Objective. Patients with RA suffer from a higher risk of periodontal attachment loss and increased oral inflammation. We hypothesize that there are pathogenetic and immunological interactions between these diseases that go beyond impaired manual dexterity accompanying advanced RA. The primary objective of the present study was to determine whether a loss of alveolar bone can be detected in RA patients during the early course of the disease. Methods. In this cross-sectional, epidemiological case–control study, 22 patients with early RA (ERA) were compared with 22 matched healthy controls. Oral and periodontal status, clinical activity, and socio-demographic parameters were determined. Oral microbiota were analysed using real-time quantitative PCR specific for leading oral pathogens. Results. More advanced forms of periodontitis were found in ERA patients compared with controls. ERA patients had a greater number of missing teeth [ERA 5.7 (s.d. 5.0), controls 1.9 (s.d. 1.0), P = 0.002], deeper periodontal pockets [clinical attachment level: ERA 3.4 (s.d. 0.5 mm), controls 2.7 (s.d. 0.3 mm), P < 0.000], and greater bleeding on probing [ERA 18.6% (s.d. 9.0%), controls 10.5% (s.d. 5.1%), P = 0.001] despite comparable oral hygiene. Tannerella forsythia (6.77-fold, P = 0.033) subgingivally and Streptococcus anginosus (3.56-fold, P = 0.028) supragingivally were the characteristic pathogens in ERA. Conclusion. Increased loss of periodontal attachment and alveolar bone can be detected in patients with ERA, therefore we propose that the consulting rheumatologists inform the patients that they have a higher risk of periodontal disease. It would be beneficial if these patients were referred directly for intensive dental care.

Background: Certain major pathogens such as Streptococcus mutans, Lactobacillus spp. and others have been reported to be involved in caries initiation and progression. Yet, in addition to those leading pathogens, microbial communities seem to be much more diverse and individually differing. The aim of this study, therefore, was to analyze the bacterial composition of carious dentin and the plaque of caries-free patients by using a custom-made, real-time quantitative polymerase chain reaction assay (RQ-PCR). Methods: The study included 26 patients with caries and 28 caries-free controls. Decayed tooth substance and plaque samples were harvested. Bacterial DNA was extracted and tested for the presence of 43 bacterial species or species groups using RQ-PCR. Results: Relative quantification revealed that Propionibacterium acidifaciens was significantly more abundant in caries samples than were other microorganisms (fold change 169.12, p = 0.023). In the caries-free samples, typical health-associated species were significantly more prevalent. Unsupervised hierarchical cluster analysis showed a high abundance of P. acidifaciens in caries subjects and distinct but individually differing bacterial clusters in the caries-free subjects. The distribution of 11 bacteria allowed full discrimination between caries and caries-free subjects. Conclusion: Within the investigated cohort, P. acidifaciens was the only pathogen significantly more abundant in caries subjects. Cluster analysis yielded a diverse flora in caries-free subjects, whereas it was narrowed down to a small range of a few outcompeting members in caries subjects.

To elicit patterns in pathogenic biofilm composition we characterized the oral microbiome present in patients with dentin caries in comparison to healthy subjects. 16S amplicon sequencing was used to analyse a total of 56 patients; 19 samples of carious dentin (pooled from at least three teeth) and 37 supragingival samples (pooled from three healthy tooth surfaces). Oral and periodontal status and socio-demographic parameters were recorded. Group assignment, smoking and further socio-demographic parameters were used as explanatory variables in the microbiome composition analysis. Overall, a total of 4,110,020 DNA high-quality sequences were yielded. Using a threshold of similarity >97% for assigning operational taxonomic units (OTU), a total of 1,537 OTUs were identified. PERMANOVA showed significant differences in microbiome composition between the groups caries/healthy (p = 0.001), smoking/non-smoking (p = 0.007) and fluoride intake during childhood yes/no (tablets p = 0.003, salt p = 0.023). The healthy microbiome had a significantly higher diversity (alpha diversity, p<0.001) and a lower dominance (Berger-Parker index, p<0.001). It was dominated by Fusobacteria. A linear discriminant analysis effect size (LEfSe) yielded a set of 39 OTUs being more abundant in carious dentin samples, including Atopobium spp. (14.9 log2FoldChange), Lactobacillus casei (11.6), Acinetobacter spp. (10.8), Lactobacillus gasseri (10.6), Parascardovia denticolens (10.5), Olsenella profusa (10.4), and others. Also Propionibacterium acidifaciens (7.2) and Streptococcus mutans (5.2) were overabundant in caries lesions. The healthy microbiome was highly diverse. The advanced caries microbiome was dominated by a set of carious associated bacteria where S. mutans played only a minor role. Smoking and fluoride intake during childhood influenced the microbiome composition significantly. The presented investigation adds knowledge to the still not fully comprehended patterns of oral microbiomes in caries compared with oral health. By analysing the genetics of biofilm samples from oral health and severe tooth decay we found distinct discriminating species which could be targets for future therapeutic approaches.

Despite the wide-spread use of antiseptics in dental practice and oral care products, there is little public awareness of potential risks associated with antiseptic resistance and potentially concomitant cross-resistance. Therefore, the aim of this study was to investigate potential phenotypic adaptation in 177 clinical isolates of early colonizers of dental plaque (Streptococcus, Actinomyces, Rothia and Veillonella spp.) upon repeated exposure to subinhibitory concentrations of chlorhexidine digluconate (CHX) or cetylpyridinium chloride (CPC) over 10 passages using a modified microdilution method. Stability of phenotypic adaptation was re-evaluated after culture in antiseptic-free nutrient broth for 24 or 72 h. Strains showing 8-fold minimal inhibitory concentration (MIC)-increase were further examined regarding their biofilm formation capacity, phenotypic antibiotic resistance and presence of antibiotic resistance genes (ARGs). Eight-fold MIC-increases to CHX were detected in four Streptococcus isolates. These strains mostly exhibited significantly increased biofilm formation capacity compared to their respective wild-type strains. Phenotypic antibiotic resistance was detected to tetracycline and erythromycin, consistent with the detected ARGs. In conclusion, this study shows that clinical isolates of early colonizers of dental plaque can phenotypically adapt toward antiseptics such as CHX upon repeated exposure. The underlying mechanisms at genomic and transcriptomic levels need to be investigated in future studies.