Microbiological and immunological characteristics of young Moroccan patients with aggressive periodontitis with and without detectable Aggregatibacter actinomycetemcomitans JP2 infection
Summary Cross‐sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis (AgP) in adolescents of northwest African descent. To gain information on why a significant part of Moroccan adolescents show clinical...
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Published in | Molecular oral microbiology Vol. 26; no. 1; pp. 35 - 51 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.02.2011
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Subjects | |
Online Access | Get full text |
ISSN | 2041-1006 2041-1014 2041-1014 |
DOI | 10.1111/j.2041-1014.2010.00593.x |
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Abstract | Summary
Cross‐sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis (AgP) in adolescents of northwest African descent. To gain information on why a significant part of Moroccan adolescents show clinical signs of periodontal disease in the absence of this pathogen we performed comprehensive mapping of the subgingival microbiota of eight young Moroccans, four of whom were diagnosed with clinical signs of AgP. The analysis was carried out by sequencing and phylogenetic analysis of a total of 2717 cloned polymerase chain reaction amplicons of the phylogenetically informative 16S ribosomal RNA gene. The analyses revealed a total of 173 bacterial taxa of which 39% were previously undetected. The JP2 clone constituted a minor proportion of the complex subgingival microbiota in patients with active disease. Rather than identifying alternative aetiologies to AgP, the recorded infection history of the subjects combined with remarkably high concentrations of antibodies against the A. actinomycetemcomitans leukotoxin suggest that disease activity was terminated in some patients with AgP as a result of elimination of the JP2 clone. This study provides information on the microbial context of the JP2 clone activity in a JP2‐susceptible population and suggests that such individuals may develop immunity to AgP. |
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AbstractList | Cross-sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis (AgP) in adolescents of northwest African descent. To gain information on why a significant part of Moroccan adolescents show clinical signs of periodontal disease in the absence of this pathogen we performed comprehensive mapping of the subgingival microbiota of eight young Moroccans, four of whom were diagnosed with clinical signs of AgP. The analysis was carried out by sequencing and phylogenetic analysis of a total of 2717 cloned polymerase chain reaction amplicons of the phylogenetically informative 16S ribosomal RNA gene. The analyses revealed a total of 173 bacterial taxa of which 39% were previously undetected. The JP2 clone constituted a minor proportion of the complex subgingival microbiota in patients with active disease. Rather than identifying alternative aetiologies to AgP, the recorded infection history of the subjects combined with remarkably high concentrations of antibodies against the A. actinomycetemcomitans leukotoxin suggest that disease activity was terminated in some patients with AgP as a result of elimination of the JP2 clone. This study provides information on the microbial context of the JP2 clone activity in a JP2-susceptible population and suggests that such individuals may develop immunity to AgP.Cross-sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis (AgP) in adolescents of northwest African descent. To gain information on why a significant part of Moroccan adolescents show clinical signs of periodontal disease in the absence of this pathogen we performed comprehensive mapping of the subgingival microbiota of eight young Moroccans, four of whom were diagnosed with clinical signs of AgP. The analysis was carried out by sequencing and phylogenetic analysis of a total of 2717 cloned polymerase chain reaction amplicons of the