Fluorescence-Aided Identification Technique (FIT) Improves Tooth Surface Clean-Up after Debonding of Buccal and Lingual Orthodontic Appliances.

The aim of this study was to evaluate the use of fluorescence inducing light to aid the clean-up of tooth surfaces after bracket removal when using buccal or lingual orthodontic appliances. Two full sets of dental arches using extracted human teeth were assembled, with 14 teeth per arch. All teeth were bonded on their buccal and lingual surfaces. After debonding, a single blinded operator performed the tooth surface clean-up, as commonly performed in clinical practice; without the use of fluorescent light (non-FIT) and with two methods using fluorescent light to identify composite remnants on the tooth surfaces (FIT; OPAL and BRACE). Tooth surfaces were scanned before bonding and after clean-up, and the two scans were superimposed using the best-fit method. The results showed that the debonding method, type of tooth and type of tooth surface had a significant effect on the presence of composite remnants, enamel defects, and on debonding time. Contrary to the non-FIT method, there were no composite remnants after clean-up with the use of fluorescence inducing light. Clean-up time was significantly reduced on the buccal surfaces when using the FIT methods. On the lingual surfaces, the FIT methods resulted in larger enamel defects.

In vitro comparison of the torsional load transfer of various commercially available stainless-steel wires used for fixed retainers in orthodontics.

OBJECTIVE: To assess the torsional load transfer of various commercially available stainless-steel wires used for fixed retainers. DESIGN: An in vitro study using a robotic device. SETTING: Department of Pediatric Oral Health and Orthodontics, University of Basel. METHODS: A 10° proclination of a maxillary lateral incisor of a 2-2 retainer was simulated with a robotic device. Eight stainless-steel wires with different shapes (round or rectangular), types (plain, braided, coaxial or chain) and dimensions were selected to measure the torsional load transfer at the adjacent central incisor. The influence of annealing was also tested. RESULTS: The 0.016 × 0.016 and Bond-A-Braid™ wires (0.02645 × 0.01055-inch, 8-stranded, braided) showed the largest relative torsional load transfer (3.7% and 3.3%, respectively). The two multistranded wires - Triple Flex™ and Respond® - showed the smallest values of 1.0% and 0.7%, respectively. The spiral direction of these two multistranded wires affected the load transfer, the twisting showing larger torsional load transfer than the untwisting one. CONCLUSION: The effective torsional load transfer depends on the dimension, shape and type of a wire. Plain and braided retainers were more predictable in torsional load transfer than multistranded retainers, which may have stored more energy in the area between the composite bonding sites. This may explain the unexpected complications reported in multistranded retainers.

Oncogenic ALK F1174L drives tumorigenesis in cutaneous squamous cell carcinoma.

Cutaneous squamous cell carcinoma (cSCC) is the second most common skin cancer characterized by increased mortality. Here, we show for the first time that anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase of the insulin receptor superfamily, plays a pivotal role in the pathogenesis of cSCC. Our data demonstrate that the overexpression of the constitutively active, mutated ALK, ALK F1174L , is sufficient to initiate the development of cSCC and is 100% penetrant. Moreover, we show that cSCC development upon ALK F1174L overexpression is independent of the cell-of-origin. Molecularly, our data demonstrate that ALK F1174L cooperates with oncogenic Kras G12D and loss of p53, well-established events in the biology of cSCC. This cooperation results in a more aggressive cSCC type associated with a higher grade histological morphology. Finally, we demonstrate that Stat3 is a key downstream effector of ALK F1174L and likely plays a role in ALK F1174L -driven cSCC tumorigenesis. In sum, these findings reveal that ALK can exert its tumorigenic potential via cooperation with multiple pathways crucial in the pathogenesis of cSCC. Finally, we show that human cSCCs contain mutations in the ALK gene. Taken together, our data identify ALK as a new key player in the pathogenesis of cSCC, and this knowledge suggests that oncogenic ALK signaling can be a target for future clinical trials.