Stability of the JP2 Clone of Aggregatibacter actinomycetemcomitans

Abstract

The JP2 clone of Aggregatibacter actinomycetemcomitans is strongly associated with aggressive periodontitis. To obtain information about colonization dynamics of the JP2 clone, we used PCR to examine its presence in 365 Moroccan juveniles from whom periodontal plaque samples were collected at baseline and after one and two years. Periodontal attachment loss was measured at baseline and at the two-year follow-up. At baseline, 43 (12%) carriers of the JP2 clone were found. Nearly half (44 %) of these were persistently colonized with the clone. The relative risk for the development of aggressive periodontitis, adjusted for the concomitant presence of other genotypes of A. actinomycetemcomitans, was highest for individuals continuously infected by the JP2 clone (RR = 13.9; 95% CI, 9.0 to 21.4), indicating a relationship between infectious dose and disease, which further substantiates the evidence for the JP2 clone as a causal factor in aggressive periodontitis.

Pathogenicity of the highly leukotoxic JP2 clone ofAggregatibacter actinomycetemcomitansand its geographic dissemination and role in aggressive periodontitis

“…Nearly half of the JP2 clone carriers were persistently infected during the 2-year follow-up period, which indicates a level of the stability of the colonization with the JP2 clone similar to that previously reported for the non-JP2 genotypes of A. actinomycetemcomitans (103, 109, 112). However, the relative risk for the development of aggressive periodontitis was highest for individuals with stable JP2 clone colonization (33, 109). Although the method used (polymerase chain reaction) in the first and the second Moroccan cohort studies was not quantitative, these results add to the evidence for a causal role of the JP2 clone in aggressive periodontitis (109).…”

“…Haraszthy and coworkers found a higher prevalence of highly leukotoxic strains in children equal to or under the age of 14 years than in subjects older than 14 years (81% versus 26%, p <0.001) (60). In addition, longitudinal data on Moroccan adolescents reports that few individuals are colonized with the JP2 clone de novo after puberty (109). Thus, it is likely that the JP2 clone preferentially infects younger individuals.…”

“…The stability of JP2 and non-JP2 genotypes of A. actinomycetemcomitans has also been studied in the Moroccan population (109). Nearly half of the JP2 clone carriers were persistently infected during the 2-year follow-up period, which indicates a level of the stability of the colonization with the JP2 clone similar to that previously reported for the non-JP2 genotypes of A. actinomycetemcomitans (103, 109, 112).…”

“…However, the relative risk for the development of aggressive periodontitis was highest for individuals with stable JP2 clone colonization (33, 109). Although the method used (polymerase chain reaction) in the first and the second Moroccan cohort studies was not quantitative, these results add to the evidence for a causal role of the JP2 clone in aggressive periodontitis (109). …”

The highly leukotoxic JP2 clone ofAggregatibacter actinomycetemcomitansin localized and generalized forms of aggressive periodontitis

“…Thus, the difference could be partly explained by these differences between the two studies. Alternatively, some of the adolescents may have developed mild disease due to transient infection with the JP2 clone, as it has been found that over a 2-year period approximately half of this age group was temporarily colonized [36], whereas those persistently infected are supposed to develop more severe disease over time, as presumed for the slightly older patient sample included in the present study. In support of this, elimination of the JP2 clone has been shown to correlate with diminishing disease activity [37].…”