phylogenetically informative 16S ribosomal RNA gene. The analyses revealed a total of 173 bacterial taxa of which 39% were previously undetected. The JP2 clone constituted a minor proportion of the complex subgingival microbiota in patients with active disease. Rather than identifying alternative aetiologies to AgP, the recorded infection history of the subjects combined with remarkably high concentrations of antibodies against the A. actinomycetemcomitans leukotoxin suggest that disease activity was terminated in some patients with AgP as a result of elimination of the JP2 clone. This study provides information on the microbial context of the JP2 clone activity in a JP2-susceptible population and suggests that such individuals may develop immunity to AgP. Summary Cross‐sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis (AgP) in adolescents of northwest African descent. To gain information on why a significant part of Moroccan adolescents show clinical signs of periodontal disease in the absence of this pathogen we performed comprehensive mapping of the subgingival microbiota of eight young Moroccans, four of whom were diagnosed with clinical signs of AgP. The analysis was carried out by sequencing and phylogenetic analysis of a total of 2717 cloned polymerase chain reaction amplicons of the phylogenetically informative 16S ribosomal RNA gene. The analyses revealed a total of 173 bacterial taxa of which 39% were previously undetected. The JP2 clone constituted a minor proportion of the complex subgingival microbiota in patients with active disease. Rather than identifying alternative aetiologies to AgP, the recorded infection history of the subjects combined with remarkably high concentrations of antibodies against the A. actinomycetemcomitans leukotoxin suggest that disease activity was terminated in some patients with AgP as a result of elimination of the JP2 clone. This study provides information on the microbial context of the JP2 clone activity in a JP2‐susceptible population and suggests that such individuals may develop immunity to AgP. Cross-sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis (AgP) in adolescents of northwest African descent. To gain information on why a significant part of Moroccan adolescents show clinical signs of periodontal disease in the absence of this pathogen we performed comprehensive mapping of the subgingival microbiota of eight young Moroccans, four of whom were diagnosed with clinical signs of AgP. The analysis was carried out by sequencing and phylogenetic analysis of a total of 2717 cloned polymerase chain reaction amplicons of the phylogenetically informative 16S ribosomal RNA gene. The analyses revealed a total of 173 bacterial taxa of which 39% were previously undetected. The JP2 clone constituted a minor proportion of the complex subgingival microbiota in patients with active disease. Rather than identifying alternative aetiologies to AgP, the recorded infection history of the subjects combined with remarkably high concentrations of antibodies against the A. actinomycetemcomitans leukotoxin suggest that disease activity was terminated in some patients with AgP as a result of elimination of the JP2 clone. This study provides information on the microbial context of the JP2 clone activity in a JP2-susceptible population and suggests that such individuals may develop immunity to AgP. Cross-sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis (AgP) in adolescents of northwest African descent. To gain information on why a significant part of Moroccan adolescents show clinical signs of periodontal disease in the absence of this pathogen we performed comprehensive mapping of the subgingival microbiota of eight young Moroccans, four of whom were diagnosed with clinical signs of AgP. The analysis was carried out by sequencing and phylogenetic analysis of a total of 2717 cloned polymerase chain reaction amplicons of the phylogenetically informative 16S ribosomal RNA gene. The analyses revealed a total of 173 bacterial taxa of which 39% were previously