口腔微生物群与牙周病
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摘要
口腔微生物群作为人体微生物群的重要组成部分,种类繁多、组成复杂,其组成和比例与各类口腔疾病密切相关。牙周炎是一种多微生物的复合感染,它由口腔内微生物群中潜在的致病微生物丰度增加引起,这些微生物通过介导炎症反应及调节口腔微生物群的基础营养环境而致病。本文综述了近年来口腔微生物群与牙周疾病之间的关系及相关影响因素,并分析了目前牙周病微生物群研究的挑战与瓶颈,为将微生物群作为预防、诊断和治疗牙周相关疾病的生物标记物并进一步应用于临床提供理论基础。
As an important part of microbial community of human body, oral microflora is composed of a wide variety of microorganisms with different proportions which are closely related to all kinds of oral diseases. Periodontitis is a multiple infection with multiple microorganisms. It is caused by the increase in abundance of potential pathogenic microorganisms in oral microflora, and these microorganisms are responsible for mediating inflammatory reactions and regulating nutritional environment of oral microflora. This article will clarify the relationship between oral microflora and periodontal diseases, explore the related influencing factors, and analyze the challenges and bottlenecks in the study on periodontal microflora, with the purpose of providing further foundation to use microbial community as a biomarker for the prevention, diagnosis and treatment of periodontal diseases.
As an important part of microbial community of human body, oral microflora is composed of a wide variety of microorganisms with different proportions which are closely related to all kinds of oral diseases. Periodontitis is a multiple infection with multiple microorganisms. It is caused by the increase in abundance of potential pathogenic microorganisms in oral microflora, and these microorganisms are responsible for mediating inflammatory reactions and regulating nutritional environment of oral microflora. This article will clarify the relationship between oral microflora and periodontal diseases, explore the related influencing factors, and analyze the challenges and bottlenecks in the study on periodontal microflora, with the purpose of providing further foundation to use microbial community as a biomarker for the prevention, diagnosis and treatment of periodontal diseases.
引文
[1] Yamanaka W,Takeshita T,Shibata Y,et al.Compositional stability of a salivary bacterial population against supragingival microbiota shift following periodontal therapy[J].PLoS One,2012,7(8):e42806.
[2] Reinhardt RA,McDonald TL,Bolton RW,et al.IgG subclasses in gingival crevicular fluid from active versus stable periodontal sites[J].J Periodontol,1989,60(1):44-50.
[3] Hajishengallis G.Immunomicrobial pathogenesis of periodontitis:keystones,pathobionts,and host response[J].Trends Immunol,2014,35(1):3-11.
[4] Wang J,Qi J,Zhao H,et al.Metagenomic sequencing reveals microbiota and its functional potential associated with periodontal disease[J].Sci Rep,2013,3:1843.
[5] Socransky SS,Haffajee AD,Cugini MA,et al.Microbial complexes in subgingival plaque[J].J Clin Periodontol,1998,25(2):134-144.
[6] Lepp PW,Brinig MM,Ouverney CC,et al.Methanogenic archaea and human periodontal disease[J].Proc Natl Acad Sci U S A,2004,101(16):6176-6181.
[7] Mikx FH.Environmental effects on the growth and proteolysis of Treponema denticola ATCC 33520[J].Oral Microbiol Immunol,1997,12(4):249-253.
[8] Slots J.Human viruses in periodontitis[J].Periodontol 2000,2010,53(1):89-110.
[9] Zijnge V,van Leeuwen MB,Degener JE,et al.Oral biofilm architecture on natural teeth[J].PLoS One,2010,5(2):e9321.
[10] Valm AM,Mark Welch JL,Rieken CW,et al.Systems-level analysis of microbial community organization through combinatorial labeling and spectral imaging[J].Proc Natl Acad Sci U S A,2011,108(10):4152-4157.
[11] Griffen AL,Beall CJ,Campbell JH,et al.Distinct and complex bacterial profiles in human periodontitis and health revealed by 16S pyrosequencing[J].ISME J,2012,6(6):1176-1185.
[12] Ge X,Rodriguez R,Trinh M,et al.Oral microbiome of deep and shallow dental pockets in chronic periodontitis[J].PLoS One,2013,8(6):e65520.
