Aggregatibacter actinomycetemcomitans in Brazil: a prospective longitudinal cohort study and the risk of aggressive periodontitis
Publicado em 11 de agosto de 2009 por EDSON COSTA
The Aggregatibacter actinomycetemcomitans in Brazil: a prospective longitudinal cohort study and the risk of aggressive periodontitis in adolescent carriers of the JP2 clone.
Summary
Background
Periodontitis is a loss of supporting connective tissue and alveolar bone around teeth, and if it occurs in an aggressive form it can lead to tooth loss before the age of 20 years. Although the cause of periodontitis in general remains elusive, a particular clone (JP2) of the gram-negative rod Aggregatibacter (Actinobacillus) actinomycetemcomitans is considered a possible aetiological agent of the aggressive form in adolescents living in or originating from south and east Brazil, where the disease is highly prevalent. We did a population-based longitudinal study of adolescents to assess the role of the JP2 clone in the initiation of aggressive periodontitis.
Methods
A total of 1000 adolescents from public schools in Guarulhos City, Brazil, were enrolled in the study. We used PCR to detect A actinomycetemcomitans in plaque samples (taken from molar and incisor sites) and to differentiate between the JP2 clone and other non-JP2 genotypes of the bacterium. 18 individuals were found to already have periodontitis and were excluded. The 710 periodontally healthy adolescents (mean age 13-1 years; SD 1•0) were classified according to their A actinomycetemcomitans carrier status at baseline. After 2 years, 645 (64•5%) individuals returned for re-examination, which included recording of periodontal attachment loss measured from the cemento-enamel junction to the bottom of the periodontal pockets of all teeth present.
Findings
Individuals who carried the JP2 clone of A actinomycetemcomitans alone (relative risk 18•0; 95% CI 7•8–41•2, p<0•0001) or together with non-JP2 clones of A actinomycetemcomitans (12•4; 5•2–29•9, p<0•0001) had a significantly increased risk of periodontal attachment loss. A much less pronounced disease risk was found in those carrying non-JP2 clones only (3•0; 1•3–7•1, p=0•012).
Interpretation
The JP2 clone of A actinomycetemcomitans is likely to be an important aetiological agent in initiation of periodontal attachment loss in children and adolescents. Co-occurrence of non-JP2 clones of A actinomycetemcomitans reduces the risk of development of periodontitis, suggesting competition for the ecological niche between the JP2 and non-JP2 clones of this species.
Summary
Background
Periodontitis is a loss of supporting connective tissue and alveolar bone around teeth, and if it occurs in an aggressive form it can lead to tooth loss before the age of 20 years. Although the cause of periodontitis in general remains elusive, a particular clone (JP2) of the gram-negative rod Aggregatibacter (Actinobacillus) actinomycetemcomitans is considered a possible aetiological agent of the aggressive form in adolescents living in or originating from south and east Brazil, where the disease is highly prevalent. We did a population-based longitudinal study of adolescents to assess the role of the JP2 clone in the initiation of aggressive periodontitis.
Methods
A total of 1000 adolescents from public schools in Guarulhos City, Brazil, were enrolled in the study. We used PCR to detect A actinomycetemcomitans in plaque samples (taken from molar and incisor sites) and to differentiate between the JP2 clone and other non-JP2 genotypes of the bacterium. 18 individuals were found to already have periodontitis and were excluded. The 710 periodontally healthy adolescents (mean age 13-1 years; SD 1•0) were classified according to their A actinomycetemcomitans carrier status at baseline. After 2 years, 645 (64•5%) individuals returned for re-examination, which included recording of periodontal attachment loss measured from the cemento-enamel junction to the bottom of the periodontal pockets of all teeth present.
Findings
Individuals who carried the JP2 clone of A actinomycetemcomitans alone (relative risk 18•0; 95% CI 7•8–41•2, p<0•0001) or together with non-JP2 clones of A actinomycetemcomitans (12•4; 5•2–29•9, p<0•0001) had a significantly increased risk of periodontal attachment loss. A much less pronounced disease risk was found in those carrying non-JP2 clones only (3•0; 1•3–7•1, p=0•012).
Interpretation
The JP2 clone of A actinomycetemcomitans is likely to be an important aetiological agent in initiation of periodontal attachment loss in children and adolescents. Co-occurrence of non-JP2 clones of A actinomycetemcomitans reduces the risk of development of periodontitis, suggesting competition for the ecological niche between the JP2 and non-JP2 clones of this species.