Upper Second Molar Distalization with Clear Aligners: A Finite Element Study

Among orthodontists and scientists, in the last years, upper molar distalization has been a debated topic in the orthodontic aligner field. However, despite that few clinical studies have been published, no insights on aligners' biomechanics regarding this movement are available. The aim of this study was to assess, through finite element analysis, the force system resulting in the upper arch during second maxillary molar distalization with clear aligners and variable attachments settings. The average tooth distalization was found to be 0.029, with buccal flaring of the upper incisors in all attachment configurations. The mesial deformation of the aligner was registered to be 0.2 mm on average. Different pressure areas on the interface between aligners and upper molars were registered, with the mesial attachment surface to be directly involved when present. Periodontal ligament pressure was reported to range between 67 g/cm(2) and 132 g/cm(2). Configurations with rectangular attachments from second molar-to-canine and from first molar-to-canine present, in an in silico environment, almost equal efficiency in distalizing the upper second molar. However, attachments from the second molar to the canine are suggested to be adopted in clinical environments due to greater feasibility in everyday practice

Mapping pathological phenotypes in a mouse model of CDKL5 disorder.

open14sihe research was supported by EMBL (E.A. and C.T.G.), the Italian Telethon Foundation (grant GGP09196, T.P. and M.G.; grant GGP10162, E.C., T.P., and M.G.), Epigenomics Flagship Project EPIGEN, MIUR-CNR to T.P., AIRETT onlus (T.P. and M.G.), the International Rett Syndrome Foundation (ISRF, M.G.), and a fellowship from the International Foundation for CDKL5 Research (IFCR) in collaboration with ISRF (E.A.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Mutations in cyclin-dependent kinase-like 5 (CDKL5) cause early-onset epileptic encephalopathy, a neurodevelopmental disorder with similarities to Rett Syndrome. Here we describe the physiological, molecular, and behavioral phenotyping of a Cdkl5 conditional knockout mouse model of CDKL5 disorder. Behavioral analysis of constitutive Cdkl5 knockout mice revealed key features of the human disorder, including limb clasping, hypoactivity, and abnormal eye tracking. Anatomical, physiological, and molecular analysis of the knockout uncovered potential pathological substrates of the disorder, including reduced dendritic arborization of cortical neurons, abnormal electroencephalograph (EEG) responses to convulsant treatment, decreased visual evoked responses (VEPs), and alterations in the Akt/rpS6 signaling pathway. Selective knockout of Cdkl5 in excitatory and inhibitory forebrain neurons allowed us to map the behavioral features of the disorder to separable cell-types. These findings identify physiological and molecular deficits in specific forebrain neuron populations as possible pathological substrates in CDKL5 disorder.openAmendola E;Zhan Y;Mattucci C;Castroflorio E;Calcagno E;Fuchs C;Lonetti G;Silingardi D;Vyssotski AL;Farley D;Ciani E;Pizzorusso T;Giustetto M;Gross CTAmendola E;Zhan Y;Mattucci C;Castroflorio E;Calcagno E;Fuchs C;Lonetti G;Silingardi D;Vyssotski AL;Farley D;Ciani E;Pizzorusso T;Giustetto M;Gross C