Abstract
Aggregatibacter actinomycetemcomitans (Aa) is a low-abundance Gram-negative oral pathobiont that is highly associated with a silent but aggressive orphan disease that results in periodontitis and tooth loss in adolescents of African heritage. For the most part Aa conducts its business by utilizing strategies allowing it to conceal itself below the radar of the host mucosal immune defense system. A great deal of misinformation has been conveyed with respect to Aa biology in health and disease. The purpose of this review is to present misconceptions about Aa and the strategies that it uses to colonize, survive, and evade the host. In the process Aa manages to undermine host mucosal defenses and contribute to disease initiation. This review will present clinical observational, molecular, and interventional studies that illustrate genetic, phenotypic, and biogeographical tactics that have been recently clarified and demonstrate how Aa survives and suppresses host mucosal defenses to take part in disease pathogenesis. At one point in time Aa was considered to be the causative agent of Localized Aggressive Periodontitis. Currently, it is most accurate to look at Aa as a community activist and necessary partner of a pathogenic consortium that suppresses the initial host response so as to encourage overgrowth of its partners. The data for Aa's activist role stems from molecular genetic studies complemented by experimental animal investigations that demonstrate how Aa establishes a habitat (housing), nutritional sustenance in that habitat (food), and biogeographical mobilization and/or relocation from its initial habitat (transportation). In this manner Aa can transfer to a protected but vulnerable domain (pocket or sulcus) where its community activism is most useful. Aa's “strategy” includes obtaining housing, food, and transportation at no cost to its partners challenging the economic theory that “there ain't no such thing as a free lunch.” This “strategy” illustrates how co-evolution can promote Aa's survival, on one hand, and overgrowth of community members, on the other, which can result in local host dysbiosis and susceptibility to infection.
Highlights
Ever since 1976 when it was discovered that Aggregatibacter actinomycetemcomitans was associated with Aggressive Periodontitis in adolescents there have been many attempts to understand its relationship to disease [1, 2]
While initially it was thought that Aa was the cause of localized aggressive periodontitis (LAgP) [5] current research suggests that Aa is implicated as an important and perhaps necessary constituent of a consortium of microorganisms related to disease [6]
It is still to be proven whether this scenario is unique to the non-JP2 strain of Aa or if this is a general strategy used to provoke local disease. This working hypothesis can be applied to other combinations of microbes that can operate under differing circumstances in populations distinct from the African American adolescents studied in Localized Aggressive Periodontitis
Summary
Ever since 1976 when it was discovered that Aggregatibacter actinomycetemcomitans (ne Actinobacillus) was associated with Aggressive Periodontitis in adolescents there have been many attempts to understand its relationship to disease [1, 2]. Results showed that while Aa was incapable of moving from HA to BECs, Aa was quite capable of moving from BECs to HA These in-vivo and in-vitro experiments clearly demonstrated the difference in the kinetics of Aa attached to BECs via specific adhesin/receptor interactions that are reversible, as compared to linear and irreversible, nonspecific aggregative adherence mediated by flp, tad, and rcp genes that facilitate Aa’s attachment to HA [32]. Confirmation of the early plaque formation of Aa came from a little known experiment conducted in 1976 by Kilian and Rolla where these investigators set out to study the dietary impact of sucrose on Streptococcus mutans colonization in a Rhesus monkey model [33] In these experiments it was clearly shown that sucrose influenced early colonization of S. mutans, but unintentionally it was demonstrated that Aa, a member of the commensal flora in these monkeys, was found on teeth within 3 h following thorough oral debridement of these Rh monkeys
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