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

While at follow-up 397 individuals were re-examined, 82 of them had had disease at baseline (one or more sites with proximal attachment loss of 3 mm or more). If possible causal agents for the development of disease are to be identified, only healthy subjects at outset should be considered. Among the 315 individuals at baseline who had not experienced at least 3 mm attachment loss., 87 developed disease status at follow-up, i.e., one or more sites with attachment loss of 3 mm or more. Of 30 subjects positive for the JP2 clone of A. actinomycetemcomitans (some had in addition also non-JP2 clones of the organism), 23 developed disease (77%). Of 123 positive for only non-JP2 clones of A. actinomycetemcomitans, 47 experienced attachment loss of at least 3 mm (38%), while 17 of 162 subjects free of A. actinomycetemcomitans (10.5%) developed disease. One may therefore calculate relative risks of 7.3 (95% confidence interval 4.5-11.9) and 3.6 (95% CI 2.2-6.0) for presence of JP2 or non-JP2 A. actinomycetemcomitans to experience significant attachment loss of 3 mm or more at one or more sites when compared to the risk of individuals free of A. actinomycetemcomitans [1]. Further analyses by the authors indicated that in particular the JP2 clone of A. actinomycetemcomitans must be considered a strong risk factor for development and progression of attachment loss in Ghanese school children.

This is one of the first reports suggesting that the highly leukotoxic clone of the organisms plays a decisive role in (aggressive) periodontitis also in sub-Saharan Africa. About 16 years ago I had come across a young immigrant from Ghana in Germany who suffered badley from localized aggressive periodontitis which had started to develop into generalized aggressive periodontitis. Several teeth were hopelessly involved. High numbers of A. actinomycetemcomitans were found in subgingival plaque samples and PCR of the promoter region of the leukotoxin gene indicated [pdf] that it was the JP2 clone.

Since I already at that time had got the impression that that would be the target, I discussed with the patient that I won’t extract any tooth for the time being but rather do non-surgical periodontal and adjunct antibiotic therapy (1.5 g amoxicillin and 1.2 g metronidazole for 10 d).

The clinical response was very good. The number of deep pockets in excess of 4 mm was instantly (say, after 8 weeks) largely reduced, clinical attachment gain occurred and it was planned to keep even severely involved teeth. By sampling subgingival plaque from every tooth and a dozen mucosal surfaces it was possible to prove, with some confidence, that A. actinomycetemcomitans was eradicated, at least for some time.

Six months later, some radiographic evidence indicated that the fate of certain highly questionable teeth was no longer doomed and remaining pockets might be managed within close supportive periodontal treatment [1].

Fullmouth survey of 24-yr old patient from Ghana with localized aggressive periodontitis

Fullmouth survey of 24-yr old patient from Ghana with localized aggressive periodontitis

 

 

Clinical situation

Clinical situation

 

 

 

 

Eight weeks after non-surgical periodontal therapy and adjunct systemic antibiotics (1.5 g amoxicillin and 1.2 g metronidazole for 10 d)

Eight weeks after non-surgical periodontal therapy and adjunct systemic antibiotics (1.5 g amoxicillin and 1.2 g metronidazole for 10 d)

 

 

 

 

 

 

 

Periapical radiographs before and six months after treatment

Periapical radiographs before and six months after treatment

 

 

 

 

 

Notes

[1] Relative risks and 95% confidence interval estimates maybe calculated by applying the formulas in the figure below. As an exercise, readers may want to check that Höglund Åberg et al. had used these formulas.

Risk

[2] The case should prove the principle that the eradication of the targeted organism, JP2, would result in healing of most of the lesions. Nothing else. In 1997, proper longitudinal studies which could prove JP2 was actually involved as a causal agent (alone or in combination with other, unknown, organism), had not been conducted. See, for further discussion, the dissertation by  Haubek (2010) [pdf].

17 January 2014 @ 3:52 pm.

Last modified January 18, 2014.

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