A study on the morphologic change of palatal alveolar bone shape after intrusion and retraction of maxillary incisors.

The purpose of this study is to evaluate the changes in the palatal alveolar bone thickness and find the factors related to the resorption of the palatal alveolar bone caused by tooth movement after the maxillary incisors were retracted and intruded during orthodontic treatment. The study group comprised of 33 skeletal Class II malocclusion patients who underwent extraction for orthodontic treatment. Palatal alveolar bone thickness changes and resorption factors were identified and analyzed. The changes of maxillary central incisors and palatal alveolar bone thickness were measured, and the corresponding sample t test was performed using SPSS (IBM SPSS version 22). The amount of palatal alveolar bone resorption was measured and various parameters were analyzed to determine which factors affected it. Correlation analysis adopting the amount of palatal alveolar bone resorption as a dependent variable demonstrated that the SNB, mandibular plane angle, and the inclination of the maxillary central incisor were significantly correlated with before treatment. On the other hand, mandibular plane angle, angle of convexity, the inclination of the upper incisor, and the occlusal plane (UOP, POP) were significantly correlated with post-treatment. In addition, the variables related to palatal contour (PP to PAS, SN to PAS, palatal surface angle) and occlusal planes (UOP/POP) were significantly correlated with the difference in palatal bone resorption. During initial diagnosis, high angle class II with normal upper incisor inclination can be signs of high-risk factors. In addition, maintaining the occlusal plane during treatment helps to prevent palatal bone loss.

Oleic acid inhibits hepatic insulin signaling through deregulation of STAT3 activation and C/EBPalpha expression.

Elevated free fatty acids (FFAs) are known to induce the impairment of insulin signaling. However, the insulin signaling components that are deregulated by FFAs in the liver remain unknown. Here, we examined the mechanisms of disruption of oleic acid on insulin signaling in hepatic cell lines. Oleic acid decreased the expression of insulin receptor substrate (IRS) 1 and augmented the expression of suppressor of cytokine signaling (SOCS) 3, which can induce the proteasome-mediated degradation of IRS. Moreover, oleic acid enhanced the phosphorylation of signal transducer and activator of transcription (STAT) 3 and induced the expression of CCAAT/enhancer-binding protein alpha (C/EBPalpha). The interaction between STAT3 and C/EBPalpha was increased by oleic acid; these proteins subsequently enhanced the promoter activity of SOCS3 in the presence of oleic acid. Finally, oleic acid impaired the insulin signaling cascades through inhibition of the alpha-associated signaling pathway.