Skip to Main Content
Text size: SmallMediumLargeExtra-Large

One, Two, Three

August 8, 2013

Aggregatibacter actinomycetemcomitants (Aa) The final verdict had remained out on an oral bacterium with the tongue-twisting name Aggregatibacter actinomycetemcomitants (Aa). But all of the evidence weighed heavily in favor of fingering it as the cause of Localized Aggressive Periodontitis, or LAP, the most common form of periodontal disease in kids, particularly among African American and Hispanic children.

The case went like this. In early clinical studies, children diagnosed with LAP often were shown to have Aa in the periodontal pocket of the affected molar, where the condition typically arises. It was also shown that removing Aa led to disease remission. In basic studies, Aa has been found to secrete toxins that can stymie communication among immune cells, providing a plausible biological mechanism for the bacterium to destabilize conditions in the periodontal pocket. Five years ago, the case seemed almost airtight when two case-controlled epidemiological studies found that healthy children with Aa will develop LAP over time. Those without the bacterium won’t.

The final piece to the causation puzzle was to show Aa resides in the gingival pocket of an at-risk molar before LAP already has flared. In short, establish that Aa was indeed there to commit the periodontal infection. That led to an NIDCR-supported study that unexpectedly turned the case in a new direction. The scientists screened over 2,000 African American and Hispanic adolescents and discovered that, of those with clinical evidence of LAP, only 67 percent had Aa in the gingival pocket. Given that more than 30 percent did not, the earlier clinical data now seemed less convincing. The NIDCR-supported scientists followed up with a case-controlled longitudinal study in which they compared the previously screened, Aa-positive students with an equal number of adolescents who were Aa free. Again, only those who had Aa to start the study developed LAP. But 70 percent with Aa at entry remained healthy. This raised the possibility that Aa alone doesn’t cause LAP. It needs a little help from its bacterial friends.

Now, as published online in the Journal of Clinical Microbiology, the scientists overseeing the ongoing NIDCR-supported study have discovered for the first time four of these friends. They are: Streptococcus parasanguinis, Filifactotor alocis, Porphorymonas gingivalis, and Veillonella spp.

The scientists drilled down further into their data and found that as LAP enters its final tooth-destructive phase, Aa seems to partner with F. alocis and S. parasanguinis to erode the bone that supports the affected molar. So much so, the scientists found that by testing for all three bacteria in the gingival pockets, they could predict with 99 percent specificity (certainty a positive test result is correct) which children would develop future bone loss compared to 75 percent when testing for Aa alone. The testing sensitivity (certainty a negative test result is correct) for the trio was nearly 90 percent.

F. alocis
is a rod-shaped anaerobic bacterium that recent studies indicate can turn virulent in the gingival pocket. S. parasanguinis is considered to be a commensal, or relatively benign, bacterium in the mouth. It is an early colonizer of oral surfaces and serves as a foundational bacterium upon which other bacteria attach to build the polymicrobial plaques in our mouth, known as biofims.

The scientists noted, “While it seems clear that Aa does not act alone, we hypothesize that Aa is a keystone pathogen and thus sets up the subgingivial environment by producing toxins resulting in immune paralysis and permitting overgrowth of specific organisms at specific time-points that would otherwise be controlled and regulated by the host.”

The paper is titled, “A consortium of Aggregatibacter actinomycetemcomitants (Aa), Streptococcus parasanguinis, and Filifactotor alocis." The article was published online on June 19, 2013 in the Journal of Clinical Microbiology. The authors are: Daniel H. Fine, Kenneth Markowitz, Karen Fairlie, Debbie Tischio-Bereski, Javier Ferrendiz, David Furgang, Bruce J. Paster, and Floyd E. Dewhirst.

Share This Page

GooglePlusExternal link – please review our disclaimer

LinkedInExternal link – please review our disclaimer


This page last updated: February 26, 2014