Spontaneous Union of an Accidentally Fractured Proximal Segment During Vertical Ramus Osteotomy.

After sawing in the intraoral vertical ramus osteotomy, in the case of an incomplete amputation, the proximal segment is split using the osteotome. Unfortunately, in this case, the proximal segment was accidentally fractured. The operation was completed without performing any other fixation. Postoperatively intermaxillary fixation was performed and kept for a week, followed by physical therapy, which was initiated immediately after. The patient was closely observed for 6 months. No abnormal findings were detected clinically, and the union of bone was verified.

Percutaneous self-injury to the femoral region caused by bur breakage during surgical extraction of a patient's impacted third molar.

Extraction of an impacted third molar is one of the most frequently performed techniques in oral and maxillofacial surgery. Surgeons can suffer numerous external injuries while extracting a tooth, with percutaneous injuries to the hand being the most commonly reported. In this article, we present a case involving a percutaneous injury of the surgeon's femoral region caused by breakage of the fissure bur connected to the handpiece during extraction of the third molar. We also propose precautions to prevent such injuries and steps to be undertaken when they occur.

Three-dimensional functional unit analysis of hemifacial microsomia mandible-a preliminary report.

BACKGROUND: The aim of this study was to present three-dimensional (3D) structural characteristics of the mandible in the hemifacial microsomia. The mandible has six distinct functional units, and its architecture is the sum of balanced growth of each functional unit and surrounding matrix. METHODS: In order to characterize the mandibular 3D architecture of hemifacial microsomia, we analyzed the mandibular functional units of four hemifacial microsomia patients using the 3D reconstructed computed tomography (CT) images. And we compared the functional unit size between affected and non-affected side. RESULTS: The length of condyle and angle showed significant differences between affected and non-affected sides. However, the length of mandibular body showed insignificant differences. The size differences between affected and non-affected side were observed at the condyle, angle, and body in descending order. CONCLUSIONS: This preliminary study suggests that the main etiopathogenic units are condyle and angle in the hemifacial microsomia mandible. Further investigation with the increased number of subjects will be helpful to establish treatment modality by etiopathogenic targeting of hemifacial microsomia.

ALS/FTLD-linked TDP-43 regulates neurite morphology and cell survival in differentiated neurons.

Tar-DNA binding protein of 43kDa (TDP-43) has been characterized as a major component of protein aggregates in brains with neurodegenerative diseases such as frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). However, physiological roles of TDP-43 and early cellular pathogenic effects caused by disease associated mutations in differentiated neurons are still largely unknown. Here, we investigated the physiological roles of TDP-43 and the effects of missense mutations associated with diseases in differentiated cortical neurons. The reduction of TDP-43 by siRNA increased abnormal neurites and decreased cell viability. ALS/FTLD-associated missense mutant proteins (A315T, Q331K, and M337V) were partially mislocalized to the cytosol and neurites when compared to wild-type and showed abnormal neurites similar to those observed in cases of loss of TDP-43. Interestingly, cytosolic expression of wild-type TDP-43 with mutated nuclear localization signals also induced abnormal neurtie morphology and reduction of cell viability. However, there was no significant difference in the effects of cytosolic expression in neuronal morphology and cell toxicity between wild-type and missense mutant proteins. Thus, our results suggest that mislocalization of missense mutant TDP-43 may contribute to loss of TDP-43 function and affect neuronal morphology, probably via dominant negative action before severe neurodegeneration in differentiated cortical neurons.