[13] Dennison DK,Van Dyke TE.The acute inflammatory response and the role of phagocytic cells in periodontal health and disease[J].Periodontol 2000,1997,14:54-78.
[14] Yamazaki K,Yoshie H,Seymour GJ.T cell regulation of the immune response to infection in periodontal diseases[J].Histol Histopathol,2003,18(3):889-896.
[15] Gamonal J,Acevedo A,Bascones A,et al.Levels of interleukin-1 beta,-8,and -10 and RANTES in gingival crevicular fluid and cell populations in adult periodontitis patients and the effect of periodontal treatment[J].J Periodontol,2000,71(10):1535-1545.
[16] Berglundh T,Donati M.Aspects of adaptive host response in periodontitis[J].J Clin Periodontol,2005,32(Suppl 6):87-107.
[17] Teng YT.The role of acquired immunity and periodontal disease progression[J].Crit Rev Oral Biol Med,2003,14(4):237-252.
[18] Eskan MA,Jotwani R,Abe T,et al.The leukocyte integrin antagonist Del-1 inhibits IL-17-mediated inflammatory bone loss[J].Nat Immunol,2012,13(5):465-473.
[19] Baker PJ,Dixon M,Evans RT,et al.CD4(+) T cells and the proinflammatory cytokines gamma interferon and interleukin-6 contribute to alveolar bone loss in mice[J].Infect Immun,1999,67(6):2804-2809.
[20] Baker PJ,Garneau J,Howe L,et al.T-cell contributions to alveolar bone loss in response to oral infection with Porphyromonas gingivalis[J].Acta Odontol Scand,2001,59(4):222-225.
[21] Takahashi K,Azuma T,Motohira H,et al.The potential role of interleukin-17 in the immunopathology of periodontal disease[J].J Clin Periodontol,2005,32(4):369-374.
[22] Bittner-Eddy PD,Fischer LA,Costalonga M.Identification of gingipain-specific I-A(b) -restricted CD4+ T cells following mucosal colonization with Porphyromonas gingivalis in C57BL/6 mice[J].Mol Oral Microbiol,2013,28(6):452-466.
[23] Costalonga M,Bittner-Eddy PD,Fischer L.Gingipain-specific Th17 do not sustain anti-Porphyromonas gingivalis IgGs[J].J Dent Res,2013:92.
[24] Rovin S,Costich ER,Gordon HA.The influence of bacteria and irritation in the initiation of periodontal disease in germfree and conventional rats[J].J Periodontal Res,1966,1(3):193-204.
[25] Colombo AP,Bennet S,Cotton SL,et al.Impact of periodontal therapy on the subgingival microbiota of severe periodontitis:comparison between good responders and individuals with refractory periodontitis using the human oral microbe identification microarray[J].J Periodontol,2012,83(10):1279-1287.
[26] Darveau RP,Hajishengallis G,Curtis MA.Porphyromonas gingivalis as a potential community activist for disease[J].J Dent Res,2012,91(9):816-820.
[27] Hajishengallis G,Lambris JD.Microbial manipulation of receptor crosstalk in innate immunity[J].Nat Rev Immunol,2011,11(3):187-200.
[28] Hajishengallis G,Liang S,Payne MA,et al.Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement[J].Cell Host Microbe,2011,10(5):497-506.
[29] Hajishengallis G,Lamont RJ.Beyond the red complex and into more complexity:the polymicrobial synergy and dysbiosis(PSD) model of periodontal disease etiology[J].Mol Oral Microbiol,2012,27(6):409-419.
[30] Liang S,Krauss JL,Domon H,et al.The C5a receptor impairs IL-12-dependent clearance of Porphyromonas gingivalis and is required for induction of periodontal bone loss[J].J Immunol,2011,186(2):869-877.
[31] Hajishengallis G,Wang M,Liang S,et al.Pathogen induction of CXCR4/TLR2 cross-talk impairs host defense function[J].Proc Natl Acad Sci U S A,2008,105(36):13532-13537.
[32] Harokopakis E,Hajishengallis G.Integrin activation by bacterial fimbriae through a pathway involving CD14,Toll-like receptor 2,and phosphatidylinositol-3-kinase[J].Eur J Immunol,2005,35(4):1201-1210.
