Advances in the Microbiology of Aggressive Periodontitis

It had long been claimed that Aggregatibacter actinomycetemcomitans is strongly associated with localized aggressive periodontitis. In particular, A. actinomycetemcomitans has even been involved in the pathogenesis of aggressive periodontitis. Later it had been realized that this bacterium occurs frequently also in other forms of periodontitis and even gingivitis. And, other bacteria, such as Porphyromonas gingivalis, may be involved in the pathogenesis of both localized and generalized aggressive periodontitis.

One of the upcoming issues of Periodontology 2000 is dedicated to all aspects of, what has turned out, very controversial aggressive periodontitis. Eija Könönen at Turku University and I had been asked to scrutinize the voluminous literature on the microbiology of aggressive periodontitis [1]. The following is a brief summary of the role of A. actinomycetemcomitans as a causative agent and new findings of open-ended molecular techniques regarding the microbiome of localized and generalized aggressive periodontitis.

Criteria for Causality

Sir Bradford Hill had described about 50 years ago criteria for possible causal relationship of certain risk factors for complex chronic diseases (Hill 1965), see [pdf] here. These criteria ultimately proved that smoking causes some forms of lung cancer. Among them, strength of association (including consistency and specificity), temporality of events (the causal factor has to be present before the onset of the disease) and experimental evidence (intervention trials) are of great importance as is for instance the biological gradient (dose-response relationship), while plausibility, coherence with laboratory findings, and analogy are not, or not so much [2].

Recently, Howick et al. (2009) have re-arranged Hill’s criteria [3], see [pdf] here, putting much emphasis on direct evidence for a causal relationship which comprises the size of the effect (after adjusting for possible confounding), the appropriate temporal and/or spatial proximity (the cause precedes the effect and the effect occurs after a plausible interval; the cause occurs at the same site as the intervention), and dose-responsiveness and reversibility. What they call mechanistic evidence (evidence for biological, chemical, or mechanical mechanisms of action; and parallel evidence (coherence, replicability, similarity) would therefore not suffice to prove causality.

Methods and Results (I)

A systematic literature search was done in PubMed using the following focused question:

“Do prospective studies exist which may indicate a causal relationship between Aggregatibacter actinomycetemcomitans and the development of periodontitis at young age?”

Search terms were: (“actinobacillus actinomycetemcomitans”[MeSH Terms] OR (“actinobacillus”[All Fields] AND “actinomycetemcomitans”[All Fields]) OR “actinobacillus actinomycetemcomitans”[All Fields] OR (“aggregatibacter”[All Fields] AND “actinomycetemcomitans”[All Fields]) OR “aggregatibacter actinomycetemcomitans”[All Fields]) AND (“aggressive periodontitis”[MeSH Terms] OR (“aggressive”[All Fields] AND “periodontitis”[All Fields]) OR  “aggressive periodontitis”[All Fields]) AND (“longitudinal studies”[MeSH Terms] OR (“longitudinal”[All Fields] AND “studies”[All Fields]) OR “longitudinal studies”[All Fields] OR “prospective”[All Fields]), which yielded 63 papers published between 1986 and 2011.  Read the rest of this entry »


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