Effective and Efficient Correction of Severe Skeletal Class II Division 1 Malocclusion with Intermaxillary Elastics.

Treatment of Class II malocclusion accompanied with a skeletal discrepancy is challenging. The approach of correction depends on several factors such as the status and pattern of growth, severity of the malocclusion, and patient cooperation. This case report describes a successful management of a 12-year-old young adolescent boy that was presented with a Class II division 1 malocclusion with an underlying skeletal discrepancy in horizontal and vertical dimensions. Growth modification was achieved by means of bite opening and unlocking the mandible together with Class II elastics and mechanics. Treatment was highly effective and efficient by achieving all treatment goals within a period of 18 months.

Social media as a learning tool: Dental students' perspectives.

OBJECTIVES: This study explored the perceptions of dental students in Saudi Arabia for implementing social media as an educational tool. METHODS: A cross-sectional survey was conducted among dental students in 3 governmental dental schools in the western region of Saudi Arabia. A validated questionnaire was used to explore social media use and student perceptions on the advantages and disadvantages of implementing social media in dental education. Descriptive statistics and Pearson's' χ2 , Kruskal-Wallis, and Fishers' exact tests were used for data analysis. RESULTS: The survey included 1034 students from third to sixth year and dental interns. WhatsApp was the most used social media platform (97.5%), followed by Snapchat (90.5%), Twitter (85.2%), and Instagram (83.4%). Social media was used for entertainment (81.4%), dental learning (70.8%), searching for general information (63.3%), exchanging general ideas (63.1%), and community general discussion (55.8%). The predominant advantages of using social media in learning were assistance in gaining more information on different subjects, making education more engaging, affording a better chance to access new resources, improving the ability for creativity and innovation, and improving research skills. In contrast, the predominant disadvantages were distraction from studying, increasing addictive potential, increased time spent, and concerns over no direct contact with the instructors. CONCLUSION: The present findings suggest that students report social media can be a valuable learning tool in dental education if appropriately used. A proper understanding of social media and its usefulness in supporting learning can benefit both students and faculty members.

Expression of Evc2 in craniofacial tissues and craniofacial bone defects in Evc2 knockout mouse.

OBJECTIVE: Our objectives were to determine the expression of EVC2 in craniofacial tissues and investigate the effect of Evc2 deficiency on craniofacial bones using Evc2 knockout (KO) mouse model. DESIGN: Evc2 KO mice were generated by introducing a premature stop codon followed by the Internal Ribosomal Entry Site fused to ß-galactosidase (LacZ). Samples from wild-type (WT), heterozygous (Het) and homozygous Evc2 KO mice were prepared. LacZ staining and immunohistochemistry (IHC) with anti-ß-galactosidase, anti-EVC2 and anti-SOX9 antibodies were performed. The craniofacial bones were stained with alcian blue and alizarin red. RESULTS: The LacZ activity in KO was mainly observed in the anterior parts of viscerocranium. The Evc2-expressing cells were identified in many cartilageous regions by IHC with anti-ß-galactosidase antibody in KO and Het embryos. The endogenous EVC2 protein was observed in these areas in WT embryos. Double labeling with anti-SOX9 antibody showed that these cells were mainly chondrocytes. At adult stages, the expression of EVC2 was found in chondrocytes of nasal bones and spheno-occipital synchondrosis, and osteocytes and endothelial-like cells of the premaxilla and mandible. The skeletal double staining demonstrated that craniofacial bones, where the expression of EVC2 was observed, in KO had the morphological defects as compared to WT. CONCLUSION: To our knowledge, our study was the first to identify the types of Evc2-expressing cells in craniofacial tissues. Consistent with the expression pattern, abnormal craniofacial bone morphology was found in the Evc2 KO mice, suggesting that EVC2 may be important during craniofacial growth and development.

Ellis Van Creveld2 is Required for Postnatal Craniofacial Bone Development.

Ellis-van Creveld (EvC) syndrome is a genetic disorder with mutations in either EVC or EVC2 gene. Previous case studies reported that EvC patients underwent orthodontic treatment, suggesting the presence of craniofacial bone phenotypes. To investigate whether a mutation in EVC2 gene causes a craniofacial bone phenotype, Evc2 knockout (KO) mice were generated and cephalometric analysis was performed. The heads of wild type (WT), heterozygous (Het) and homozygous Evc2 KO mice (1-, 3-, and 6-week-old) were prepared and cephalometric analysis based on the selected reference points on lateral X-ray radiographs was performed. The linear and angular bone measurements were then calculated, compared between WT, Het and KO and statistically analyzed at each time point. Our data showed that length of craniofacial bones in KO was significantly lowered by ∼20% to that of WT and Het, the growth of certain bones, including nasal bone, palatal length, and premaxilla was more affected in KO, and the reduction in these bone length was more significantly enhanced at later postnatal time points (3 and 6 weeks) than early time point (1 week). Furthermore, bone-to-bone relationship to cranial base and cranial vault in KO was remarkably changed, i.e. cranial vault and nasal bone were depressed and premaxilla and mandible were developed in a more ventral direction. Our study was the first to show the cause-effect relationship between Evc2 deficiency and craniofacial defects in EvC syndrome, demonstrating that Evc2 is required for craniofacial bone development and its deficiency leads to specific facial bone growth defect. Anat Rec, 299:1110-1120, 2016. © 2016 Wiley Periodicals, Inc.