Craniomaxillofacial (CMF) trauma occurs in isolation or in combination with other serious injuries, including intracranial, spinal, and upper- and lower-body injuries. It is a major cause of expensive treatment and rehabilitation requirements, temporary or lifelong morbidity, and loss of human productivity. The aim of this study was to evaluate patterns of CMF trauma in a large patient sample within a 15-year time frame. Between 1991 and 2005, CMF trauma data were collected from 14,654 patients with 35,129 injuries at the Department of Cranio-Maxillofacial and Oral Surgery in Innsbruck, assessing a plethora of parameters such as injury type and mechanism as well as age and gender distribution over time. Three main groups of CMF trauma were evaluated: facial bone fractures, dentoalveolar trauma, and soft tissue injuries. Statistical comparisons were carried out using a chi-square test. This was followed by a logistic regression analysis to determine the impact of the five main causes for CMF injury. Older people were more prone to soft tissue lesions with a rising risk of 2.1% per year older, showing no significant difference between male and female patients. Younger patients were at higher risk of suffering from dentoalveolar trauma with an increase of 4.4% per year younger. This number was even higher (by 19.6%) for female patients. The risk of sustaining facial bone fractures increased each year by 4.6%. Male patients had a 66.4% times higher risk of suffering from this type of injury. In addition, 2550 patients (17.4%) suffered from 3834 concomitant injuries of other body parts. In summary, we observed changing patterns of CMF trauma over the last 15 years, paralleled by advances in refined treatment and management options for rehabilitation and reconstruction of patients suffering from CMF trauma.

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Organic layers of salivary biopolymers adsorbed on soft and hard oral tissues, referred to also as salivary pellicle, play a critical role with respect to all surface phenomena taking place in the oral cavity. The initial stages of pellicle formation are of great interest since they determine the ensuing processes of salivary biopolymer adsorption and subsequent adherence of bacteria. In spite of the important physiological role of the pellicle in protecting the enamel surface against short-term acidic attacks, the composition and ultrastructure of the pellicle layer are not yet understood and resolved in detail. The present study utilized atomic force microscopy (AFM), for the first time, to elucidate the morphogenesis and ultrastructural pattern of initial salivary pellicle formation taking place in situ on solid substrates of mica, silicon wafer and graphite. Using tapping mode AFM, salivary pellicles were found in all intraorally exposed specimens and revealed a globular surface morphology of the adsorbed protein layer. The average diameter and height of the adsorbed salivary proteins were determined to be 15 +/- 3 nm and 2.0 +/- 0.5 nm, respectively. It was also found that the surface energy of the substrates affects the rate of pellicle formation, while the overall size of the adsorbed salivary proteins appears to be identical on all studied substrates.

Hydrophilicity influences the connective tissue healing at polished implant surfaces in vivo positively. The attachment of connective tissue and the number of cells in contact to the surface were increased. Moreover, the inflammatory response is decreased at the hydrophilic surface.

AimsDespite the lower patency of venous compared with arterial coronary artery bypass grafts, ∼50% of grafts used are saphenous vein conduits because of their easier accessibility. In a search for ways to increase venous graft patency, we applied the results of a previous pharmacological study screening for non-toxic compounds that inhibit intimal hyperplasia of saphenous vein conduits in organ cultures. Here we analyse the effects and mechanism of action of leoligin [(2S,3R,4R)-4-(3,4-dimethoxybenzyl)-2-(3,4-dimethoxyphenyl)tetrahydrofuran-3-yl]methyl (2Z)-2-methylbut-2-enoat, the major lignan from Edelweiss (Leontopodium alpinum Cass.).Methods and resultsWe found that leoligin potently inhibits vascular smooth muscle cell (SMC) proliferation by inducing cell cycle arrest in the G1-phase. Leoligin induced cell death neither in SMCs nor, more importantly, in endothelial cells. In a human saphenous vein organ culture model for graft disease, leoligin potently inhibited intimal hyperplasia, and even reversed graft disease in pre-damaged vessels. Furthermore, in an in vivo mouse model for venous bypass graft disease, leoligin potently inhibited intimal hyperplasia.ConclusionOur data suggest that leoligin might represent a novel non-toxic, non-thrombogenic, endothelial integrity preserving candidate drug for the treatment of vein graft disease.