Tagged: D. Haubek

Aggregatibacter actinomycetemcomitans JP2 in Ghana

Another longitudinal study by Höglund Åberg et al. (2014) [pdf] has linked the development and progression of periodontal attachment loss in teenagers with the highly leukotoxic clone of Aggregatibacter actinomycetemcomitans, JP2, in Ghana. It confirms several previous reports by Haubek et al. on adolescents in Morocco (see her PhD thesis here [pdf]) in that JP2 is strongly associated with the onset and progression of aggressive periodontitis, a term which is noticeably avoided by Höglund Åberg et al. in her present paper.

A random sample cohort of students from public and private schools in Greater Accra, Ghana’s capital, had been recruited in 2009. The mean age was 13.2 yr with a standard deviation of 1.5 yr. At follow-up after 2 yr, 397 participants (79.4%) showed in 2011. Periodontal probing was done at the “mesiobuccal [sic] aspect of the mesial and distal surfaces of all fully erupted teeth (except third molars). At baseline and follow-up, attachment loss was calculated as the difference between the distance from the gingival margin to the cemento-enamel junction and the recorded probing pocket depth measurement. Several subgingival plaque samples were collected with paper points for PCR analysis (including determination of the 530 bp deletion in the leukotoxin promoter region pointing to JP2) and cultivation. Only presence or absence of A. actinomycetemcomitans was determined, not its quantity nor the presence of other bacteria.

Disease status at the individual level (case definition) was set at interproximal attachment loss of 3 mm or more in one or more sites in the dentition. Individuals were defined as having progressing disease if they showed one or more sites with a progression of attachment loss of 3 mm or more.

Åberg

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Not So Much Evidence That Destructive Periodontal Disease Etiology is Associated With Specific Infection

My colleague Professor Eija Könönen at Turku University had asked me some time ago whether I wanted to contribute to an invited review on the microbiology of aggressive periodontitis. Not being a microbiologist (in contrast to Eija) I was a bit hesitant. But the topic was interesting and research into the matter promised to end, once and forever, persisting myths about Aggregatibacter, something which I found tempting. So, I agreed. Meanwhile, the issue had been dealt with from different perspectives, including necessarily large portions of narrative review of the literature beginning with the 1970s, and systematic searches for the role of Aggregatibacter actinomycetemcomitans and recent studies on the microbiota/microbiome of aggressive periodontitis using whole genomic DNA probes and, in particular, 16S ribosomal RNA genomic analyses. It will be published later this year in Periodontology 2000.

One of the few longitudinal studies identified by our systematic search [1] for a possible role of A. actinomycetemcomitans in the etiology of aggressive periodontitis was the study by Fine et al. (2007) [2], who

“… screened 1075 students clinically and microbiologically, and subgingival plaque, saliva and buccal epithelial-cell samples were examined for A. actinomycetemcomitans. Of those who carried the organism, 38 were followed for at least 1 year after the initial examination (test group); at the screening visit, 36 students had been diagnosed as periodontally healthy (up to one 5-mm pocket without attachment loss) or as ‘borderline’ healthy (two or more 5-mm pockets with <2 mm of attachment loss), and two were ‘potentially diseased’ (pocket depth 6 mm with attachment loss of >2 mm in one or two teeth). In addition, 58 age- and gender-matched students, confirmed negative for A. actinomycetemcomitans, formed the control group; 55 were periodontally healthy and the others were ‘borderline’ healthy at the outset of the study (see Fig. 2 in the original article). Among all 1075 students, 13 (1.2%) had already developed localized aggressive periodontitis and 13.7% were culture positive for A. actinomycetemcomitans. The majority of students were African-American or Hispanic, and the former had a slightly higher carrier rate than the latter (16.6% and 11.5%, respectively). At recall, eight students presented with bone loss, which was visible on bitewing radiographs taken yearly. All were A. actinomycetemcomitans-positive and two harbored the JP2 clone. Four had been classified at baseline as healthy, two as ‘borderline’ and two as ‘potentially diseased’. No subject in the A. actinomycetemcomitans-negative control group presented with bone loss at any recall. Survival analysis indicated a higher likelihood for carriers of A. actinomycetemcomitans to develop pockets and attachment loss over time compared with control subjects who were negative for A. actinomycetemcomitans. The authors concluded that the detection of A. actinomycetemcomitans in periodontally healthy children can serve as a risk marker for the initiation of localized aggressive periodontitis; however, given the sparseness and heterogeneity of the data (i.e. the groups seemed to differ clinically at the outset, so some carriers of A. actinomycetemcomitans might have already developed periodontitis), the evidence may be considered weak.”

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