Does Condylar Morphology Affect Maxillary Repositioning in Bimaxillary Orthognathic Surgery?

This study aimed to measure the association between condylar morphology and a measure of the maxillary centroid following bimaxillary surgery using mandibular-dependent splints. The study included skeletal Class III and Class II malocclusion patients, excluding those with facial asymmetry. Based on computed tomography imaging patients were characterized into normal or abnormal temporomandibular joint (TMJ) groups. A computer-aided design/computer-aided manufacturing splints were fabricated to reposition the maxilla in Le Fort I osteotomy. The primary outcome measure was the absolute differences between the maxillary centroid's the planned and actual postoperative positions calculated by superimposing computed tomography scans. The secondary outcome was the measure of other variations in linear and angular maxilla discrepancies. The demographic covariates included the age and sex of the patients. The operative covariates consisted of the dentofacial deformity and the planned movement of the maxilla. Seventy patients with skeletal maxillofacial deformities were included for analysis: 44 patients in the normal and 26 in the abnormal TMJ group. The average maxillary misalignment was 1.04±0.48 mm in the normal and 1.53±0.63 mm in the abnormal TMJ group (P<0.001). A statistically significant relationship existed between the discrepancies of the maxillary centroid and dentofacial deformity (η=0.656, P<0.001). These findings suggest an increased propensity for maxillary malposition in skeletal Class II patients. Furthermore, condylar morphology is a significant prognostic factor influencing maxillary repositioning errors in bimaxillary surgery with mandibular-dependent splints.

Microarray and gene co-expression analysis reveals that melatonin attenuates immune responses and modulates actin rearrangement in macrophages.

Melatonin produced by the pineal gland suppresses inflammatory responses in innate immune cells. However, the mechanism of how melatonin affects inflammatory gene regulation remains unclear. Here we performed comprehensive microarray analysis combined with transcription factor binding site (TFBS) analysis using LPS-induced mouse macrophages to investigate the effect of melatonin treatment. The results showed that melatonin preferentially downregulated interferon regulatory factors (IRFs) and signal transducers and activators of transcription (STATs) related signaling. The results also showed that melatonin strongly suppressed virus infection related gene expression. Furthermore, TFBS analysis implicated that melatonin downregulated the binding activity of hypoxia inducible factors (HIFs), following destabilizing actin cytoskeleton which are indispensable for induction of the TRIF-dependent signaling pathway. Indeed, it was demonstrated that melatonin treatment caused impaired phagocytosis in macrophages. Thus, melatonin regulates inflammatory responses by inhibiting specific subsets of transcription factors (TFs) by disrupting actin dynamics in the macrophage.