Variables associated with stability after Le Fort I osteotomy for skeletal class III malocclusion.

The purpose of this study was to assess skeletal stability and predictors of relapse in patients undergoing an isolated Le Fort I osteotomy. A retrospective cohort study of 92 subjects undergoing Le Fort I osteotomy for Class III malocclusion was implemented. Predictor variables were demographic and perioperative factors. The primary outcome variable was postoperative skeletal position with relapse defined as >2mm sagittal and/or vertical change at A-point on serial lateral cephalograms at immediate postoperative, 1 year, and latest follow-up time points. Mean advancement at A-point was 6.28±2.63mm and mean lengthening was 0.92±1.76mm. Eight subjects (8.70%) had relapse (>2mm) in the sagittal plane, and two subjects (2.17%) in the vertical plane. No subjects required reoperation for relapse as overbite and overjet remained in an acceptable range due to dental compensation. In regression analysis, magnitude of maxillary advancement was an independent predictor of relapse in the sagittal plane (P=0.008). There were no significant predictors of relapse in the vertical plane. This study suggests that isolated Le Fort I osteotomy for correction of skeletal Class III malocclusion is a stable procedure and that greater advancement is an independent risk factor for sagittal relapse.

Frequency of cervical spine injuries in patients with midface fractures.

The aim of this retrospective cohort study was to determine the frequency and risk factors for cervical spine injury (CSI) in patients with midface fractures. Patients ≥18 years of age entered in the Massachusetts General Hospital Trauma Registry from 2007 to 2017 were identified. Those with a midface fracture, computed tomography and/or magnetic resonance imaging of the cervical spine, and complete medical records were included. There were 23,394 patients in the registry; 3950 (16.9%) had craniomaxillofacial fractures and 1822 (7.8%) had a CSI. Craniomaxillofacial fractures included fractures of the midface (n=2803, 71.0%), mandible (n=873, 22.1%), and midface plus mandible (n=274, 6.9%). The overall frequency of CSI in patients with midface fractures was 11.4% (350/3077). Patients with midface fractures had a higher risk for CSI compared to patients without a midface fracture (odds ratio 2.4, 95% confidence interval 2.1-2.4, P<0.001). In a multivariate model, nasal and orbital fractures, chest injuries, age, injury severity score, and motor vehicle crash or fall as the etiology were independent risk factors for CSI. Mortality was two times higher in subjects with CSI. Early and accurate diagnosis of CSI is a critical factor when planning the treatment of patients with these fractures.

Oncogenic transformation of HPV-immortalized human oral keratinocytes is associated with the genetic instability of cells.

HPV-immortalized human oral keratinocytes can convert to tumorigenic cells when exposed to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), but normal human oral keratinocytes cannot transform with a similar exposure. The different responses of these cells could be due to different genetic stability of cells. In as much as genetic stability is determined by cell cycle control and of repair of damaged DNA, we studied the effect of MNNG exposure upon cell cycle progression, expression of p53, WAF1/CIP1 and gadd45, and the mutation frequency of a shuttle vector pS189 in normal human oral keratinocytes, in HPV-immortalized oral keratinocytes, and in an oral cancer cell line expressing mutant p53. Normal cells demonstrated transient cell cycle arrest after exposure to MNNG, but the other tested cells did not. While MNNG exposure significantly increased the levels of intranuclear wt p53 protein and the expression of WAF1/CIP1 and gadd45 genes in normal cells, it did not alter them in the immortalized and cancer cells. The mutation frequency of pS189 plasmid was significantly lower in normal cells than in the other tested cells. These data indicate that malignant conversion of HPV-immortalized oral keratinocytes may, in part, be associated with the cells' genetic instability. The genetic instability may be due to cells' (1) inability to accumulate intranuclear wt p53 to a threshold level at which p53 upregulates the transcription of WAF1/CIP1 and gadd45, resulting in the loss of cell cycle control and (2) inefficient repair of DNA damage caused by genotoxic agents.