undetected. The JP2 clone constituted a minor proportion of the complex subgingival microbiota in patients with active disease. Rather than identifying alternative aetiologies to AgP, the recorded infection history of the subjects combined with remarkably high concentrations of antibodies against the A. actinomycetemcomitans leukotoxin suggest that disease activity was terminated in some patients with AgP as a result of elimination of the JP2 clone. This study provides information on the microbial context of the JP2 clone activity in a JP2-susceptible population and suggests that such individuals may develop immunity to AgP. Cross‐sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis (AgP) in adolescents of northwest African descent. To gain information on why a significant part of Moroccan adolescents show clinical signs of periodontal disease in the absence of this pathogen we performed comprehensive mapping of the subgingival microbiota of eight young Moroccans, four of whom were diagnosed with clinical signs of AgP. The analysis was carried out by sequencing and phylogenetic analysis of a total of 2717 cloned polymerase chain reaction amplicons of the phylogenetically informative 16S ribosomal RNA gene. The analyses revealed a total of 173 bacterial taxa of which 39% were previously undetected. The JP2 clone constituted a minor proportion of the complex subgingival microbiota in patients with active disease. Rather than identifying alternative aetiologies to AgP, the recorded infection history of the subjects combined with remarkably high concentrations of antibodies against the A. actinomycetemcomitans leukotoxin suggest that disease activity was terminated in some patients with AgP as a result of elimination of the JP2 clone. This study provides information on the microbial context of the JP2 clone activity in a JP2‐susceptible population and suggests that such individuals may develop immunity to AgP. |
Author | Reinholdt, J. Rylev, M. Ennibi, O.-K. Kilian, M. Bek-Thomsen, M. |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21214871$$D View this record in MEDLINE/PubMed |
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(2007) Identification of oral bacterial species associated with halitosis. J Am Dent Assoc 138: 1113-1120. Jumas-Bilak, E., Roudiere, L. and Marchandin, H. (2009) Description of 'Synergistetes' phyl. nov. and emended description of the phylum 'Deferribacteres' and of the family Syntrophomonadaceae, phylum 'Firmicutes'. Int J Syst Evol Microbiol 59: 1028-1035. Levin, L., Baev, V., Lev, R., Stabholz, A. and Ashkenazi, M. (2006) Aggressive periodontitis among young Israeli army personnel. J Periodontol 77: 1392-1396. Faveri, M., Mayer, M.P., Feres, M., de Figueiredo, L.C., Dewhirst, F.E. and Paster, B.J. (2008) Microbiological diversity of generalized aggressive periodontitis by 16S rRNA clonal analysis. Oral Microbiol Immunol 23: 112-118. Califano, J.V., Gunsolley, J.C., Nakashima, K., Schenkein, H.A., Wilson, M.E. and Tew, J.G. (1996) Influence of anti-Actinobacillus actinomycetemcomitans Y4 (serotype b) lipopolysaccharide on severity of generalized early-onset periodontitis. Infect Immun 64: 3908-3910. Haubek, D., Poulsen, K., Asikainen, S. and Kilian, M. (1995) Evidence for absence in northern Europe of especially virulent clonal types of Actinobacillus actinomycetemcomitans. J Clin Microbiol 33: 395-401. Nibali, L., Donos, N., Brett, P.M. et al. (2008) A familial analysis of aggressive periodontitis - clinical and genetic findings. J Periodontal Res 43: 627-634. Armitage, G.C. (1996) Consensus report. Periodontal diseases: pathogenesis and microbial factors. Ann Periodontol 1: 926-932. Armitage, G.C. (1999) Development of a classification system for periodontal diseases and conditions. Ann Periodontol 4: 1-6. Paster, B.J., Boches, S.K., Galvin, J.L. et al. (2001) Bacterial diversity in human subgingival plaque. J Bacteriol 183: 3770-3783. Saxen, L. (1980) Prevalence of juvenile periodontitis in Finland. J Clin Periodontol 7: 177-186. Brogan, J.M., Lally, E.T., Poulsen, K., Kilian, M. and