Int J Stomatol

Inter J Stomatol ›› 2017, Vol. 44 ›› Issue (6): 642-646.doi: 10.7518/gjkq.2017.06.004

• Microbiology • Previous Articles     Next Articles

Research progress on the relationship of periodontal microbes and metabolic syndrome

He Linlin, Yang Zhuo, Liu Chengcheng, Ding Yi.   

  1. 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:2016-11-29 Revised:2017-07-09 Online:2017-11-01 Published:2017-11-01
  • Supported by:
    This work was supported by National Natural Science Foundation of China(81600871), National Key Clinical Specialist Foundation(2010) and The Scientific Research Foundation for Young Teachers, Sichuan University(2016SCU11056).

RichHTML

10

PDF (PC)

255

Abstract: A metabolic syndrome is characterized by symptoms of metabolic disorders, such as proteins, fats, and carbohydrates associated with increased risks of cardiovascular diseases and diabetes mellitus. Recent evidence has proposed the relationship between periodontitis and metabolic syndrome. In this review, progress on the role of inflammation and oxidative stress and the relationship of oral microbes with the main characteristics of metabolic syndrome is presented to provide new insights into the prevention and intervention of metabolic syndrome.

Key words: periodontal microbiome, metabolic syndrome, hyperlipidemia, prothrombotic state, insulin resistance, proinflammatory state, abdominal obesity

CLC Number: 

