Evaluation of human and microbial DNA content in subgingival plaque samples collected by paper points or curette.

Host DNA may adversely affect metagenomic studies focusing on the prokaryotic microbiota. This study compared the levels of host DNA in subgingival plaque collected by paper points and curette, using quantitative PCR. Lower proportions of host DNA and higher proportions of bacterial DNA were recovered from samples collected with curettes.

Do subjects with aggressive and chronic periodontitis exhibit a different cytokine/chemokine profile in the gingival crevicular fluid? A systematic review.

BACKGROUND AND OBJECTIVE: Microbiological and immunological hypotheses have been raised to explain the differences in the clinical manifestations of aggressive periodontitis and chronic periodontitis. However, studies comparing the cytokine/chemokine profiles in gingival crevicular fluid between these two clinical conditions have so far not been compiled. This systematic review aimed to answer the following question: "Do subjects with aggressive periodontitis and chronic periodontitis have a different profile of cytokines/chemokines in the gingival crevicular fluid?" MATERIAL AND METHODS: An electronic database search of MEDLINE/PubMed and Embase was performed from 1990 up to and including August 2013, using MeSH terms and other keywords. Titles and abstracts were screened and the papers that satisfied eligibility criteria were assessed. RESULTS: Of 1954 titles, 17 studies reporting the levels of 21 different cytokines/chemokines were included. Most studies did not find any significant differences in the gingival crevicular fluid levels of cytokines/chemokines between aggressive periodontitis and chronic periodontitis. Some studies demonstrated that the levels of specific proinflammatory and anti-inflammatory cytokines/chemokines were higher (n = 5) and lower (n = 3), respectively, in aggressive periodontitis than in chronic periodontitis. The studies differed in the manner in which they reported the results (e.g. concentrations or total amounts). It was not clear in some studies whether the sample sites from both groups were matched for disease severity. Some studies did not take into account confounders, such as smoking. CONCLUSION: The current weight of evidence is not sufficient to prove that there are distinct gingival crevicular fluid cytokine/chemokine profiles for patients with aggressive periodontitis and chronic periodontitis.

Newly identified pathogens associated with periodontitis: a systematic review.

There is substantial evidence supporting the role of certain oral bacteria species in the onset and progression of periodontitis. Nevertheless, results of independent-culture diagnostic methods introduced about a decade ago have pointed to the existence of new periodontal pathogens. However, the data of these studies have not been evaluated together, which may generate some misunderstanding on the actual role of these microorganisms in the etiology of periodontitis. The aim of this systematic review was to determine the current weight of evidence for newly identified periodontal pathogens based on the results of "association" studies. This review was conducted and reported in accordance with the PRISMA statement. The MEDLINE, EMBASE, and Cochrane databases were searched up to September 2013 for studies (1) comparing microbial data of subgingival plaque samples collected from subjects with periodontitis and periodontal health and (2) evaluating at least 1 microorganism other than the already-known periodontal pathogens. From 1,450 papers identified, 41 studies were eligible. The data were extracted and registered in predefined piloted forms. The results suggested that there is moderate evidence in the literature to support the association of 17 species or phylotypes from the phyla Bacteroidetes, Candidatus Saccharibacteria, Firmicutes, Proteobacteria, Spirochaetes, and Synergistetes. The phylum Candidatus Saccharibacteria and the Archaea domain also seem to have an association with disease. These data point out the importance of previously unidentified species in the etiology of periodontitis and might guide future investigations on the actual role of these suspected new pathogens in the onset and progression of this infection.

[Bacteremia of oral origin]. / Bactériémies d'origine buccale.

Transient bacteremia from oral cavity related to oral anaerobic bacteria may occur as a result of dental healthcare procedures but also as a result of daily gestures involving the gums (chewing and oral hygiene). The risk of presenting a transient bacteremia is related to oral cavity bacterial load and to the severity of inflammation in the oral cavity. Although bacteremia is transient, in patients with immunodeficiency or comorbidity, this bacteremia may cause extra-oral infections. The bacteremia rate and the identified bacteria vary from one study to the next, depending on the method used to isolate and identify bacteria. Nevertheless, the risk for bacteremia is determined by the infectious and inflammatory conditions of each patient.

fimA genotypes and PFGE profile patterns in Porphyromonas gingivalis isolates from subjects with periodontitis.

BACKGROUND AND OBJECTIVES: Porphyromonas gingivalis is frequently identified to type by evaluation of fimA polymorphisms and less often by pulsed-field gel electrophoresis (PFGE) because of the technical intricacies of PFGE. To compare these techniques, we genotyped P. gingivalis clinical isolates as to (i) their fimA type and (ii) their whole genome restriction profile (PFGE analysis). MATERIAL AND METHODS: Thirty-two P. gingivalis strains were isolated from 16 unrelated periodontitis patients. Two strains were isolated from each patient. Strains were subjected to a fimA-typing polymerase chain reaction (PCR) assay. Strains that could not be typed by PCR were submitted to sequencing of the entire fimA gene. The PFGE profiles of clinical strains were compared using bioinformatic analysis. RESULTS: Seven of the 32 isolates were not typeable by PCR and so their entire fimA gene was sequenced. The sequencing identified each strain as belonging to a single fimA type. In one case, sequencing of the fimA gene did not agree with the result obtained using fimA PCR typing. With the exception of one patient, each patient presented isolates bearing the same fimA type. However, in three patients, isolates with the same fimA type presented different PFGE pulsotypes. CONCLUSION: The P. gingivalis typing using fimA PCR has limitations in typeability and discriminatory power. A typing technique for P. gingivalis that is easy to perform but that presents adequate typeability and discriminatory power is needed if we want to better understand the epidemiology of periodontal disease.