Three-dimensional Evaluation of the Carriere Motion 3D Appliance in the treatment of Class II malocclusion.

INTRODUCTION: This study aimed to quantify the outcomes of adolescent patients with Class II malocclusion treated with the Carriere Motion 3D Appliance (CMA) combined with full fixed appliances. METHODS: Cone-beam computed tomography scans of 22 patients were available before orthodontic treatment (T1), at removal of the CMA (T2), and posttreatment (T3). The average age of the patients was 13.5 ± 1.6 years at T1, 14.1 ± 0.2 years at T2, and 15.6 ± 0.5 years at T3. The 3-dimensional image analysis procedures were performed using ITK-SNAP (version 3.6.0; www.itksnap.org, Hatfield, Pa) and SlicerCMF (version 4.11.0; http://www.slicer.org, Cambridge, Mass); skeletal and dentoalveolar changes relative to cranial base, maxillary, and mandibular regional superimpositions were evaluated. RESULTS: Changes were analyzed with 1 sample t tests using the mean differences during the CMA phase (T1 to T2) and total treatment time (T1 to T3). Significant skeletal changes included a slight reduction of ANB from T1 to T3, mandibular growth (Co-Gn increment of 1.2 mm and 3.3 mm from T1 to T2 and T1 to T3, respectively), inferior displacement of point A, and anterior and inferior displacement of point B. The mandibular plane did not change significantly during treatment. During the CMA treatment, posterior tipping and distal rotation of the maxillary molars, tip back and inferior displacement of the maxillary canines, significant mesial rotation, and superior displacement of the mandibular molars were observed. These movements rebounded during the full fixed appliance phase except for the molar and canine vertical displacements. Clinically significant dental changes during treatment included a reduction in overjet and overbite, Class II correction of the molar and canine relationship, and proclination of the mandibular incisors. CONCLUSIONS: The CMA is an effective treatment modality for Class II correction in growing patients because of a combination of mesial movement of the mandibular molar, distal rotation of the maxillary molar, and anterior displacement of the mandible.

Treatment effects of the Carriere® Motion 3D™ appliance for the correction of Class II malocclusion in adolescents.

OBJECTIVES: To determine the treatment effects produced in Class II patients by the Carriere® Motion 3D™ appliance (CMA) followed by full fixed appliances (FFA). MATERIALS AND METHODS: This retrospective study evaluated 34 adolescents at three time points: T1 (pretreatment), T2 (removal of CMA), and T3 (posttreatment). The comparison group comprised 22 untreated Class II subjects analyzed at T1 and T3. Serial cephalograms were traced and digitized, and 12 skeletal and 6 dentoalveolar measures were compared. RESULTS: Phase I with CMA lasted 5.2 ± 2.8 months; phase II with FFA lasted 13.0 ± 4.2 months. CMA treatment restricted the forward movement of the maxilla at point A. There was minimal effect on the sagittal position of the chin at pogonion. The Wits appraisal improved toward Class I by 2.1 mm during the CMA phase but not during FFA. Lower anterior facial height increased twice as much in the treatment group as in controls. A clockwise rotation (3.9°) of the functional occlusal plane in the treatment group occurred during phase I; a substantial rebound (-3.6°) occurred during phase II. Overjet and overbite improved during treatment, as did molar relationship; the lower incisors proclined (4.2°). CONCLUSIONS: The CMA appliance is an efficient and effective way of correcting Class II malocclusion. The changes were mainly dentoalveolar in nature, but some skeletal changes also occurred, particularly in the sagittal position of the maxilla and in the vertical dimension.

The G protein-coupled receptor GALR2 promotes angiogenesis in head and neck cancer.

Squamous cell carcinoma of the head and neck (SCCHN) is an aggressive disease with poor patient survival. Galanin receptor 2 (GALR2) is a G protein-coupled receptor that induces aggressive tumor growth in SCCHN. The objective of this study was to investigate the mechanism by which GALR2 promotes angiogenesis, a critical oncogenic phenotype required for tumor growth. The impact of GALR2 expression on secretion of proangiogenic cytokines in multiple SCCHN cell lines was investigated by ELISA and in vitro angiogenesis assays. Chemical inhibitor and genetic knockdown strategies were used to understand the key regulators. The in vivo impact of GALR2 on angiogenesis was investigated in mouse xenograft, chick chorioallantoic membrane, and the clinically relevant mouse orthotopic floor-of-mouth models. GALR2 induced angiogenesis via p38-MAPK-mediated secretion of proangiogenic cytokines, VEGF, and interleukin-6 (IL-6). Moreover, GALR2 activated small-GTP-protein, RAP1B, thereby inducing p38-mediated inactivation of tristetraprolin (TTP), which functions to destabilize cytokine transcripts. This resulted in enhanced secretion of proangiogenic cytokines and angiogenesis in vitro and in vivo. In SCCHN cells overexpressing GALR2, inactivation of TTP increased secretion of IL-6 and VEGF, whereas inhibition of p38 activated TTP and decreased cytokine secretion. Here, we report that GALR2 stimulates tumor angiogenesis in SCCHN via p38-mediated inhibition of TTP with resultant enhanced cytokine secretion. Given that p38 inhibitors are in clinical use for inflammatory disorders, GALR2/p38-mediated cytokine secretion may be an excellent target for new adjuvant therapy in SCCHN.