[33] Sendide K,Reiner NE,Lee JS,et al.Cross-talk between CD14 and complement receptor 3 promotes phagocytosis of mycobacteria:regulation by phosphatidylinositol 3-kinase and cytohesin-1[J].J Immunol,2005,174(7):4210-4219.
[34] Hajishengallis G,Shakhatreh MA,Wang M,et al.Complement receptor 3 blockade promotes IL-12-mediated clearance of Porphyromonas gingivalis and negates its virulence in vivo[J].J Immunol,2007,179(4):2359-2367.
[35] Jiao Y,Darzi Y,Tawaratsumida K,et al.Induction of bone loss by pathobiont-mediated Nod1 signaling in the oral cavity[J].Cell Host Microbe,2013,13(5):595-601.
[36] You M,Mo S,Leung WK,et al.Comparative analysis of oral treponemes associated with periodontal health and disease[J].BMC Infect Dis,2013,13:174.
[37] Abusleme L,Dupuy AK,Dutzan N,et al.The subgingival microbiome in health and periodontitis and its relationship with community biomass and inflammation[J].ISME J,2013,7(5):1016-1025.
[38] Haubek D.The highly leukotoxic JP2 clone of Aggregatibacter actinomycetemcomitans:evolutionary aspects,epidemiology and etiological role in aggressive periodontitis[J].APMIS,2010,118(suppl 130):1-53.
[39] Meng H,Xu L,Li Q,et al.Determinants of host susceptibility in aggressive periodontitis[J].Periodontol 2000,2007,43:133-159.
[40] Haubek D,Ennibi OK,Poulsen K,et al.Risk of aggressive periodontitis in adolescent carriers of the JP2 clone of Aggregatibacter(Actinobacillus) actinomycetemcomitans in Morocco:a prospective longitudinal cohort study[J].Lancet,2008,371(9608):237-242.
[41] Fine DH,Markowitz K,Furgang D,et al.Aggregatibacter actinomycetemcomitans and its relationship to initiation of localized aggressive periodontitis:longitudinal cohort study of initially healthy adolescents[J].J Clin Microbiol,2007,45(12):3859-3869.
[42] Teles R,Teles F,Frias-Lopez J,et al.Lessons learned and unlearned in periodontal microbiology[J].Periodontol 2000,2013,62(1):95-162.
[43] Michalowicz BS,Hodges JS,Pihlstrom BL.Is change in probing depth a reliable predictor of change in clinical attachment loss?[J].J Am Dent Assoc,2013,144(2):171-178.
[44] Pihlstrom BL.Measurement of attachment level in clinical trials:probing methods[J].J Periodontol,1992,63(12 Suppl):1072-1077.
[45] Vartoukian SR,Palmer RM,Wade WG.Diversity and morphology of members of the phylum "synergistetes" in periodontal health and disease[J].Appl Environ Microbiol,2009,75(11):3777-3786.
[46] Hutter G,Schlagenhauf U,Valenza G,et al.Molecular analysis of bacteria in periodontitis:evaluation of clone libraries,novel phylotypes and putative pathogens[J].Microbiology,2003,149(Pt 1):67-75.
[47] Kumar PS,Griffen AL,Moeschberger ML,et al.Identification of candidate periodontal pathogens and beneficial species by quantitative 16S clonal analysis[J].J Clin Microbiol,2005,43(8):3944-3955.
[2] Reinhardt RA,McDonald TL,Bolton RW,et al.IgG subclasses in gingival crevicular fluid from active versus stable periodontal sites[J].J Periodontol,1989,60(1):44-50.
[3] Hajishengallis G.Immunomicrobial pathogenesis of periodontitis:keystones,pathobionts,and host response[J].Trends Immunol,2014,35(1):3-11.
[4] Wang J,Qi J,Zhao H,et al.Metagenomic sequencing reveals microbiota and its functional potential associated with periodontal disease[J].Sci Rep,2013,3:1843.
[5] Socransky SS,Haffajee AD,Cugini MA,et al.Microbial complexes in subgingival plaque[J].J Clin Periodontol,1998,25(2):134-144.
[6] Lepp PW,Brinig MM,Ouverney CC,et al.Methanogenic archaea and human periodontal disease[J].Proc Natl Acad Sci U S A,2004,101(16):6176-6181.
[7] Mikx FH.Environmental effects on the growth and proteolysis of Treponema denticola ATCC 33520[J].Oral Microbiol Immunol,1997,12(4):249-253.
