This review aimed to systematically compare microbial profiles of peri-implantitis to those of periodontitis and healthy implants. Therefore, an electronic search in five databases was conducted. For inclusion, studies assessing the microbiome of peri-implantitis in otherwise healthy patients were considered. Literature was assessed for consistent evidence of exclusive or predominant peri-implantitis microbiota. Of 158 potentially eligible articles, data of 64 studies on 3730 samples from peri-implant sites were included in this study. Different assessment methods were described in the studies, namely bacterial culture, PCR-based assessment, hybridization techniques, pyrosequencing, and transcriptomic analyses. After analysis of 13 selected culture-dependent studies, no microbial species were found to be specific for peri-implantitis. After assessment of 28 studies using PCR-based methods and a meta-analysis on 19 studies, a higher prevalence of Aggregatibacter actinomycetemcomitans and Prevotella intermedia (log-odds ratio 4.04 and 2.28, respectively) was detected in peri-implantitis biofilms compared with healthy implants. Actinomyces spp., Porphyromonas spp. and Rothia spp. were found in all five pyrosequencing studies in healthy-, periodontitis-, and peri-implantitis samples. In conclusion, the body of evidence does not show a consistent specific profile. Future studies should focus on the assessment of sites with different diagnosis for the same patient, and investigate the complex host-biofilm interaction.

Objectives The aim of the article was to present an overview of the management strategies of dentin hypersensitivity (DHS) and summarize and discuss the therapeutic options. Materials and methods A PubMed literature search was conducted to identify articles dealing with dentin hypersensitivity prophylaxis and treatment. We focussed on meta-analyses of available or controlled clinical trials. Results DHS therapy should start with noninvasive individual prophylactic home-care approaches. In-office therapy follows with nerve desensitizing, precipitating, or plugging agents. If the hypersensitivity persists, depending on the hard and soft tissue components at reevaluation, i.e., presence or absence of cervical lesions and the gingival contour, adhesive restorations including sealing or mucogingival surgery may be an option. They allow for the establishment of a physicomechanical barrier. As the placebo effect may play an important role, adequate patient management strategies and positive reinforcement may improve the management of DHS in the future. Conclusions Lifelong maintenance under the premise of strict control of the causative factors is crucial in the management of DHS. Clinical relevance Clinicians are faced with a broad spectrum of therapeutic options. Therapy should not only focus on pain reduction or better elimination but also on the modification of the exposed cervical dentin area based on the defect type.

To assess the re-hardening potential of enamel matrix derivatives (EMD) and self-assembling peptides in vitro, hypothesizing that these materials may increase the mineralization of artificial carious lesions and improve hardness profiles. Forty-eight enamel samples were prepared from extracted bovine lower central incisors. After embedding and polishing, nail varnish was applied, leaving a defined test area. One third of this area was covered with a flowable composite (non-demineralized control). The remaining area was demineralized in an acidic buffer solution for 18 d to simulate a carious lesion. Half the demineralized area was then covered with composite (demineralized control), while the last third was left open for three test and one control treatments: (A) Application of enamel-matrix proteins (EMD - lyophilized protein fractions dissolved in acetic acid, Straumann), (B) self-assembling peptides (SAP, Curodont), or (C) amine fluoride solution (Am-F, GABA) for 5 min each. Untreated samples (D) served as control. After treatment, samples were immersed in artificial saliva for four weeks (remineralization phase) and microhardness (Knoop) depth profiles (25-300 µm) were obtained at sections. Two-way ANOVA was calculated to determine differences between the areas (re-hardening or softening). Decalcification resulted in significant softening of the subsurface enamel in all groups (A-D). A significant re-hardening up to 125 µm was observed in the EMD and SAP groups. This study showed that EMD and SAP were able to improve the hardness profiles when applied to deep demineralized artificial lesions. However, further research is needed to verify and improve this observed effect.