RESUMO
Background and Objective: Loosening of abutment screws in dental implants is a mechanical complication that affects prosthetic treatments and hence, patient satisfaction. Blood contamination of abutment screws may play a role in this phenomenon. However, only limited research attention has been given to this issue. In the present study, we determined the effect of blood contamination and decontamination protocol on the reverse torque value (RTV) of abutment screws. Materials and Methods: A questionnaire-based survey was sent to 210 implantologists requesting feedback on their attitude to the blood contamination issue and the decontamination protocols used. The survey responses were used in a selection of the decontamination solutions that were used in the subsequent in vitro study on the effects of blood decontamination protocol on the RTV of abutment screws. Thus, three study groups were used (n = 20 abutment screws in each group): Group 1 (control group; blood-contaminated screws); Group 2 (screws decontaminated with 5.25% sodium hypochlorite (NaOCl) solution); and Group 3 (screws decontaminated with normal saline solution (0.9%)). Then, each of the connections were subjected to thermocycling, and RTVs of the screw were measured using a digital torque meter. Intragroup and intergroup RTVs were analyzed for significance using analysis of variance (ANOVA) and Tukey's honestly significant difference (HSD) tests. Results: 48% of the implantologists responded to the survey; 80% of them were concerned with blood contamination in the implant connection, especially before abutment loading and 85% of them used either chlorhexidine solution or normal saline solution as the decontamination agent. The mean RTV for Group 2 screws (30.27 ± 2.8 N.cm) was significantly greater than that for Group 3 screws (26.02 ± 1.99 N.cm) which, in turn, was significantly greater than that for Group 1 screws (23.64 ± 1.84 N.cm). Conclusion: Decontamination of blood-covered connections using 5.25% NaOCl solution or normal saline solution restores the RTV of abutment screws. This finding may have clinical relevance in that the decontaminated screws may contribute to the low incidence of screw loosening and, ultimately, improved patient satisfaction.
RESUMO
Knowledge of photo-oxidative stress responses in bacteria that survive antimicrobial photodynamic therapy (aPDT) is scarce. Whereas aPDT is attracting growing clinical interest, subsequent stress responses are crucial to evaluate as they may lead to the up-regulation of pathogenic traits. Here, we aimed to assess transcriptional responses to sublethal aPDT-stress and identify potential connections with virulence-related genes. Six Enterococcus faecalis strains were investigated; ATCC 29212, three dental root-canal isolates labelled UmID1, UmID2 and UmID3 and two vancomycin-resistant isolates labelled A1 and A2. TMPyP was employed as a photosensitiser. A viability dose-response curve to increasing concentrations of TMPyP was determined by culture plating. Differential expression of genes involved in oxidative stress responses (dps and hypR), general stress responses (dnaK, sigma-factorV and relA), virulence-related genes (ace, fsrC and gelE) and vancomycin-resistance (vanA) was assessed by reverse-transcription qPCR. TMPyP-mediated aPDT inactivated all strains with comparable efficiencies. TMPyP at 0.015 µM was selected to induce sublethal photo-oxidative stress. Despite heterogeneities in gene expression between strains, transcriptional profiles revealed up-regulations of transcripts dps, hypR as well as dnaK and sigma factorV after exposure to TMPyP alone and to light-irradiated TMPyP. Specifically, the alternative sigma factorV reached up to 39 ± 113-fold (median ± IQR) (p = 0.0369) in strain A2. Up-regulation of the quorum sensing operon, fsr, and its downstream virulence-related gelatinase gelE were also observed in strains ATCC-29212, A1, A2 and UmID3. Finally, photo-oxidative stress induced vanA-type vancomycin-resistance gene in both carrier isolates, reaching up to 3.3 ± 17-fold in strain A2 (p = 0.015). These findings indicate that, while aPDT successfully inactivates vancomycin-resistant and naïve strains of E. faecalis, subpopulations of surviving cells respond by co-ordinately up-regulating a network of genes involved in stress survival and virulence. This includes the induction of vancomycin-resistance genes in carrier isolates. These data may provide the mechanistic basis to circumvent bacterial responses and improve future clinical protocols.
