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The biocompatibility of metal implants is related to their surface electrochemical characterizations. The in situ growing process of osteoblast-like U-2 OS cells on polished Ti and Ti-6Al-4V alloy during 72h incubation was monitored using the electrochemical impedance spectroscopy (EIS) measurement technique. The results showed that the presence of cells on metals led to an increase in the impedance and polarization resistance (R(p)) of metals. The impedance and R(p) increased as the cells grew (i.e., from adhesion, spreading to proliferation period). A trace amount of V element released from Ti-6Al-4V alloy led to a lower R(p) with respect to Ti metal during cell culture. In this study, a satisfactory equivalent circuit simulating the electrochemical characterizations of Ti and Ti-6Al-4V alloy cultured with cells was proposed. The EIS measurement technique was applied successfully to monitor the in situ growing process of U-2 OS cells on Ti and Ti-6Al-4V alloy.  相似文献   

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ObjectivesStromal cell‐derived factor‐1 (SDF‐1) actively directs endogenous cell homing. Exendin‐4 (EX‐4) promotes stem cell osteogenic differentiation. Studies revealed that EX‐4 strengthened SDF‐1‐mediated stem cell migration. However, the effects of SDF‐1 and EX‐4 on periodontal ligament stem cells (PDLSCs) and bone regeneration have not been investigated. In this study, we aimed to evaluate the effects of SDF‐1/EX‐4 cotherapy on PDLSCs in vitro and periodontal bone regeneration in vivo.MethodsCell‐counting kit‐8 (CCK8), transwell assay, qRT‐PCR and western blot were used to determine the effects and mechanism of SDF‐1/EX‐4 cotherapy on PDLSCs in vitro. A rat periodontal bone defect model was developed to evaluate the effects of topical application of SDF‐1 and systemic injection of EX‐4 on endogenous cell recruitment, osteoclastogenesis and bone regeneration in vivo.ResultsSDF‐1/EX‐4 cotherapy had additive effects on PDLSC proliferation, migration, alkaline phosphatase (ALP) activity, mineral deposition and osteogenesis‐related gene expression compared to SDF‐1 or EX‐4 in vitro. Pretreatment with ERK inhibitor U0126 blocked SDF‐1/EX‐4 cotherapy induced ERK signal activation and PDLSC proliferation. SDF‐1/EX‐4 cotherapy significantly promoted new bone formation, recruited more CXCR4+ cells and CD90+/CD34 stromal cells to the defects, enhanced early‐stage osteoclastogenesis and osteogenesis‐related markers expression in regenerated bone compared to control, SDF‐1 or EX‐4 in vivo.ConclusionsSDF‐1/EX‐4 cotherapy synergistically regulated PDLSC activities, promoted periodontal bone formation, thereby providing a new strategy for periodontal bone regeneration.  相似文献   

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