Conditional deletion of the human ortholog gene Dicer1 in Pax2-Cre expression domain impairs orofacial development.

BACKGROUND: Orofacial clefts are common worldwide and result from insufficient growth and/or fusion during the genesis of the derivatives of the first pharyngeal arch and the frontonasal prominence. Recent studies in mice carrying conditional and tissue-specific deletions of the human ortholog Dicer1, an RNAse III family member, have highlighted its importance in cell survival, differentiation, proliferation, and morphogenesis. Nevertheless, information regarding Dicer1 and its dependent microRNAs (miRNAs) in mammalian palatogenesis and orofacial development is limited. AIMS: To describe the craniofacial phenotype, gain insight into potential mechanisms underlying the orofacial defects in the Pax2-Cre/Dicer1 CKO mouse, and shed light on the role of Dicer1 in mammalian palatogenesis. MATERIALS AND METHODS: Histological and molecular assays of wild type (WT) and Pax2-Cre/Dicer1(loxP/loxP) (Dicer1 CKO) mice dissected tissues have been performed to characterize and analyze the orofacial dysmorphism in Pax2-Cre/Dicer1(loxP/loxP) mouse. RESULTS: Dicer1 CKO mice exhibit late embryonic lethality and severe craniofacial dysmorphism, including a secondary palatal cleft. Further analysis suggest that Dicer1 deletion neither impacts primary palatal development nor the initial stages of secondary palatal formation. Instead, Dicer1 is implicated in growth, differentiation, mineralization, and survival of cells in the lateral palatal shelves. Histological and molecular analysis demonstrates that secondary palatal development becomes morphologically arrested prior to mineralization around E13.5 with a significant increase in the expression levels of apoptotic markers (P < 0.01). CONCLUSIONS: Pax2-Cre-mediated Dicer1 deletion disrupts lateral palatal outgrowth and bone mineralization during palatal shelf development, therefore providing a mammalian model for investigating the role of miRNA-mediated signaling pathways during palatogenesis.

Master in oral biology program: A path to addressing the need for future dental educators.

In dental education, the anatomical sciences, which include gross anatomy, histology, embryology, and neuroanatomy, encompass an important component of the basic science curriculum. At Creighton University School of Dentistry, strength in anatomic science education has been coupled with a solid applicant pool to develop a novel Master of Science in Oral Biology, Anatomic Sciences track degree program. The program provides a heavy emphasis on developing teaching skills in predoctoral students as well as exposure to research processes to encourage the cohort to pursuing a career in academic dentistry. The individuals considered for this program are applicants for admission to the School of Dentistry that have not been accepted into the entering dental class for that year. The students undertake a two year curriculum, studying anatomic sciences with a special emphasis on teaching. The students also must complete a research project that requires a thesis. The students in the program are guaranteed acceptance to dental school upon successful completion of the program. After six years, the first ten students have received their Master of Science degrees and continued in dental school. The program is favorably viewed by the faculty and participating students. It is also considered successful by metrics. Nine of the ten graduates have said they would like to participate in academic dentistry in some capacity during their careers. Anat Sci Educ 10: 607-612. © 2017 American Association of Anatomists.

Bony Exostosis After Treatment of Gingival Recession With Subepithelial Connective Tissue Graft and Enamel Matrix Derivative.

INTRODUCTION: Biologic materials, such as enamel matrix derivative (EMD), are often used to improve the regenerative outcome of periodontal treatment. On occasion, unintended effects of such treatment may occur. To the best of the authors' knowledge, this is the first case report to document the development and treatment of a bony exostosis subsequent to a subepithelial connective tissue (CT) graft with the addition of EMD. CASE PRESENTATION: A healthy female patient received a CT graft and the application of EMD for the treatment of gingival recession at a maxillary premolar. In the following year, a bony exostosis developed and was excised using a piezoelectric surgical device and examined histologically. At the 1-year follow-up, the lesion had not recurred. CONCLUSION: The use of EMD in conjunction with a CT graft represents a new potential contributing factor in the etiology of bony exostoses occurring after gingival augmentation procedures that warrants additional investigation.

Conditional deletion of the human ortholog gene Dicer1 in Pax2-Cre expression domain impairs orofacial development.

Background: Orofacial clefts are common worldwide and result from insufficient growth and/or fusion during the genesis of the derivatives of the first pharyngeal arch and the frontonasal prominence. Recent studies in mice carrying conditional and tissue-specific deletions of the human ortholog Dicer1, an RNAse III family member, have highlighted its importance in cell survival, differentiation, proliferation, and morphogenesis. Nevertheless, information regarding Dicer1 and its dependent microRNAs (miRNAs) in mammalian palatogenesis and orofacial development is limited. Aims: To describe the craniofacial phenotype, gain insight into potential mechanisms underlying the orofacial defects in the Pax2-Cre/Dicer1 CKO mouse, and shed light on the role of Dicer1 in mammalian palatogenesis. Materials And Methods: Histological and molecular assays of wild type (WT) and Pax2-Cre/Dicer1 loxP/loxP (Dicer1 CKO) mice dissected tissues have been performed to characterize and analyze the orofacial dysmorphism in Pax2-Cre/Dicer1 loxP/loxP mouse. Results: Dicer1 CKO mice exhibit late embryonic lethality and severe craniofacial dysmorphism, including a secondary palatal cleft. Further analysis suggest that Dicer1 deletion neither impacts primary palatal development nor the initial stages of secondary palatal formation. Instead, Dicer1 is implicated in growth, differentiation, mineralization, and survival of cells in the lateral palatal shelves. Histological and molecular analysis demonstrates that secondary palatal development becomes morphologically arrested prior to mineralization around E13.5 with a significant increase in the expression levels of apoptotic markers (P < 0.01). Conclusions: Pax2-Cre-mediated Dicer1 deletion disrupts lateral palatal outgrowth and bone mineralization during palatal shelf development, therefore providing a mammalian model for investigating the role of miRNA-mediated signaling pathways during palatogenesis.

Unique origin of the inferior alveolar artery.

The inferior alveolar artery is the major blood supply to the mandible and mandibular teeth. This artery has a very consistent path, originating from the maxillary artery and passing inferiorly until it enters the mandibular foramen, accompanied by the inferior alveolar nerve and vein. During routine dissection of a 90-year-old female cadaver, a unique origin of the inferior alveolar artery was observed on the left side. The artery branched off the external carotid artery, just superior to the stylohyoid and posterior belly of the digastric muscle in the posterior region of the submandibular triangle. From its starting point the artery passed superiorly in the stylomandibular fascia and made a curving arch into the pterygomandibular space to enter the mandibular foramen with the inferior alveolar nerve. The position and branching pattern of the maxillary artery were otherwise typical. The inferior alveolar artery on the right side displayed a normal branching pattern within the infratemporal fossa. Results of surgical procedures in this area, such as sliding osteotomy of the mandible, could be impacted by this anomaly.