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Objectives: Narrow-diameter implants (NDI) are claimed to be a reasonable alternative to bone augmentation procedures. The aim of this comprehensive literature review was to conduct a meta-analysis comparing the implant survival of NDI and standard diameter implants (SDI) and to provide recommendations and guidelines for application of NDI.Material and methods: An extensive systematic literature search was performed in the PubMed/MEDLINE and the Cochrane Library databases. NDI were classified into Category 1 (implant diameter <3.0 mm, "mini-implants"), Category 2 (implant diameter 3-3.25 mm) and Category 3 (implant diameters 3.3-3.5 mm). Clinical studies at all levels of evidence with at least 10 patients included and a follow-up time of at least 12 months were included. The primary outcome criterion was the survival rates of NDI. Results: Seventy-six studies were identified for qualitative and 16 studies for quantitative synthesis. Quality assessment illustrated a high risk of bias for the included literature. Mean implant survival rates were 94.7 ± 5%, 97.3 ± 5% and 97.7 ± 2.3% for Categories 1, 2 and 3. Meta-analysis indicated a statistically significant lower implant survival of Category 1 NDI compared to SDI ([OR], 4.54; [CI], 1.51-13.65). For Category 2 and Category 3, no statistical significant differences in implant survival were seen compared to SDI ([OR], 1.06; [CI], 0.31-3.61 and [OR], 1.19; [CI], 0.83-1.70).Conclusion: NDI of Category 1 performed statistically significantly worse than SDI and were mainly described for the rehabilitation of the highly atrophic maxilla or mandible. Category 2 and Category 3 NDI showed no difference in implant survival compared to SDI. Category 2 NDI were mostly used for the rehabilitation of limited interdental spaces in anterior single-tooth restorations. NDI of Category 3 were described in all regions, including posterior single-tooth restorations. However, resilient long-term data and data on the possible risk of biological and technical complications with wide platform teeth on NDI are missing so far. K E Y W O R D Smeta-analysis, narrow diameter, review, small dental implants, survivalThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

BackgroundThe augmentation of the jaw has been and continues to be a sophisticated therapy in implantology. Modern CAD-CAM technologies lead to revival of old and established augmentation techniques such as the use of titanium mesh (TM) for bone augmentation. The aim of this retrospective study was to evaluate the clinical outcome of an individualized CAD-CAM-produced TM based on the CT/DVT-DICOM data of the patients for the first time.MethodsIn 17 patients, 21 different regions were augmented with an individualized CAD-CAM-produced TM (Yxoss CBR®, Filderstadt, Germany). For the augmentation, a mixture of autologous bone and deproteinized bovine bone mineral (DBBM) or autologous bone alone was used. Reentry with explantation of the TM and simultaneous implantation of 44 implants were performed after 6 months. Preoperative and 6-month postoperative cone beam computed tomographies (CBCT) were performed to measure the gained bone height.ResultsThe success rate for the bone grafting procedure was 100%. Thirty-three percent of cases presented an exposure of the TM during the healing period. However, premature removal of these exposed meshes was not necessary. Exposure rate in augmentations performed with mid-crestal incisions was higher than in augmentations performed with a modified poncho incision (45.5 vs. 20%, p = 0.221). In addition, exposure rates in the maxilla were significantly higher than in the mandible (66.7 vs. 8.3%, p = 0.009). Gender, smoking, periodontal disease, gingiva type, used augmentation material, and used membrane had no significant influence on the exposure rate (p > 0.05). The mean vertical augmentation was 6.5 ± 1.7 mm, and the mean horizontal augmentation was 5.5 ± 1.9 mm. Implant survival rate after a mean follow-up of 12 ± 6 months after reentry was 100%.ConclusionWithin the limits of the retrospective character of this study, this study shows for the first time that individualized CAD-CAM TM provide a sufficient and safe augmentation technique, especially for vertical and combined defects. However, the soft tissue handling for sufficient mesh covering remains one of the most critical steps using this technique.

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The evolution of implant hardware and improvement of treatment strategies during the last years have affirmed dental implant-supported concepts as a valuable treatment option for patients with a history of radiation in the head and neck region.

Resorption of the alveolar ridge cannot be totally stopped by ARP, while it still can be prevented compared with unassisted healing. No reliable predictions on the histological effects could be made due to limited data. Further on, no recommendation for a specific technique of ARP could be made. In conclusion, there is still need for ongoing research on the topic, even though the lower percentage of implant sites that needed additional augmentation in test sockets seemed to bring a patient benefit.

Nonetheless, INR should be less than 4, local hemostatic measures are of high importance and patients need to be instructed and closely monitored as minor bleedings might occur more often in OAT patients.

Growth differentiation factor 15 (GDF15) is induced during heart failure development, and may influence different processes in cardiac remodeling. While its anti-apoptotic action under conditions of ischemia-reperfusion have been shown, it remained unclear if this is a broadly protective effect applicable to other apoptotic stimuli. Furthermore, effects on cardiac hypertrophy remained obscure. Therefore, we investigated the effects of GDF15 on induction of hypertrophy and apoptosis in ventricular cardiomyocytes. GDF15 (3 ng/ml) enhanced hypertrophic growth of cardiomyocytes as determined by an increase in cell size by 27 +/- 5% and rate of protein synthesis by 47 +/- 15%. In addition, a time and dose-dependent increase in SMAD-binding affinity was found, as well as enhanced phosphorylation of R-SMAD1. Inhibition of SMADs by transformation of cardiomyocytes with SMAD-decoy oligonucleotides abolished the hypertrophic growth effect. Specific inhibitors of PI3K (10 microM LY290042 or 10 nM wortmannin) or ERK (10 microM PD98059) also blocked GDF15-induced hypertrophy and SMAD activation. Apoptosis induction by three different agents, 100 nM angiotensin II, 1 ng/ml TGFbeta(1), or the NO-donor SNAP (100 microM) was blocked by addition of GDF15 (3 ng/ml). Scavenging of SMADs by transformation of cardiomyocytes with SMAD-decoy oligonucleotides abolished the anti-apoptotic effect of GDF15. In conclusion, GDF15 protects ventricular cardiomyocytes against different apoptotic stimuli and enhances hypertrophic growth. Hypertrophic signaling is thereby mediated via the kinases PI3K and ERK and the transcription factor R-SMAD1. Thus, GDF15 may influence cardiac remodeling via two different mechanisms, apoptosis protection and induction of hypertrophy.