Infective endocarditis (IE) is an inflammatory disease usually caused by bacteria entering the bloodstream and settling in the heart lining valves or blood vessels. Despite modern antimicrobial and surgical treatments, IE continues to cause substantial morbidity and mortality. Thus, primary prevention and enhanced diagnosis remain the most important strategies to fight this disease. In this regard, it is worth noting that for over 50 years, oral microbiota has been considered one of the significant risk factors for IE. Indeed, among the disparate recommendations from the American heart association and the European Society of Cardiology, there are good oral hygiene and prophylaxis for high-risk patients undergoing dental procedures. Thus, significant interest has grown in the role of oral microbiota and it continues to be a subject of research interest, especially if we consider that antimicrobial treatments can generate drug-resistant mutant bacteria, becoming a severe social problem. This review will describe the current knowledge about the relationship between oral microbiota, dental procedures, and IE. Further, it will discuss current methods used to prevent IE cases that originate from oral pathogens and how these should be focused on improving oral hygiene, which remains the significant persuasible way to prevent bacteremia and systemic disorders.

The microbiological monitoring of mineral bottled waters results is crucial for the prevention of outbreaks in consumers. European and International regulations establish the quality of water intended for human consumption in order to preserve human health from the negative effects deriving from water contamination. Advanced methods targeting the faster detection of potential pathogens in drinking water may consent to the creation of an early warning system, enhancing water quality management. This study aimed to suggest the implementation of standard water quality evaluations, based on the characterization of the microbial composition of mineral bottled water brands, contributing to the periodic control of the water’s microbiological stability along with the shelf life, and, consequently, the stability of the supplying sources. Bottled water microbiota analysis was combined with the qualitative and quantitative evaluation of microbial loads in time, and the monitoring was performed in two seasons and two different storage conditions for a total of sixty days. The employment of molecular microbiology techniques (NGS and Sanger sequencing), compared to standardized cultural methods and integrated with metagenomic analysis, combining chemical and physical indicators for each sample, allowing for the generation of specific fingerprints for mineral bottled waters, pointing at simplifying and improving the foreseen risk assessment strategies to ensure the adequate traceability, quality and safety management of drinking water.

The aim of the present study was to compare the effects of folinic acid chitosan hydrogel and botulinum toxin A on the wound repair of cleft lip surgery in rat animal models. Cleft lip defects were simulated by triangular incisions in the upper lip of 40 Wistar rats. Then, the rats were randomly assigned to four groups: control (CTRL), chitosan hydrogel (CHIT), and folinic acid chitosan hydrogel (FOLCHIT), in which the wounds were covered by a gauze pad soaked in normal saline, chitosan hydrogel, and folinic acid chitosan hydrogel, respectively for 5 min immediately after closure; and botulinum toxin A (BOT) with the injection of 3 units of botulinum toxin A in the wound region. Fibroblast proliferation, collagen deposition, inflammatory cell infiltration, neovascularization, and epithelial proliferation and each parameter were rated on days 14 and 28. Statistical analysis was performed by Kolmogorov-Smirnov test, Shapiro-Wilk test, Kruskal-Wallis, and post-hoc tests (α = 0.05). The mean score for fibroblast proliferation was significantly higher in the FOLCHIT group compared with the BOT group at days 14 and 28 (p < 0.001, p = 0.012, respectively). At day 28, collagen deposition was significantly higher in the FOLCHIT group compared with the BOT group (p = 0.012). No significant difference was observed between the inflammatory infiltration of the study groups at the two time points (p = 0.096 and p = 1.000, respectively). At day 14, vascular proliferation of group FOLCHIT was significantly higher than groups CTRL and CHIT (p = 0.001 and p = 0.006, respectively). The epithelial proliferation in the FOLCHIT group was significantly higher than groups CHIT and CTRL at day 14 (p = 0.006 and p = 0.001, respectively) and day 28 (p = 0.012). In simulated lip cleft defects, topical application of folinic acid induces faster initial regeneration by higher inflammation and cellular proliferation, at the expense of a higher tendency for scar formation by slightly higher fibroblast proliferation and collagen deposition. While injection of botulinum toxin A provides less fibroblast proliferation and collagen deposition, and thus lower potential for scar formation compared with the folinic acid group. Therefore, in wounds of the esthetic zone, such as cleft lip defects, the application of botulinum toxin A shows promising results.

Objectives: The aim of the current in vitro study was to assess the effect of simvastatin on the early-stage differentiation of human dental pulp stem cells (hDPSCs) in an odontogenic pattern by evaluating the expression of specific odontogenic-related genes. Methods: hDPSCs were cultured in the presence of different concentrations of simvastatin (0.1, 0.5, 1, 5, and 10 µM) to evaluate cytotoxicity. Moreover, osteogenic differentiation was assessed by Alkaline Phosphatase (ALP) activity and alizarin red staining (ARS) after 7 days of culture. Finally, odontogenic-related gene (OCN, MEPE, DSPP, and DMP-1) expression analysis was performed. Results: Three days after treatment, higher concentrations of simvastatin (1, 5, and 10 µM) significantly limited cell viability. Upregulation of ALP activity and odontoblastic cell-related genes (OCN and MEPE) was observed in the presence of 1 µM simvastatin. The expression was statistically higher for ALP (p = 0.0001) and OCN (p = 0.0231). On the other hand, comparable or slightly less effect concerning mineralization ability with respect to the control group, as well as in the expression of DSPP and DMP-1, was observed. Conclusions: Simvastatin demonstrated a positive influence on dentinogenesis by improving the expression of specific markers such as MEPE and OCN. However, its effect on inflammation reduction and the potential to be used in combination with other materials should be further assessed. Simvastatin might be successfully applied in the regeneration of damaged dental pulp tissues and promotion of reparative dentinogenesis. Additional studies should be carried out to support the obtained outcomes.