Chin-Soo Kim

Stability of Mandibular Setback Surgery With and Without Presurgical Orthodontics

PURPOSE The purpose of this study was to compare stability after mandibular setback surgery in patients with skeletal Class III malocclusion with and without presurgical orthodontics. MATERIALS AND METHODS This retrospective cohort study included consecutive patients with skeletal Class III malocclusion who underwent only mandibular surgery. Patients treated with the surgery-first approach without presurgical orthodontics (SF group) were compared with a control group (conventional surgery with presurgical orthodontics; CS group) using lateral cephalograms taken preoperatively, immediately postoperatively, and at the time of debonding. Predictor variables (group and timing), outcome variables (cephalometric measurements over time), and other variables, such as baseline characteristics, were evaluated to determine the difference in stability of mandibular positions such as the B point. RESULTS Sixty-one patients were enrolled in this study (CS group, n = 38; SF group, n = 23). Baseline demographic variables were similar in the 2 groups except for orthodontic treatment period. The mean setback of the mandible at the B point was similar (CS group, 8.7 mm; SF group, 9.1 mm; difference, P > .05), but the horizontal relapse in the SF group (2.4 mm) was significantly greater than in the CS group (1.6 mm; P < .05). Patients with a horizontal relapse greater than 3 mm comprised 39.1% of the SF group compared with 15.8% of the CS group (P < .05). CONCLUSION Mandibular sagittal split ramus osteotomy without presurgical orthodontic treatment was less stable than conventional orthognathic surgery for mandibular prognathism. Before performing a surgery-first approach, skeletal stability needs to be considered.

Aspirin induces apoptosis in YD-8 human oral squamous carcinoma cells through activation of caspases, down-regulation of Mcl-1, and inactivation of ERK-1/2 and AKT.

NSAIDs and COX-2 inhibitors show anti-cancer activities in many cancer cells. In this study, we investigated the effects of NSAIDs (aspirin or indomethacin) and COX-2 inhibitor (NS-398) on growth of YD-8 human oral squamous carcinoma cells. Interestingly, among drugs tested, aspirin showed strongest inhibitory effects on viability and survival of YD-8 cells. Profoundly, aspirin treatment resulted in severe cell shrinkage and nuclear DNA fragmentation in YD-8 cells, suggesting the aspirin-induced apoptosis in YD-8 cells. Data of Western blot further demonstrated that aspirin treatment caused activation of caspases, down-regulation of Mcl-1 protein, dephosphorylation of ERK-1/2 and AKT, and also IkappaB-alpha proteolysis-dependent NF-kappaB activation in YD-8 cells. Aspirin, however, had no effect on expressions of Bcl-2, XIAP, and HIAP-1 in YD-8 cells. Importantly, pretreatment with z-VAD-fmk, a pan-caspase inhibitor blocked the aspirin-induced apoptosis and Mcl-1 down-regulation in YD-8 cells. These findings collectively suggest that aspirin induces apoptosis in YD-8 cells and the induction may be correlated to activation of caspases, caspase-dependent Mcl-1 proteolysis, inactivation of ERK-1/2 and AKT, and activation of NF-kappaB. It is suggested that aspirin may be applied a potential anti-cancer drug against human oral squamous carcinoma.