[8] Slots J.Human viruses in periodontitis[J].Periodontol 2000,2010,53(1):89-110.
[9] Zijnge V,van Leeuwen MB,Degener JE,et al.Oral biofilm architecture on natural teeth[J].PLoS One,2010,5(2):e9321.
[10] Valm AM,Mark Welch JL,Rieken CW,et al.Systems-level analysis of microbial community organization through combinatorial labeling and spectral imaging[J].Proc Natl Acad Sci U S A,2011,108(10):4152-4157.
[11] Griffen AL,Beall CJ,Campbell JH,et al.Distinct and complex bacterial profiles in human periodontitis and health revealed by 16S pyrosequencing[J].ISME J,2012,6(6):1176-1185.
[12] Ge X,Rodriguez R,Trinh M,et al.Oral microbiome of deep and shallow dental pockets in chronic periodontitis[J].PLoS One,2013,8(6):e65520.
[13] Dennison DK,Van Dyke TE.The acute inflammatory response and the role of phagocytic cells in periodontal health and disease[J].Periodontol 2000,1997,14:54-78.
[14] Yamazaki K,Yoshie H,Seymour GJ.T cell regulation of the immune response to infection in periodontal diseases[J].Histol Histopathol,2003,18(3):889-896.
[15] Gamonal J,Acevedo A,Bascones A,et al.Levels of interleukin-1 beta,-8,and -10 and RANTES in gingival crevicular fluid and cell populations in adult periodontitis patients and the effect of periodontal treatment[J].J Periodontol,2000,71(10):1535-1545.
[16] Berglundh T,Donati M.Aspects of adaptive host response in periodontitis[J].J Clin Periodontol,2005,32(Suppl 6):87-107.
[17] Teng YT.The role of acquired immunity and periodontal disease progression[J].Crit Rev Oral Biol Med,2003,14(4):237-252.
[18] Eskan MA,Jotwani R,Abe T,et al.The leukocyte integrin antagonist Del-1 inhibits IL-17-mediated inflammatory bone loss[J].Nat Immunol,2012,13(5):465-473.
[19] Baker PJ,Dixon M,Evans RT,et al.CD4(+) T cells and the proinflammatory cytokines gamma interferon and interleukin-6 contribute to alveolar bone loss in mice[J].Infect Immun,1999,67(6):2804-2809.
[20] Baker PJ,Garneau J,Howe L,et al.T-cell contributions to alveolar bone loss in response to oral infection with Porphyromonas gingivalis[J].Acta Odontol Scand,2001,59(4):222-225.
[21] Takahashi K,Azuma T,Motohira H,et al.The potential role of interleukin-17 in the immunopathology of periodontal disease[J].J Clin Periodontol,2005,32(4):369-374.
[22] Bittner-Eddy PD,Fischer LA,Costalonga M.Identification of gingipain-specific I-A(b) -restricted CD4+ T cells following mucosal colonization with Porphyromonas gingivalis in C57BL/6 mice[J].Mol Oral Microbiol,2013,28(6):452-466.
[23] Costalonga M,Bittner-Eddy PD,Fischer L.Gingipain-specific Th17 do not sustain anti-Porphyromonas gingivalis IgGs[J].J Dent Res,2013:92.
[24] Rovin S,Costich ER,Gordon HA.The influence of bacteria and irritation in the initiation of periodontal disease in germfree and conventional rats[J].J Periodontal Res,1966,1(3):193-204.
[25] Colombo AP,Bennet S,Cotton SL,et al.Impact of periodontal therapy on the subgingival microbiota of severe periodontitis:comparison between good responders and individuals with refractory periodontitis using the human oral microbe identification microarray[J].J Periodontol,2012,83(10):1279-1287.
[26] Darveau RP,Hajishengallis G,Curtis MA.Porphyromonas gingivalis as a potential community activist for disease[J].J Dent Res,2012,91(9):816-820.
[27] Hajishengallis G,Lambris JD.Microbial manipulation of receptor crosstalk in innate immunity[J].Nat Rev Immunol,2011,11(3):187-200.
[28] Hajishengallis G,Liang S,Payne MA,et al.Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement[J].Cell Host Microbe,2011,10(5):497-506.
