Comparison of the mandibular hinge axis in adult patients with facial asymmetry with and without posterior unilateral crossbite.

BACKGROUND/OBJECTIVES: Although it has been suggested that adult patients with facial asymmetry with posterior unilateral crossbite (PUXB) may have a more tilted mandibular hinge axis (MHA) than those without PUXB, whether craniofacial morphology is associated with the MHA remains unclear. The purpose of this study was to compare the craniofacial morphology and MHA in adult subjects with post-growth facial asymmetry with and without PUXB. SUBJECTS/METHODS: Thirty pre-orthodontic patients (PUXB and non-PUXB groups, n = 15 each, 9 females and 6 males, mean age: 23.2 years) participated in the study. The MHA was measured by computerized axiography and duplicated on posteroanterior and submentovertex cephalometric radiographs. Morphological asymmetry was evaluated for both skeletal and dental components and positional deviation of the mandible by cephalometric analysis. The Mann-Whitney U-test and Spearman's correlation coefficient by rank were used for statistical analysis. The level of statistical significance was set at P < 0.05. RESULTS: Significant differences in both skeletal and dental components were found between the PUXB and non-PUXB groups. In both the frontal and horizontal dimensions, the inclination of the MHA towards the mandibular shifted side was greater in the PUXB group than in the non-PUXB group. CONCLUSIONS/IMPLICATIONS: The present findings suggest that facially asymmetric adult subjects with malocclusions associated with PUXB exhibit not only mandibular asymmetry but also remodelling of the condylar head and glenoid fossa that accompanies the three-dimensional shifting of the MHA.

TGFß regulates epithelial-mesenchymal interactions through WNT signaling activity to control muscle development in the soft palate.

Clefting of the soft palate occurs as a congenital defect in humans and adversely affects the physiological function of the palate. However, the molecular and cellular mechanism of clefting of the soft palate remains unclear because few animal models exhibit an isolated cleft in the soft palate. Using three-dimensional microCT images and histological reconstruction, we found that loss of TGFß signaling in the palatal epithelium led to soft palate muscle defects in Tgfbr2(fl/fl);K14-Cre mice. Specifically, muscle mass was decreased in the soft palates of Tgfbr2 mutant mice, following defects in cell proliferation and differentiation. Gene expression of Dickkopf (Dkk1 and Dkk4), negative regulators of WNT-ß-catenin signaling, is upregulated in the soft palate of Tgfbr2(fl/fl);K14-Cre mice, and WNT-ß-catenin signaling is disrupted in the palatal mesenchyme. Importantly, blocking the function of DKK1 and DKK4 rescued the cell proliferation and differentiation defects in the soft palate of Tgfbr2(fl/fl);K14-Cre mice. Thus, our findings indicate that loss of TGFß signaling in epithelial cells compromises activation of WNT signaling and proper muscle development in the soft palate through tissue-tissue interactions, resulting in a cleft soft palate. This information has important implications for prevention and non-surgical correction of cleft soft palate.

Association between intraoral pressure and molar position and inclination in subjects with facial asymmetry.

Although it has been suggested that an imbalance in buccolingual pressure may play a role in dental compensation of the molars and asymmetry in the mandibular dental arch in subjects with facial asymmetry, it is still unclear whether buccolingual pressure is associated with this phenomenon. Thus, the purpose of this study was to test the null hypothesis that there are no differences in cheek and tongue pressure between the shifted and non-shifted sides in 12 (8 females and 4 males, mean age: 24.9 years) subjects with facial asymmetry defined as 4 mm or more deviation of the midline in the mandibular incisors. The resting buccolingual pressure on the bilateral mandibular first molars was measured simultaneously using four miniature pressure sensors. Moreover, a postero-anterior (PA) cephalogram was used to determine the buccolingual positions and the inclination of the mandibular first molars. Wilcoxon t-, Kruskal-Wallis H-, and Mann-Whitney U-tests and Spearman correlation coefficient by rank were used for statistical analysis. Significance was set at P < 0.05. Cheek pressure was significantly greater on the shifted than that on the non-shifted side, while tongue pressure on the shifted side was significantly less than that on the non-shifted side. On the other hand, tongue/cheek pressure ratio on the shifted side was significantly less than that on the non-shifted side. There were significant differences between the shifted and non-shifted sides in the buccolingual positions and inclination of the mandibular first molars. Regardless of the side, there were significant negative correlations between the buccolingual position of the mandibular first molars and cheek pressure and significant positive correlations between the buccolingual position of the mandibular first molars and tongue/cheek pressure ratio. There were also significant negative correlations between tongue/cheek pressure ratio and inclination of the mandibular first molars on both the shifted and the non-shifted sides. Thus, the present findings reject the null hypothesis. The imbalance in buccolingual pressure in subjects with facial asymmetry appears to be related to dental compensation of the molars and mandibular asymmetry.