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 inMolecular oral microbiology Vol. 26; no. 1; pp. 35 - 51
Main Authors Rylev, M., Bek-Thomsen, M., Reinholdt, J., Ennibi, O.-K., Kilian, M.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.02.2011
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ISSN2041-1006
2041-1014
2041-1014
DOI10.1111/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.
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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Hutter, G., Schlagenhauf, U., Valenza, G. et al. (2003) Molecular analysis of bacteria in periodontitis: evaluation of clone libraries, novel phylotypes and putative pathogens. Microbiology 149: 67-75.
Bek-Thomsen, M., Lomholt, H.B. and Kilian, M. (2008) Acne is not associated with yet-uncultured bacteria. J Clin Microbiol 46: 3355-3360.
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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.
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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
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Snippet Summary 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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StartPage 35
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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https://www.ncbi.nlm.nih.gov/pubmed/21214871
https://www.proquest.com/docview/835118119
https://www.proquest.com/docview/879470449
Volume 26
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