[29] Hajishengallis G,Lamont RJ.Beyond the red complex and into more complexity:the polymicrobial synergy and dysbiosis(PSD) model of periodontal disease etiology[J].Mol Oral Microbiol,2012,27(6):409-419.
[30] Liang S,Krauss JL,Domon H,et al.The C5a receptor impairs IL-12-dependent clearance of Porphyromonas gingivalis and is required for induction of periodontal bone loss[J].J Immunol,2011,186(2):869-877.
[31] Hajishengallis G,Wang M,Liang S,et al.Pathogen induction of CXCR4/TLR2 cross-talk impairs host defense function[J].Proc Natl Acad Sci U S A,2008,105(36):13532-13537.
[32] Harokopakis E,Hajishengallis G.Integrin activation by bacterial fimbriae through a pathway involving CD14,Toll-like receptor 2,and phosphatidylinositol-3-kinase[J].Eur J Immunol,2005,35(4):1201-1210.
[33] Sendide K,Reiner NE,Lee JS,et al.Cross-talk between CD14 and complement receptor 3 promotes phagocytosis of mycobacteria:regulation by phosphatidylinositol 3-kinase and cytohesin-1[J].J Immunol,2005,174(7):4210-4219.
[34] Hajishengallis G,Shakhatreh MA,Wang M,et al.Complement receptor 3 blockade promotes IL-12-mediated clearance of Porphyromonas gingivalis and negates its virulence in vivo[J].J Immunol,2007,179(4):2359-2367.
[35] Jiao Y,Darzi Y,Tawaratsumida K,et al.Induction of bone loss by pathobiont-mediated Nod1 signaling in the oral cavity[J].Cell Host Microbe,2013,13(5):595-601.
[36] You M,Mo S,Leung WK,et al.Comparative analysis of oral treponemes associated with periodontal health and disease[J].BMC Infect Dis,2013,13:174.
[37] Abusleme L,Dupuy AK,Dutzan N,et al.The subgingival microbiome in health and periodontitis and its relationship with community biomass and inflammation[J].ISME J,2013,7(5):1016-1025.
[38] Haubek D.The highly leukotoxic JP2 clone of Aggregatibacter actinomycetemcomitans:evolutionary aspects,epidemiology and etiological role in aggressive periodontitis[J].APMIS,2010,118(suppl 130):1-53.
[39] Meng H,Xu L,Li Q,et al.Determinants of host susceptibility in aggressive periodontitis[J].Periodontol 2000,2007,43:133-159.
[40] Haubek D,Ennibi OK,Poulsen K,et al.Risk of aggressive periodontitis in adolescent carriers of the JP2 clone of Aggregatibacter(Actinobacillus) actinomycetemcomitans in Morocco:a prospective longitudinal cohort study[J].Lancet,2008,371(9608):237-242.
[41] Fine DH,Markowitz K,Furgang D,et al.Aggregatibacter actinomycetemcomitans and its relationship to initiation of localized aggressive periodontitis:longitudinal cohort study of initially healthy adolescents[J].J Clin Microbiol,2007,45(12):3859-3869.
[42] Teles R,Teles F,Frias-Lopez J,et al.Lessons learned and unlearned in periodontal microbiology[J].Periodontol 2000,2013,62(1):95-162.
[43] Michalowicz BS,Hodges JS,Pihlstrom BL.Is change in probing depth a reliable predictor of change in clinical attachment loss?[J].J Am Dent Assoc,2013,144(2):171-178.
[44] Pihlstrom BL.Measurement of attachment level in clinical trials:probing methods[J].J Periodontol,1992,63(12 Suppl):1072-1077.
[45] Vartoukian SR,Palmer RM,Wade WG.Diversity and morphology of members of the phylum "synergistetes" in periodontal health and disease[J].Appl Environ Microbiol,2009,75(11):3777-3786.
[46] Hutter G,Schlagenhauf U,Valenza G,et al.Molecular analysis of bacteria in periodontitis:evaluation of clone libraries,novel phylotypes and putative pathogens[J].Microbiology,2003,149(Pt 1):67-75.
[47] Kumar PS,Griffen AL,Moeschberger ML,et al.Identification of candidate periodontal pathogens and beneficial species by quantitative 16S clonal analysis[J].J Clin Microbiol,2005,43(8):3944-3955.