytokines, DNA damage, autophagy

中图分类号: 

  • R781.4
[1] Teeuw WJ, Kosho MX, Poland DC, et al. Periodon-titis as a possible early sign of diabetes mellitus[J]. BMJ Open Diabetes Res Care, 2017, 5(1):e000326.
[2] Chapple IL, Genco R. Diabetes and periodontal diseases: consensus report of the joint EFP/AAP workshop on periodontitis and systemic diseases[J]. J Clin Periodontol, 2013, 40(Suppl 14):S106-S112.
[3] Prattichizzo F, De Nigris V, La Sala L, et al. “In-flammaging” as a druggable target: a senescence-associated secretory phenotype-centered view of type 2 diabetes[J]. Oxid Med Cell Longev, 2016, 2016:1810327.
[4] Franceschi C, Bonafè M, Valensin S, et al. Inflamm-aging. An evolutionary perspective on immuno-senescence[J]. Ann N Y Acad Sci, 2000, 908:244- 254.
[5] 夏世金, 孙涛, 郑松柏, 等. 炎性衰老的研究[J]. 成都医学院学报, 2012, 7(3):336-343.
Xia SJ, Sun T, Zheng SB, et al. Research of inflam-maging[J]. J Chengdu Med Col, 2012, 7(3):336-343.
[6] Childs BG, Durik M, Baker DJ, et al. Cellular sene-scence in aging and age-related disease: from me-chanisms to therapy[J]. Nat Med, 2015, 21(12):1424- 1435.
[7] Johnson SC, Dong X, Vijg J, et al. Genetic evidence for common pathways in human age-related diseases [J]. Aging Cell, 2015, 14(5):809-817.
[8] Xia S, Zhang X, Zheng S, et al. An update on in-flamm-aging: mechanisms, prevention, and treat-ment[J]. J Immunol Res, 2016, 2016:8426874.
[9] De la Fuente M, Miquel J. An update of the oxida-tion-inflammation theory of aging: the involvement of the immune system in oxi-inflamm-aging[J]. Curr Pharm Des, 2009, 15(26):3003-3026.
[10] Cannizzo ES, Clement CC, Sahu R, et al. Oxidative stress, inflamm-aging and immunosenescence[J]. J Proteomics, 2011, 74(11):2313-2323.
[11] Marchal J, Pifferi F, Aujard F. Resveratrol in ma-mmals: effects on aging biomarkers, age-related diseases, and life span[J]. Ann N Y Acad Sci, 2013, 1290:67-73.
[12] Adams AA, Breathnach CC, Katepalli MP, et al. Advanced age in horses affects divisional history of T cells and inflammatory cytokine production[J]. Mech Ageing Dev, 2008, 129(11):656-664.
[13] Michaud M, Balardy L, Moulis G, et al. Proinflam-matory cytokines, aging, and age-related diseases[J]. J Am Med Dir Assoc, 2013, 14(12):877-882.
[14] Minciullo PL, Catalano A, Mandraffino G, et al. Inflammaging and anti-inflammaging: the role of cytokines in extreme longevity[J]. Arch Immunol Ther Exp(Warsz), 2016, 64(2):111-126.
[15] Bartek J, Hodny Z, Lukas J. Cytokine loops driving senescence[J]. Nat Cell Biol, 2008, 10(8):887-889.
[16] Watanabe S, Kawamoto S, Ohtani N, et al. Impact of senescence-associated secretory phenotype and its potential as a therapeutic target for senescence-associated diseases[J]. Cancer Sci, 2017, 108(4):563- 569.
[17] Choubey D, Panchanathan R. IFI16, an amplifier of DNA-damage response: role in cellular senescence and aging-associated inflammatory diseases[J]. Ageing Res Rev, 2016, 28:27-36.
[18] Olivieri F, Albertini MC, Orciani M, et al. DNA damage response(DDR) and senescence: shuttled inflamma-miRNAs on the stage of inflamm-aging[J]. Oncotarget, 2015, 6(34):35509-35521.
[19] Bonafè M, Storci G, Franceschi C. Inflamm-aging of the stem cell niche: breast cancer as a paradigmatic example: breakdown of the multi-shell cytokine net-work fuels cancer in aged people[J]. Bioessays, 2012, 34(1):40-49.
[20] Levine B, Mizushima N, Virgin HW. Autophagy in immunity and inflammation[J]. Nature, 2011, 469 (7330):323-335.
[21] Juhász G, Erdi B, Sass M, et al. Atg7-dependent autophagy promotes neuronal health, stress tolerance, and longevity but is dispensable for metamorphosis in drosophila[J]. Genes Dev, 2007, 21(23):3061- 3066.
[22] Salminen A, Kaarniranta K, Kauppinen A. Inflamm-aging: disturbed interplay between autophagy and inflammasomes[J]. Aging(Albany NY), 2012, 4(3): 166-175.
[23] Eke PI, Dye BA, Wei L, et al. Update on prevalence of periodontitis in adults in the United States: NHANES 2009 to 2012[J]. J Periodontol, 2015, 86 (5):611-622.
[24] Huang ES, Laiteerapong N, Liu JY, et al. Rates of complications and mortality in older patients with diabetes mellitus: the diabetes and aging study[J]. JAMA Intern Med, 2014, 174(2):251-258.
[25] Patil VS, Patil VP, Gokhale N, et al. Chronic perio-dontitis in type 2 diabetes mellitus: oxidative stress as a common factor in periodontal tissue injury[J]. J Clin Diagn Res, 2016, 10(4):BC12-BC16.
[26] Pradeep AR, Agarwal E, Bajaj P, et al. 4-Hydroxy-2-nonenal, an oxidative stress marker in crevicular fluid and serum in type 2 diabetes with chronic periodontitis[J]. Contemp Clin Dent, 2013, 4(3):281- 285.
[27] Preshaw PM, Alba AL, Herrera D, et al. Periodontitis and diabetes: a two-way relationship[J]. Diabetolo-gia, 2012, 55(1):21-31.
[28] Mesia R, Gholami F, Huang H, et al. Systemic in-flammatory responses in patients with type 2 dia-betes with chronic periodontitis[J]. BMJ Open Dia-betes Res Care, 2016, 4(1):e000260.
[29] Sriram S, Subramanian S, Juvvuna PK, et al. Myos-tatin induces DNA damage in skeletal muscle of streptozotocin-induced type 1 diabetic mice[J]. J Biol Chem, 2014, 289(9):5784-5798.
[30] Öngöz Dede F, Bozkurt Doğan Ş, Ballı U, et al. The effect of initial periodontal treatment on plasma, gingival crevicular fluid and salivary levels of 8-hydroxy-deoxyguanosine in obesity[J]. Arch Oral Biol, 2016, 62:80-85.
[31] Ayilavarapu S, Kantarci A, Hasturk H, et al. IPLA2 mRNA expression by human neutrophils in type 2 diabetes and chronic periodontitis[J]. J Int Acad Periodontol, 2014, 16(4):121-126.
[32] 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 Med, 2012, 10:122.
[33] Qian M, Fang X, Wang X. Autophagy and in-flammation[J]. Clin Transl Med, 2017, 6(1):24.
[34] Tang D, Kang R, Livesey KM, et al. Endogenous HMGB1 regulates autophagy[J]. J Cell Biol, 2010, 190(5):881-892.
[35] Wang Y, Li YB, Yin JJ, et al. Autophagy regulates inflammation following oxidative injury in diabetes [J]. Autophagy, 2013, 9(3):272-277.
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