In-vitro comparison of bonding time and strength of adhesive pre-coated and standard metal orthodontic brackets

To compare the shear bond strength and bond time of 3M Unitek's APC (Adehesive Pre-Coated) Flash-Free™system applied to metal brackets. An in vitro study was performed on 40 extracted sound human premolar teeth randomly divided into two groups (20 per group) bonded either with Adhesive Pre-Coated Flash-Free metal brackets or metal brackets coated manually with Transbond XT™ light-cure adhesive. Bonding time was measured using a stopwatch. Thermoycling was performed on the samples (500 cycles) to simulate the oral environment between baths of 5°C and 55°C distilled water. Debonding shear bond strength measurements were performed in an Instron universal testing machine. The APC Flash-Free group bonded in significantly (p<0.001) less time (mean 34.06s/tooth) than the manually coated group (mean 55.14s/tooth). Shear bond strength of the manually coated group was significantly (p<0.001) higher (mean 13.32 MPa) than the APC Flash-Free group (mean 10.95 MPa). The APC Flash-Free free system is efficient and allows for reduced chair time during the bonding appointment while attaining a mean shear bond strength of 10.95MPa, which is higher than the minimum shear bond strength of between 4MPa and 7MPa

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)