Comparison of intraoral and extraoral scanners on the accuracy of digital model articulation.

Digital dental technology is increasingly becoming an integral part of the modern orthodontic practice. The accuracy of digitally articulated models is critical when developing orthodontic treatment plans. OBJECTIVE: to determine the accuracy of model articulation generated by extraoral and intraoral scanners. DESIGN: One extraoral scanner with a wax (EOW) or vinyl polysiloxane bite registration (EOVPS), and three intraoral digital scanners utilizing confocal static (IOCS), confocal continuous (IOCC), and blue LED light technologies (IOLED) were used. METHODS: On each scanned image (n = 25 per group), measurements between the maxillary and mandibular molars and canines were performed and then compared to the gold standard values. A deviation of ± 0.5 mm from the gold standard value was considered acceptable. The significance level was kept at 0.05. RESULTS: IOCS and IOCC were accurate for all six interarch measurements. IOLED and EOVPS groups produced the next most accurate articulation of the digital models. EOW group resulted in the least accurate articulation. Also, of the software platforms used, the OrthoCAD™ was found to be the most accurate system for making measurements on digital casts. CONCLUSIONS: Only the scanners with the confocal imaging technology produced accurately articulated models. Differences between the scanners may be related to measurement errors inherent to the technologies employed and the software systems used to process the images.

Embryonic overexpression of receptors for advanced glycation end-products by alveolar epithelium induces an imbalance between proliferation and apoptosis.

Receptors for advanced glycation end-products (RAGEs) are multiligand cell surface receptors highly expressed in the lung that contribute to alveolar epithelial cell differentiation during embryogenesis and the modulation of pulmonary inflammation during disease. When RAGEs are overexpressed throughout embryogenesis, severe lung hypoplasia ensues, culminating in perinatal lethality. However, the possible mechanisms that lead to the disappearance of pulmonary tissue remain unclear. A time course of lung organogenesis, commencing on Embryonic Day (E) 12.5, demonstrated that increased RAGE expression primarily alters lung morphogenesis beginning on E16.5. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) immunohistochemistry and immunoblotting for active caspase-3 confirmed a shift toward apoptosis in lungs from RAGE-overexpressing mice, compared with wild-type control mice. This observation supports previous work where electron microscopy identified the cellular blebbing of alveolar epithelium in embryonic RAGE-overexpressing mice. Assaying for NF-κB also revealed elevated nuclear translocation in lungs from transgenic mice compared with control mice. An RT-PCR assessment of genes regulated by NF-κB demonstrated the elevated expression of Fas ligand, suggesting increased activity of the Fas-mediated signal transduction pathway in which ligand-receptor interactions trigger cell death. These data provide evidence that the expression of RAGEs must be tightly regulated during homeostatic organogenesis. Further elucidations of the RAGE signaling potentially involved in cell-cycle abnormalities may provide insights into the progression of RAGE-mediated lung diseases.

Immunohistochemical detection and regulation of α5 nicotinic acetylcholine receptor (nAChR) subunits by FoxA2 during mouse lung organogenesis.

BACKGROUND: α5 nicotinic acetylcholine receptor (nAChR) subunits structurally stabilize functional nAChRs in many non-neuronal tissue types. The expression of α5 nAChR subunits and cell-specific markers were assessed during lung morphogenesis by co-localizing immunohistochemistry from embryonic day (E) 13.5 to post natal day (PN) 20. Transcriptional control of α5 nAChR expression by FoxA2 and GATA-6 was determined by reporter gene assays. RESULTS: Steady expression of α5 nAChR subunits was observed in distal lung epithelial cells during development while proximal lung expression significantly alternates between abundant prenatal expression, absence at PN4 and PN10, and a return to intense expression at PN20. α5 expression was most abundant on luminal edges of alveolar type (AT) I and ATII cells, non-ciliated Clara cells, and ciliated cells in the proximal lung at various periods of lung formation. Expression of α5 nAChR subunits correlated with cell differentiation and reporter gene assays suggest expression of α5 is regulated in part by FoxA2, with possible cooperation by GATA-6. CONCLUSIONS: Our data reveal a highly regulated temporal-spatial pattern of α5 nAChR subunit expression during important periods of lung morphogenesis. Due to specific regulation by FoxA2 and distinct identification of α5 in alveolar epithelium and Clara cells, future studies may identify possible mechanisms of cell differentiation and lung homeostasis mediated at least in part by α5-containing nAChRs.