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Study Design: Retrospective, descriptive observational study. Objective: The need for revision surgery after mandibular fractures is an indicator for severe postoperative complications. This study aimed to characterise this patient cohort, describe solutions to deal with complications and evaluate treatment quality as a risk variable for complications. Methods: Patients with revision surgery with refixation after open reduction and internal fixation (ORIF) of a mandible fracture were included. Patient- and therapy-specific information were assessed together with postoperative complications. The quality of fixation was evaluated individually by 6 specialists. Interobserver agreement was analysed using Fleiss' kappa. Results: Out of 630 patients, inclusion criteria were met by 17 patients (14 male, 3 female) with an average age of 43.3 (±15.5) years. Complications at the mandible body/angle/symphysis led to refixation in all cases. Main indications for refixation were osteomyelitis (52.9%) or pseudarthrosis (41.2%). Risk factors were drug-related immune suppression, local infection or substance abuse (nicotine, alcohol or drugs). Six patients did not present any of these predictors. Of these, treatment of 4 patients was rated as not in accordance to the AO principles. The interrater reliability of treatment quality assessments was.239. Conclusions: Patients with risk factors need to be carefully observed perioperatively after ORIF of mandibular fractures and treatments need to be adapted to these patients. Discrepancies of treatments to common guidelines may also be an independent predictor for treatment failure in patients without risk factors. Current treatment guidelines should be re-evaluated concerning additional treatment strategies for patients with specific risk factors. [ABSTRACT FROM AUTHOR]

Bite force measuring devices that are generally suitable for edentulous patients or patients undergoing mandibular reconstruction are missing. This study assesses the validity of a new bite force measuring device (prototype of loadpad®, novel GmbH) and evaluates its feasibility in patients after segmental mandibular resection. Accuracy and reproducibility were analyzed with two different protocols using a universal testing machine (Z010 AllroundLine, Zwick/Roell, Ulm, Germany). Four groups were tested to evaluate the impact of silicone layers around the sensor: no silicone ("pure"), 2.0 mm soft silicone ("2-soft"), 7.0 mm soft silicone ("7-soft") and 2.0 mm hard silicone ("2-hard"). Thereafter, the device was tested in 10 patients prospectively who underwent mandibular reconstruction using a fibula free flap. Average relative deviations of the measured force in relation to the applied load reached 0.77% ("7-soft") to 5.28% ("2-hard"). Repeated measurements in "2-soft" revealed a mean relative deviation of 2.5% until an applied load of 600 N. Maximum bite force decreased postoperatively by 51.8% to a maximum mean bite force of 131.5 N. The novel device guarantees a high accuracy and degree of reproducibility. Furthermore, it offers new opportunities to quantify perioperative oral function after reconstructive surgery of the mandible also in edentulous patients. [ABSTRACT FROM AUTHOR]

Multiple sclerosis is the most frequent chronic inflammatory disease of the CNS. The entry and survival of pathogenic T cells in the CNS are crucial for the initiation and persistence of autoimmune neuroinflammation. In this respect, contradictory evidence exists on the role of the most potent type of antigenpresenting cells, dendritic cells. Applying intravital two-photon microscopy, we demonstrate the gatekeeper function of CNS professional antigen-presenting CD11c+ cells, which preferentially interact with Th17 cells. IL-17 expression correlates with expression of GM-CSF by T cells and with accumulation of CNS CD11c+ cells. These CD11c+ cells are organized in perivascular clusters, targeted by T cells, and strongly express the inflammatory chemokines Ccl5, Cxcl9, and Cxcl10. Our findings demonstrate a fundamental role of CNS CD11c+ cells in the attraction of pathogenic T cells into and their survival within the CNS. Depletion of CD11c+ cells markedly reduced disease severity due to impaired enrichment of pathogenic T cells within the CNS. [ABSTRACT FROM AUTHOR]

Introduction. Human mesenchymal stromal cells (hMSCs) exhibit the potential to accelerate bone healing by enhanced osteogenic differentiation. Interleukin-1β is highly expressed during fracture healing and has been demonstrated to exert a significant impact on the differentiation behaviour of hMSCs. Here, we investigate the effect of 2-hour IL-1β stimulation on the differentiation and paracrine activity of hMSCs in coculture with osteosarcoma cells in vitro. Methods. hMSCs from 3 donors were incubated for 2 hours with 10 ng/mL IL-1β and subsequently cocultured with MG63-GFP cells either in control or in differentiation medium in a transwell system for 28 days. Genetic and functional effects were investigated. Results. hMSCs cultured in control medium exhibited a regulatory effect on cocultured MG63-GFP cells, resulting in upregulation of osteogenic gene expression in combination with increased ALP activity. However, while stimulated hMSCs cultured under differentiation conditions exhibit signs of osteogenic differentiation, osteogenic differentiation also caused an impaired regulatory effect on the cocultured MG63-GFP cells. Conclusion. Short stimulation of hMSCs has the potential to modify their long-term behaviour. In addition, undifferentiated hMSCs are able to regulate osteoblast differentiation; however, this regulatory function is lost upon osteogenic differentiation in vitro. This offers a novel approach for clinical cell therapy protocols. [ABSTRACT FROM AUTHOR]

Multiple sclerosis is the most frequent chronic inflammatory disease of the CNS. The entry and survival of pathogenic T cells in the CNS are crucial for the initiation and persistence of autoimmune neuroinflammation. In this respect, contradictory evidence exists on the role of the most potent type of antigen-presenting cells, dendritic cells. Applying intravital two-photon microscopy, we demonstrate the gatekeeper function of CNS professional antigen-presenting CD11c(+) cells, which preferentially interact with Th17 cells. IL-17 expression correlates with expression of GM-CSF by T cells and with accumulation of CNS CD11c(+) cells. These CD11c(+) cells are organized in perivascular clusters, targeted by T cells, and strongly express the inflammatory chemokines Ccl5, Cxcl9, and Cxcl10. Our findings demonstrate a fundamental role of CNS CD11c(+) cells in the attraction of pathogenic T cells into and their survival within the CNS. Depletion of CD11c(+) cells markedly reduced disease severity due to impaired enrichment of pathogenic T cells within the CNS., (© 2015 The Authors.)