No abstract

The data suggest that pregnancy, especially in the early periods, promotes the proliferation of microorganisms in the oral cavity and facilitates a colonization of periodontal pathogens.

Fixed orthodontic appliances are common and effective tools to treat malocclusion. Adverse effects of these appliances, such as dental caries and periodontitis, may be associated with alteration of the microbiome. This study investigated the impact of these appliances on the dynamics of the oral microbiome. Seventy-one patients were selected. Supragingival plaque samples were collected before placement (T0) and six months after placement (T1). Saliva samples were collected at T0 and T1, and then when appliance removal (T2). Microbial DNA was analyzed by 16S rRNA meta-sequencing. The diversity analysis indicated dynamic changes in the structure of the oral microbiome. Taxonomic analysis at phylum level showed a significant increase in Bacteroidetes and Saccharibacteria (formally TM7) and decrease in Proteobacteria and Actinobacteria over time, in both plaque and saliva. Genus level analysis of relative abundance indicated a significant increase in anaerobic and facultative anaerobes in both plaque and saliva. Fixed orthodontic appliances induced measurable changes in the oral microbiome. This was characterized by an increase in relative abundance of obligate anaerobes, including periodontal pathogens. It can be concluded that this dysbiosis induced by fixed orthodontic appliances is likely to represent a transitional stage in the shift in microbiome from healthy to periodontitis.

Cytolethal distending toxin (CDT) is a bacterial toxin that induces G 2 /M cell cycle arrest, cell distension, and/or apoptosis in mammalian cells. It is produced by several Gram-negative species and may contribute to their pathogenicity. The catalytic subunit CdtB has homology with DNase I and may act as a genotoxin. However, the mechanism by which CdtB leads to cell death is not yet clearly understood. Here, we used Saccharomyces cerevisiae as a model to study the molecular pathways involved in the function of CdtB from Aggregatibacter actinomycetemcomitans, a cause of aggressive periodontitis. We show that A. actinomycetemcomitans CdtB (AaCdtB) expression induces S/G 2 arrest and death in a DNase-catalytic residue and nuclear localization-dependent manner in haploid yeasts. Yeast strains defective in homologous recombination (HR) repair, but not other DNA repair pathways, are hypersensitive to AaCdtB, suggesting that HR is required for survival upon CdtB expression. In addition, yeast does not harbor the substrate for the other activity proposed for CdtB function, which is phosphatidylinositol-3,4,5-triphosphate phosphatase. Thus, these results suggest that direct DNA-damaging activity alone is sufficient for CdtB toxicity. To investigate how CdtB induces cell death, we examined the effect of CdtB in yeast strains with mutations in apoptotic regulators. Our results suggest that yeast death occurs independently of the yeast metacaspase gene YCA1 and the apoptosis-inducing factor AIF1 but is partially dependent on histone H2B serine 10 phosphorylation. Therefore, we report here the evidence that AaCdtB causes DNA damage that leads to nonapoptotic death in yeast and the first mutation that confers resistance to CdtB.

We re-evaluated several antibiotics including newer ones, for their in vitro killing activity, as well as their inhibitory activity, against clinical isolates of periodontopathic bacteria. Tetracyclines were active against Porphyromonas gingivalis, and were highly active against Prevotella intermedia, but demonstrated only a low killing activity against Actinobacillus actinomycetemcomitans. Rokitamycin, a new macrolide, and clindamycin were highly active against P. gingivalis and P. intermedia, but showed very weak killing activity against A. actinomycetemcomitans. Quinolones demonstrated excellent bactericidal activity against A. actinomycetemcomitans, and good inhibitory and bactericidal activity against P. gingivalis and P. intermedia. Metronidazole had an activity almost equivalent to quinolones against P. gingivalis and P. intermedia; but it was the least active against A. actinomycetemcomitans.