BackgroundPrimary failure of eruption (PFE) is a rare disease defined as incomplete tooth eruption despite the presence of a clear eruption pathway. Orthodontic extrusion is not feasible in this case because it results in ankylosis of teeth. To the best of our knowledge, besides the study of Ahmad et al. (Eur J Orthod 28:535-540, 2006), no study has systematically analysed the clinical features of and factors associated with PFE. Therefore, the aim of this study was to systematically evaluate the current literature (from 2006 to 2017) for new insights and developments on the aetiology, diagnosis, genetics, and treatment options of PFE.MethodsFollowing the PRISMA guidelines, a systematic search was performed using the PubMed/Medline database for studies reporting on PFE. The following terms were used: “primary failure of tooth eruption”, “primary failure of eruption”, “tooth eruption failure”, and “PFE”.ResultsOverall, 17 articles reporting clinical data of 314 patients were identified. In all patients, the molars were affected. In 81 reported cases, both the molars and the premolars were affected by PFE. Further, 38 patients’ primary teeth were also affected. In 27 patients, no family members were affected. Additional dental anomalies were observed in 39 patients. A total of 51 different variants of the PTH1R gene associated with PFE were recorded.ConclusionsInfraocclusion of the posterior teeth, especially if both sides are affected, is the hallmark of PFE. If a patient is affected by PFE, all teeth distal to the most mesial tooth are also affected by PFE. Primary teeth can also be impacted; however, this may not necessarily occur. If a patient is suspected of having PFE, a genetic test for mutation in the PTH1R gene should be recommended prior to any orthodontic treatment to avoid ankylosis. Treatment options depend on the patient’s age and the clinical situation, and they must be evaluated individually.

The aim of this study was to evaluate the effect of an epoxy resin-based (AH-Plus), a zinc oxide eugenol containing (Pulp-Canal-Sealer) and two calcium silicate containing (MTA-Fillapex and BioRoot-RCS) sealers on primary human osteoblasts (hOB) in freshly mixed and set state. All sealers were mixed strictly according to the manufacturers´ instructions and identically samples were produced. In a pretest cytotoxic sealer concentrations were determined. Thus, for the main cell culture study, dilutions of sealer extract 1:1, 1:2, and 1:10 were used. To simulate a clinical scenario, extracts from freshly mixed sealer were added to the cells on day one. Extracts form set sealers were used for subsequent culturing for 24h, 7d, 14d, and 21d. Cell viability was analyzed by living-cell-count, MTT-assay, and living/dead-staining, cytotoxicity by LDH-assay, and changes by Richardson-staining. All data were statistically evaluated by one way ANOVA and a posthoc analysis with Bonferroni-Holm testing (p<0.05). AH-Plus was cytotoxic in a freshly mixed state, but not when the sealer was set. MTA-Fillapex and Pulp-Canal-Sealer were cytotoxic in a fresh as well as in a set state. BioRoot-RCS showed the lowest toxicity in both states; where as a regeneration of the cells could be observed over time (p<0.05). Contact of freshly mixed AH-Plus to osteoblasts should be avoided. Pulp Canal Sealer and MTA-Fillapex showed no biocompatibility in contact with osteoblasts at all. BioRoot-RCS had a positive influence on the cell metabolism (bioactivity) and is biocompatible.

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The aim of this study was to evaluate the biocompatibility of two comparatively new calcium silicate containing sealers (MTA-Fillapex and BioRoot-RCS) with that of two established sealers (AH-Plus, epoxy resin-based; Pulp-Canal-Sealer, zinc oxide eugenol containing). Human periodontal ligament cells (PDL-cells) were brought in contact with eluates from freshly mixed and set sealer. The sealers were mixed strictly according to the manufacturers' instructions and identically samples were produced. 1:1, 1:2, and 1:10 dilutions of sealers extract were used. Extracts from freshly mixed sealer were added to the PDL-cells on day one to simulate a clinical scenario. Subsequently, at 24 h, 7, 14, and 21 days extracts form set sealers were used for PDL-cell culturing. PDL-cell viability was analyzed by living-cell-count, MTT-assay, and living/dead-staining, cytotoxicity by LDH-assay, and changes by Richardson-staining. All data were statistically evaluated by one way ANOVA and a posthoc analysis with Bonferroni-Holm testing (p < 0.05). In contact with BioRoot-RCS a regeneration of the PDL-cells were observed over time. This sealer showed the lowest toxicity in a freshly mixed and set state (p < 0.05). MTA-Fillapex and Pulp-Canal-Sealer were cytotoxic in a fresh as well as in a set state, whereas AH-Plus was cytotoxic in a freshly mixed state, but not when the sealer was set. BioRoot-RCS is biocompatible and bioactive because it seems to have a positive influence on the PDL-cell metabolism. Pulp Canal Sealer and MTA-Fillapex showed no biocompatibility in contact with PDL-cells at all. Freshly mixed AH Plus is less biocompatible on PDL than in a set state.

