Aggregatibacter actinomycetemcomitans, Filifactor alocis, and Streptococcus parasanguinis

In an extension of a previous report in 2007 [1]Fine et al. (2013) shed more light last month on the microbiological cause of localized aggressive periodontitis in African Americans and Hispanics. In the new report [2] of the more interesting longitudinal part of the study, 134 periodontally healthy teenagers (mean age 12-13 yr) had been followed for more than 2 years. Sixty-three subjects harboring Aggregatibacter actinomycetemcomitans in sugingival plaque and/or buccal swab samples had been matched with 71 subjects in which that particular organism could not been found. Twenty-three subjects developed one (first molar) site [3] with a 6 mm or deeper pocket in combination with 2 mm or more attachment loss. Twenty of these harbored A. actinomycetecomitans at the time of screening. Among the eight subjects who developed two or more (first molar) sites with a pocket depth of at least 6 mm and 2 mm or more attachment loss (thus fitting the Löe & Brown “soft tissue” definition of localized aggressive periodontitis [4]), all were A. actinomycetemcomitans-positive. Likewise, all 16 subjects who developed alveolar bone loss (identified on standardized bitewing radiographs) harbored A. actinomycetemcomitans.

Among those subjects who developed (according to the definition by Löe and Brown [4]) localized aggressive periodontitis, seven had been subjected to subject level microbial assessment of pooled samples prior to pocket development and attachment using the 300 taxa of HOMIM (human oral microbe identification microarray). In comparison, ten healthy subjects (five with A. actinomycetemcomitans and five without) served as healthy controls. While healthy controls had higher prevalence of species of the Streptococcus, Actinomyces, Veillonella, Gemella, Granulocitella, Fusobacterium and Campylobacter genera, in those who developed localized aggressive periodontitis, A. actinomycetemcomitans, Filifactor alocis, Treponema socranskii, Tannerella forsythia, Porphyromonas gingivalis, Eubacterium nodatum, Eubacterium infirmum, Eubacterium brachy, Selenomonas sputigena, Prevotella intermedia, and certain unnamed taxa of the Peptostreptococcaceae, Lachnospiracea, and Desulfobulbus genera were among the prominent named species with increased prevalence in subjects prior to development of disease as compared to subjects who remained healthy.

Site-specific microbial assessments using HOMIM were done on all 16 subjects who went from periodontal health to bone loss at a specific tooth site (in total 18 sites). HOMIM analyses were done six months prior to bone loss and at the time when bone loss was detected. Further molar sites in these subjects which remained healthy (i.e., did not develop alveolar bone loss) were also studied, typically three in each subject. Four microbial species had highly elevated DNA probe levels in HOMIM in sites prior to subsequent bone loss, namely A. actinomycetemcomitans, F. alocis, P. gingivalis, and Streptococcus parasanguinis. A group of three Veillonella spp. was also highly elevated while several other species were elevated to a lesser extent in sites prior to bone loss. In sites which stayed healthy, the Fusobacterium cluster and Veillonella dispar were highly elevated. In an attempt to use these site-specific data for a diagnostic tests, it turned out that the presence of a combination of A. actinomycetemcomitans, F. alocis, and S. parasanguinis yielded 89% sensitivity and 99% specificity for subsequent bone loss in these 16 subjects.

There is emerging information about F. alocis as a periodontal pathogen. The organism exerts a number of potent virulence factors which enables it to evade or perturb host defense mechanisms. S. parasanguinis would appear to be an antagonist of A. actinomycetemcomitans given its production of hydrogen peroxide, which, on the other hand is neutralized A. actinomycetemcomitans‘ catalase activity. Authors mention, in their discussion, that viridans streptococci, to which S. parasanguinis belongs, and A. actinomycetemcomitans share certain trophic food chains. Much of the study appears having been designed with a strong bias towards possible proof that A. actinomycetemcomitans was the main cause of localized aggressive periodontitis in these mainly African American and Hispanic subjects. For instance, there was much screening in the beginning to identify subjects colonized with that particular organism. Furthermore, P. gingivalis, which was highly elevated in pooled samples prior to periodontal breakdown, probably only in certain subjects, was later omitted from further analyses due to a “low sensitivity value” of 50%.

Anyway, despite the highly complicated overall design which makes it difficult to extract pertinent information the study yields a substantial wealth of new data and probably correctly takes temporality into account, i.e., assessing microbiological information before periodontal breakdown occurs.


[1] Fine DH, Markowitz K, Furgang D, Fairlie K, Ferrandiz J, Nasri C, McKiernan M, Gunsolley J. Aggregatibacter actinomycetemcomitans and its relationship to initiation of localized aggressive periodontitis: Longitudinal cohort study of initially healthy adolescents. J Clin Microbiol 2007; 45: 3859-3869. See a critical analysis of the paper here.

[2] Fine DH, Markowitz K, Fairlie K, Tischio-Bereski D, Ferrendiz J, Furgang D, Paster BJ, Dewhirst FE. A consortium of Aggregatibacter actinomycetemcomitans, Streptococcus parasanguinis, and Filifactor alocis is present in sites prior to bone loss in a longitudinal study of localized aggressive periodontitis. J Clin Microbiol 2013; 51: 2850-2861. As in the the previous paper, see [1], periodontal health was defined if pockets up to but not more than 5 mm depth were found without any clinical attachment loss.

[3] The respective Table 4 in the manuscript indicates “one or more” but this may be a glitch.

[4] Löe H, Brown LJ. Early onset periodontitis in the United States of America. J Periodontol 1991; 62: 608-616.

1 October 2013 @ 11: 50 am.

Last modified October 1, 2013.


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