Bacterial antagonism against periodontopathogens.

Background: The aim of the current study is to compare the prevalence of commensal bacteria, with beneficial properties, for healthy and diseased individuals and additionally to examine the inhibitory effect of some commercial dietary probiotics on periodontopathogens, comparing this inhibitory effect to that of orally derived beneficial bacteria.

Methods: Subgingival plaque samples from 35 patients (healthy and periodontitis patients) were analyzed. Growth inhibition of the periodontal pathogens Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, and Aggregatibacter actinomycetemcomitans was examined using the agar overlay technique and agar well diffusion method.

Do periodontopathogens disappear after full-mouth tooth extraction?

Aim: To monitor the intra-oral microbiological changes after full-mouth extraction using quantitative polymerase chain reaction (qPCR).

Material And Methods: Nine patients with severe, aggressive periodontitis, for whom a full-mouth tooth extraction was the only remaining treatment option were recruited. Before and 6 months after extraction, microbial samples were obtained (tongue, saliva and subgingival plaque) and analysed by qPCR.

Effect of mouthrinses on Aggregatibacter actinomycetemcomitans biofilms in a hydrodynamic model.

The aim of the study was to evaluate the effects of Listerine, Meridol, and Perioaid on the viability and total number of bacteria in established biofilms using an in vitro model under hydrodynamic conditions. Biofilms of Aggregatibacter actinomycetemcomitans were placed in a modified Robbins device and rinsed twice daily during 4 days. Bacteria were quantified by culture and quantitative polymerase chain reaction.

Absence of the Kilifi mutation in the rhinovirus-binding domain of ICAM-1 in a Caucasian population.

Human rhinoviruses (HRV), responsible for approximately 60% of the common colds, are divided into two groups, according to their receptor specificity. The major group of HRVs gains access to human cells by binding to the intercellular adhesion molecule-1 (ICAM-1), whereas HRVs of the minor group use members of the low-density lipoprotein receptor (LDLR) family for cell entry. Previous studies confirmed that the HRV-binding region of ICAM-1 is located in the amino-terminal immunoglobulin-like (Ig) domain 1, which is encoded by exon 2 of the ICAM-1 gene.