Demuth, D.R. (1994) Regulation of Actinobacillus actinomycetemcomitans leukotoxin expression: analysis of the promoter regions of leukotoxic and minimally leukotoxic strains. Infect Immun 62: 501-508. Hansen, M.C., Tolker-Nielsen, T., Givskov, M. and Molin, S. (1998) Biased 16S rDNA PCR amplification caused by interference form DNA flanking template region. FEMS Microbiol Ecol 26: 141-149. Haubek, D., Ennibi, O.K., Poulsen, K., Vaeth, M., Poulsen, S. and Kilian, M. (2008) Risk of aggressive periodontitis in adolescent carriers of the JP2 clone of Aggregatibacter (Actinobacillus) actinomycetemcomitans in Morocco: a prospective longitudinal cohort study. Lancet 371: 237-242. Haubek, D., DiRienzo, J.M., Tinoco, E 1995; 74 2009; 88 2009; 47 2006; 74 2001; 183 1991; 59 1993; 61 1997; 272 2006; 77 1995; 33 2003; 57 2008; 35 1995; 332 2007; 75 2007; 78 1994; 62 2003; 55 1996; 34 1994; 21 1996; 75 Spec No 2007; 138 2002a; 40 2000; 15 2002; 40 1997; 12 2008; 23 2002; 148 2005; 32 2005; 76 1996; 1 2009; 361 2003; 82 2005; 38 1985; 12 2003; 41 2007; 24 1996; 64 2009; 59 1998; 13 1998; 26 1989; 4 1976; 84 2006; 56 1995; 59 2002; 73 2002b; 7 1986; 13 2000; 71 1999; 4 2002; 81 1999; 20 2003; 31 1985; 48 2001; 80 2009; 36 2006; 42 2002; 29 2003; 149 1997; 76 1997; 35 1991; 62 2003; 69 2008; 46 1980; 7 2008; 43 1999; 70 2007; 45 2008; 371 1990; 5 e_1_2_6_51_1 e_1_2_6_74_1 e_1_2_6_53_1 e_1_2_6_32_1 e_1_2_6_70_1 e_1_2_6_30_1 e_1_2_6_72_1 e_1_2_6_19_1 e_1_2_6_13_1 e_1_2_6_36_1 e_1_2_6_59_1 e_1_2_6_11_1 e_1_2_6_34_1 e_1_2_6_17_1 e_1_2_6_55_1 e_1_2_6_15_1 e_1_2_6_38_1 e_1_2_6_57_1 e_1_2_6_62_1 e_1_2_6_64_1 e_1_2_6_43_1 e_1_2_6_20_1 e_1_2_6_41_1 e_1_2_6_60_1 Califano J.V. (e_1_2_6_14_1) 1996; 64 e_1_2_6_9_1 Slots J. (e_1_2_6_67_1) 1976; 84 e_1_2_6_5_1 e_1_2_6_7_1 e_1_2_6_24_1 e_1_2_6_49_1 e_1_2_6_3_1 e_1_2_6_22_1 e_1_2_6_66_1 e_1_2_6_28_1 e_1_2_6_45_1 e_1_2_6_26_1 e_1_2_6_47_1 e_1_2_6_68_1 e_1_2_6_52_1 e_1_2_6_73_1 e_1_2_6_54_1 e_1_2_6_75_1 e_1_2_6_10_1 e_1_2_6_31_1 e_1_2_6_50_1 e_1_2_6_71_1 e_1_2_6_35_1 e_1_2_6_12_1 e_1_2_6_33_1 e_1_2_6_18_1 e_1_2_6_39_1 e_1_2_6_56_1 e_1_2_6_16_1 e_1_2_6_37_1 e_1_2_6_58_1 e_1_2_6_63_1 e_1_2_6_42_1 e_1_2_6_65_1 e_1_2_6_21_1 e_1_2_6_40_1 e_1_2_6_61_1 e_1_2_6_8_1 e_1_2_6_4_1 e_1_2_6_6_1 e_1_2_6_25_1 e_1_2_6_48_1 e_1_2_6_23_1 e_1_2_6_2_1 e_1_2_6_29_1 e_1_2_6_44_1 e_1_2_6_27_1 e_1_2_6_46_1 e_1_2_6_69_1 |
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Cross‐sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive... Cross‐sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis... Cross-sectional and longitudinal studies identify the JP2 clone of Aggregatibacter actinomycetemcomitans as an aetiological agent of aggressive periodontitis... |
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SubjectTerms | Actinobacillus Infections - immunology Actinobacillus Infections - microbiology Adolescence Adolescent aetiology Aggregatibacter actinomycetemcomitans - classification Aggregatibacter actinomycetemcomitans - genetics Aggregatibacter actinomycetemcomitans - immunology aggressive periodontitis Aggressive Periodontitis - immunology Aggressive Periodontitis - microbiology Antibodies Antibodies, Bacterial - blood Bacterial Toxins - immunology Case-Control Studies Clone Cells Disease Susceptibility - immunology Exotoxins - immunology Gingival Hemorrhage - immunology Gingival Hemorrhage - microbiology Humans Immunity Immunosuppressive Agents - immunology Infection leukotoxin Morocco Nucleic Acid Amplification Techniques Pathogens Periodontal Attachment Loss - immunology Periodontal Attachment Loss - microbiology Periodontal diseases Periodontal Pocket - immunology Periodontal Pocket - microbiology Periodontitis Phylogeny Polymerase Chain Reaction RNA, Ribosomal, 16S - genetics rRNA 16S Sequence Analysis, DNA Young Adult |
Title | Microbiological and immunological characteristics of young Moroccan patients with aggressive periodontitis with and without detectable Aggregatibacter actinomycetemcomitans JP2 infection |
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