  • R37

TrendMD: 
[1] Savage DC. Microbial ecology of the gastrointestinal tract[J]. Annu Rev Microbiol, 1977, 31:107-133.
[2] Avila M, Ojcius DM, Yilmaz O. The oral microbiota: living with a permanent guest[J]. DNA Cell Biol, 2009, 28(8):405-411.
[3] Hajishengallis G. Periodontitis: from microbial im-mune subversion to systemic inflammation[J]. Nat Rev Immunol, 2015, 15(1):30-44.
[4] Hussain M, Stover CM, Dupont A. P. gingivalis in periodontal disease and atherosclerosis—scenes of action for antimicrobial peptides and complement[J]. Front Immunol, 2015, 6:45.
[5] Inaba H, Sugita H, Kuboniwa M, et al. Porphyromonas gingivalis promotes invasion of oral squamous cell carcinoma through induction of proMMP9 and its activation[J]. Cell Microbiol, 2014, 16(1):131-145.
[6] Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease[J]. Diabetes, 1988, 37 (12):1595-1607.
[7] Oda E. Metabolic syndrome: its history, mechanisms, and limitations[J]. Acta Diabetol, 2012, 49(2):89-95.
[8] Grundy SM, Brewer HB Jr, Cleeman JI, et al. De-finition of metabolic syndrome: report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition[J]. Circulation, 2004, 109(3):433-438.
[9] Friend A, Craig L, Turner S. The prevalence of me-tabolic syndrome in children: a systematic review of the literature[J]. Metab Syndr Relat Disord, 2013, 11 (2):71-80.
[10] Saxlin T, Suominen-Taipale L, Kattainen A, et al. Association between serum lipid levels and perio-dontal infection[J]. J Clin Periodontol, 2008, 35(12): 1040-1047.
[11] Awartani F, Atassi F. Evaluation of periodontal status in subjects with hyperlipidemia[J]. J Contemp Dent Pract, 2010, 11(2):33-40.
[12] Fentoğlu O, Sözen T, Oz SG, et al. Short-term effects of periodontal therapy as an adjunct to anti-lipemic treatment[J]. Oral Dis, 2010, 16(7):648-654.
[13] 马丽, 潘亚萍, 张建全. 2型糖尿病伴慢性牙周炎患者牙周可疑致病菌的定植研究[J]. 上海口腔医学, 2010, 19(6):611-615.
Ma L, Pan YP, Zhang JQ. Study of putative perio-dontal pathogens colonies in type 2 diabetes with chronic periodontitis[J]. Shanghai J Stomatol, 2010, 19(6):611-615.
[14] 李厚轩, 雷浪, 陈帅, 等. 高脂血症促进载脂蛋白E基因敲除小鼠牙周炎进展的实验研究[J]. 福建医科大学学报, 2012, 46(2):77-80.
Li HX, Lei L, Chen S, et al. Effect of hyperlipidemia on periodontitis progress in apolipoprotein E knockout mice[J]. J Fujian Med Univ, 2012, 46(2):77-80.
[15] Blasco-Baque V, Serino M, Vergnes JN, et al. High-fat diet induces periodontitis in mice through lipopo-lysaccharides(LPS) receptor signaling: protective action of estrogens[J]. PLoS One, 2012, 7(11):e48220.
[16] Doxey DL, Nares S, Park B, et al. Diabetes-induced impairment of macrophage cytokine release in a rat model: potential role of serum lipids[J]. Life Sci, 1998, 63(13):1127-1136.
[17] Fentoğlu Ö, Köroğlu BK, Hiçyılmaz H, et al. Pro-inflammatory cytokine levels in association between periodontal disease and hyperlipidaemia[J]. J Clin Periodontol, 2011, 38(1):8-16.
[18] Wada H. Pre-thrombotic(hypercoagulable) state/hypercoagulable disease[J]. Rinsho Byori, 2015, 63 (12):1405-1411.
[19] Sharma A, Novak EK, Sojar HT, et al. Porphyro - monas gingivalis platelet aggregation activity: outer membrane vesicles are potent activators of murine platelets[J]. Oral Microbiol Immunol, 2000, 15(6): 393-396.
[20] Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis[J]. Circulation, 2002, 105(9):1135- 1143.
[21] Al Batran R, Al-Bayaty F, Al-Obaidi MM, et al. Evaluation of the effect of andrographolide on athe-rosclerotic rabbits induced by Porphyromonas gin-givalis [J]. Biomed Res Int, 2014, (11):724718.
[22] Mahendra J, Mahendra L, Felix J, et al. Genetic analysis of Porphyromonas gingivalis (fimA), Aggre - gatibacter actinomycetemcomitans , and red complex in coronary plaque[J]. J Investig Clin Dent, 2014, 5(3):201-207.
[23] Figuero E, Sánchez-Beltrán M, Cuesta-Frechoso S, et al. Detection of periodontal bacteria in atheroma-tous plaque by nested polymerase chain reaction[J]. J Periodontol, 2011, 82(10):1469-1477.
[24] Amar S, Wu SC, Madan M. Is Porphyromonas gin-givalis cell invasion required for atherogenesis Pharmacotherapeutic implications[J]. J Immunol, 2009, 182(3):1584-1592.
[25] Jia R, Kurita-Ochiai T, Oguchi S, et al. Periodontal pathogen accelerates lipid peroxidation and athero-sclerosis[J]. J Dent Res, 2013, 92(3):247-252.
[26] Lamont RJ, Hajishengallis G. Polymicrobial synergy and dysbiosis in inflammatory disease[J]. Trends Mol Med, 2015, 21(3):172-183.
[27] Hajishengallis G. Periodontitis: from microbial im-mune subversion to systemic inflammation[J]. Nat Rev Immunol, 2015, 15(1):30-44.
[28] Bhat UG, Ilievski V, Unterman TG, et al. Porphyro - monas gingivalis lipopolysaccharide upregulates insulin secretion from pancreatic β cell line MIN6[J]. J Periodontol, 2014, 85(11):1629-1636.
[29] Blasco-Baque V, Garidou L, Pomié C, et al. Perio-dontitis induced by Porphyromonas gingivalis drives periodontal microbiota dysbiosis and insulin resis-tance via an impaired adaptive immune response[J]. Gut, 2017, 66(5):872-885.
[30] Geurts L, Lazarevivc V, Derrien M, et al. Altered gut microbiota and endocannabinoid system tone in obese and diabetic leptin-resistant mice: impact on apelin regulation in adipose tissue[J]. Front Micro-biol, 2011, 2(2):149.
[31] Matsushita K, Hamaguchi M, Hashimoto M, et al. The novel associat ion between red complex of oral microbe and body mass index in healthy Japanese: a population based cross-sectional study[J]. J Clin Biochem Nutr, 2015, 57(2):135-139.
[32] Bjerke W. The impact of infectious disease on chronic disease: a review of contemporary findings[J]. J Soc Behav Health Sci, 2011, 5(1):45-57.
[33] Rosen HR. Clinical practice. Chronic hepatitis C infection[J]. N Engl J Med, 2011, 364(25):2429- 2438.
[34] Amar S, Zhou Q, Shaik-Dasthagirisaheb Y, et al. Diet-induced obesity in mice causes changes in immune responses and bone loss manifested by bacterial challenge[J]. Proc Natl Acad Sci U S A, 2007, 104(51): 20466-20471.
[35] Richard G, Trivedi N, Belta C, et al. Partial restora-tion of macrophage alteration from diet-induced obesity in response to Porphyromonas gingivalis infection[J]. PLoS One, 2013, 8(7):e70320.
[36] Holden JA, Attard TJ, Laughton KM, et al. Por - phyromonas gingivalis lipopolysaccharide weakly activates M1 and M2 polarized mouse macrophages but induces inflammatory cytokines[J]. Infect Immun, 2014, 82(10):4190-4203.
[37] Poletto AC, Furuya DT, David-Silva A, et al. Oleic and linoleic fatty acids downregulate Slc2a4/GLUT4 expression via NFKB and SREBP1 in skeletal muscle cells[J]. Mol Cell Endocrinol, 2015, 401:65-72.
[38] Han CY. Roles of reactive oxygen species on insulin resistance in adipose tissue[J]. Diabetes Metab J, 2016, 40(4):272-279.
[39] Rani V, Deep G, Singh RK, et al. Oxidative stress and metabolic disorders: pathogenesis and thera-peutic strategies[J]. Life Sci, 2016, 148:183-193.
[40] Paudel KR, Panth N, Kim DW. Circulating endothe-lial microparticles: a key hallmark of atherosclerosis progression[J]. Scientifica, 2016, 2016:8514056.
[1] Lü Chunxu, Sun Qinfeng. Correlation and mechanism between periodontitis and hyperlipidemia [J]. Inter J Stomatol, 2013, 40(5): 612-615.
[2] ZHANG Lin, WU Ya- fei. Review of the r esear ch of concerning mechanisms between diabetes mellitus and p [J]. Inter J Stomatol, 2008, 35(3): 295-295～297，300.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
[1] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[2] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[3] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[4] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[5] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[6] . [J]. Foreign Med Sci: Stomatol, 1999, 26(04): .
[7] . [J]. Foreign Med Sci: Stomatol, 2005, 32(06): 458 -460 .
[8] . [J]. Foreign Med Sci: Stomatol, 2005, 32(06): 452 -454 .
[9] . [J]. Inter J Stomatol, 2008, 35(S1): .
[10] . [J]. Inter J Stomatol, 2008, 35(S1): .