"Crack under pressure"-Inducing life-like mandible fractures as a potential benefit to surgical education in oral and maxillofacial surgery.

The aim of this study was to investigate whether life-like fractures of human cadaveric mandibles with a focus on the condylar process and the intact soft tissue envelope could be simulated. A total of nine fresh-frozen human head specimens were fractured in a custom-made drop-test bench. This reproducible method is based on a weight falling from a defined height onto the fixed specimens, simulating a direct blow to the symphysis of the mandible. All the fractures were analyzed by fluoroscopy and CT-scans. In all the specimens that were included in this study, several typical lesions could be created, resulting in a total of 27 mandible fractures. Seven condylar head fractures with intracapsular fracture patterns, three high, two low and five subcondylar fractures as well as different corpus fractures occurred. Human cadaveric mandibles as part of a complete head specimen with intact soft tissue can be successfully fractured by means of a drop-test bench setup. The amount of load and the exact angle at which the load is applied seem to be of high relevance. Such fractured specimens can be implemented in surgical education courses to teach and improve osteosynthetic techniques.

Simvastatin reduces mortality and hepatic injury after hemorrhage/resuscitation in rats.

Statins are established in the prevention and therapy of chronic cardiovascular diseases because of inhibition of HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A), thus lowering blood cholesterol levels. However, their cholesterol-independent effects include regulation of Rho/Rho-kinases (ROCK) and eNOS, proteins centrally involved in various models of acute inflammation. Therefore, we tested the hypothesis that simvastatin confers protection after rat hemorrhage/resuscitation (H/R) and wanted to elucidate the mechanisms involved. Fifty-two female Lewis rats (180-250 g) were pretreated with simvastatin 5 mg/kg per day or vehicle for 6 days (i.p.). Then, rats were hemorrhaged to a mean arterial pressure of 30 +/- 2 mmHg for 60 min and resuscitated. Control group underwent surgical procedures without H/R. Two hours after resuscitation, tissues were harvested. Mortality was assessed 72 h after H/R. Simvastatin pretreatment increased survival after H/R from 20% to 80%. Serum alanine aminotransferase after H/R increased 2.2-fold in vehicle as compared with simvastatin-treated rats. Histopathological analysis revealed decreased hepatic necrosis in simvastatin-treated rats after H/R. Hepatic oxidative (4-hydroxynonenal) and nitrosative (3-nitrotyrosine) stress, inflammatory markers (serum IL-6 and hepatic infiltration with polymorphonuclear leukocytes), and actin cytoskeleton rearrangements were decreased after simvastatin pretreatment compared with vehicle-treated rats after H/R. Simvastatin increased eNOS and heme oxygenase 1 expression and eNOS activation. Expression of Rho/Rho-kinase and myosin phosphatase targeting subunit, Thr-MYPT1, a marker for Rho-kinase activity, decreased after simvastatin treatment compared with vehicle-treated rats after H/R. Simvastatin pretreatment exerts beneficial effects in this model of acute inflammation by supporting protective mechanisms that are important for hepatic microcirculation after H/R.