Objectives:The aim of this study was to evaluate and compare the morphometric components and the histological properties of pristine bone and bone grafted with a biphasic ß-tricalcium phosphate in humans using the maxillary sinus model. Reparative mesenchymal stem cells in the pristine bone and graft were also evaluated. Materials and Methods:For this prospective case series, sinus augmentation was performed using a biphasic ß-tricalcium phosphate. After 6 months of healing, a core of remnant native alveolar bone and grafted bone was collected with a trephine.Histological, histomorphometrical, and immunohistochemical techniques were performed. Radiological analysis through cone beam computerized tomography was also conducted.Results: A total of 10 patients were enrolled in this study. Radiologically, patients showed an average increase of crestal bone of 8.03 ± 1.72 mm. Morphologically, the grafted area was composed by 34.93 ± 14.68% of new mineralized tissue, 9.82 ± 11.42% of remnant biomaterial particles, and 55.23 ± 11.03% non-mineralized tissue. Histologically, we found no differences in the number of osteocytes per mm 2 (p = 0.674), osteoblasts (p = 0.893), and blood vessels (p = 0.894) in the grafted area compared to the pristine bone. Differences were found on the number of osteoclasts (15.57 ± 27.50 vs. 5.37 ± 16.12, p = 0.027). The number of Musashi-1 positive mesenchymal cells (239.61 ± 177.4 vs. 42.11 ± 52.82, p = 0.027) was also significantly higher in the grafted area than in the pristine bone.Conclusion: Biphasic ß-tricalcium phosphate is a suitable biomaterial to be used in the formation of new bone in sinus floor elevation procedures in humans, not only from the histomorphometrical point of view, but also regarding the cellular and vascular quality of the regenerated bone. K E Y W O R D Sbiomaterial, biphasic ß-tricalcium phosphate, hydroxyapatite, implant dentistry, maxillary sinus augmentation, sinus lift | 337 OLAECHEA Et AL.
Background and Objective: Current evidence suggests that statins exert an anabolic effect on bone and may therefore impact on osteogenic differentiation and proliferation. These effects can be useful for their use in guided bone regeneration. The objective of this study was to determine the in vitro effects of simvastatin on the differentiation and proliferation of MG63 human osteoblast tumor cells. that may be useful against infections associated with bone healing. Experimental studies of implants in rodents found that simvastatin administration improved the bone contact ratio, bone density and osseointegration, 10,11 which was also found to be enhanced by topical fluvastatin application around implants. 12 In contrast, other authors found no increase in bone density in statin-treated defects, 13 and a recent study reported that simvastatin loading of implant surfaces exerted significant effects for only 2 weeks. 14 Formation of new bone tissue was observed in calvaria of rats after the topical injection of fluvastatin using tricalcium phosphate as carrier. 15 However, high doses of local statin can cause inflammation when used for bone regeneration, as reported by two studies in which simvastatin was applied to calvarial defects in rodents. 13,16 Simvastatin was found to affect osteogenic differentiation in a murine model, 17 while an in vitro study showed that exposure to this drug slightly increased osteoblast expression of osteocalcin, osteoprotegerin, alkaline phosphatase and other bone markers. Material and Methods 18The objective of the present study was to determine the in vitro effects of simvastatin on the differentiation and proliferation of the MG63 human tumor osteoblast cell line. | MATERIAL AND METHODSAll procedures in this study were performed in accordance with the 1964 Helsinki declaration and its later amendments. The study was approved by the Ethics Committee of the School of Dentistry of the University of Granada (reference: FOD/UGR/08/2016). | Cell line | MaterialsSimvastatin and dimethyl sulfoxide (DMSO) were obtained from Sigma-Aldrich LLC (St. Louis, MO, USA). Simvastatin was resuspended at a concentration of 20 mg/mL in DMSO and stored at −20°C. | Proliferation assayAfter
Vasculogenic Mimicry (VM) refers to the capacity to form a blood network from aggressive cancer cells in an independent way of endothelial cells, to provide nutrients and oxygen leading to enhanced microenvironment complexity and treatment failure. In a previous study, we demonstrated that VE-Cadherin and its phosphorylation at Y658 modulated kaiso-dependent gene expression (CCND1 and Wnt 11) through a pathway involving Focal Adhesion kinase (FAK). In the present research, using a proteomic approach, we have found that β-catenin/TCF-4 is associated with nuclear VE-cadherin and enhances the capacity of malignant melanoma cells to undergo VM in cooperation with VE-Cadherin; in addition, preventing the phosphorylation of Y658 of VE-cadherin upon FAK disabling resulted in VE-Cadherin/β-catenin complex dissociation, increased β-catenin degradation while reducing TCF-4-dependent genes transcription (C-Myc and Twist-1). Uveal melanoma cells knockout for VE-Cadherin loses β-catenin expression while the rescue of VE-Cadherin (but not of the phosphorylation defective VE-Cadherin Y658F mutant) permits stabilization of β-catenin and tumor growth reduction in vivo experiments. In vivo, the concomitant treatment with the FAK inhibitor PF-271 and the anti-angiogenic agent bevacizumab leads to a strong reduction in tumor growth concerning the single treatment. In conclusion, the anomalous expression of VE-Cadherin in metastatic melanoma cells (from both uveal and cutaneous origins), together with its permanent phosphorylation at Y658, favors the induction of the aggressive VM phenotype through the cooperation of β-catenin with VE-Cadherin and by enhancing TCF-4 genes-dependent transcription.
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