The purpose of this study was to compare the accuracy of stereolithographic casts (SCs) with those obtained using conventional implant impressions. An epoxy resin model containing dental implants was used as master model. Dental casts (n = 10) were fabricated through both conventional and digital implant impressions. The conventional casts (CCs), SCs, and the master model were digitized, and the accuracy was determined through a deviation analysis and linear measurements. Data were analyzed using paired Student t test with P &lt; .05. The SCs showed higher deviation at the vestibular area (CC: 41 ± 28.87 μm; SC: 117 ± 36.83 μm) and lingual cusps (CC: 40.70 ± 19.79 μm; SC: 80 ± 42.95 μm) in comparison with CCs. No statistically significant difference was found for linear measurements of conventional and digital casts. The entire-arch accuracy was comparable between casts. However, SCs were less accurate at the cusp level in comparison with CCs.

Background: Most simulation models used at university dental clinics are typodonts. Usually, models show idealized eugnathic situations, which are rarely encountered in everyday practice. The aim of this study was to use 3D printing technology to manufacture individualized surgical training models for root tip resection (apicoectomy) on the basis of real patient data and to compare their suitability for dental education against a commercial typodont model. Methods: The training model was designed using CAD/CAM (computer-aided design/computer-aided manufacturing) technology. The printer used to manufacture the models employed the PolyJet technique. Dental students, about one year before their final examinations, acted as test persons and evaluated the simulation models on a visual analogue scale (VAS) with four questions (Q1–Q4). Results: A training model for root tip resection was constructed and printed employing two different materials (hard and soft) to differentiate anatomical structures within the model. The exercise was rated by 35 participants for the typodont model and 33 students for the 3D-printed model. Wilcoxon rank sum tests were carried out to identify differences in the assessments of the two model types. The alternative hypothesis for each test was: “The rating for the typodont model is higher than that for the 3D-printed model”. As the p-values reveal, the alternative hypothesis has to be rejected in all cases. For both models, the gingiva mask was criticized. Conclusions: Individual 3D-printed surgical training models based on real patient data offer a realistic alternative to industrially manufactured typodont models. However, there is still room for improvement with respect to the gingiva mask for learning surgical incision and flap formation.

Tumor development and progression is the consequence of genetic as well as epigenetic alterations of the cell. As part of the epigenetic regulatory system, histone acetyltransferases (HATs) and deacetylases (HDACs) drive the modification of histone as well as non-histone proteins. Derailed acetylation-mediated gene expression in cancer due to a delicate imbalance in HDAC expression can be reversed by histone deacetylase inhibitors (HDACi). Histone deacetylase inhibitors have far-reaching anticancer activities that include the induction of cell cycle arrest, the inhibition of angiogenesis, immunomodulatory responses, the inhibition of stress responses, increased generation of oxidative stress, activation of apoptosis, autophagy eliciting cell death, and even the regulation of non-coding RNA expression in malignant tumor cells. However, it remains an ongoing issue how tumor cells determine to respond to HDACi treatment by preferentially undergoing apoptosis or autophagy. In this review, we summarize HDACi-mediated mechanisms of action, particularly with respect to the induction of cell death. There is a keen interest in assessing suitable molecular factors allowing a prognosis of HDACi-mediated treatment. Addressing the results of our recent study, we highlight the role of p53 as a molecular switch driving HDACi-mediated cellular responses towards one of both types of cell death. These findings underline the importance to determine the mutational status of p53 for an effective outcome in HDACi-mediated tumor therapy.