Barrier membranes have been extensively used in dentistry to prevent soft tissue down-growth into the bone defects and to promote alveolar ridge augmentation. Previous studies of our group showed that the Poly(vinylidene-trifluoroethylene)/barium titanate composite (PVDF) enhances both the in vitro osteoblastic differentiation and the in vivo bone repair compared with a commercially available polytetrafluoroethylene (PTFE) membrane. As bone formation may be regulated by post-transcriptional events such as temporary expression of microRNAs (miRs), the aim of this study was to investigate a possible mechanism involving miRs and RANKL in the osteogenic potential of the PVDF membrane. Rat calvarial bone defects were implanted with either PVDF or PTFE membrane, under the approval of the Committee of Ethics in Animal Research. At 4 and 8 weeks, the new-formed bone was submitted to a large-scale analysis of miRs by microarray, followed by the evaluation of the expression of miR-34a (microarray validation) and RANKL, one of its targets, by quantitative real-time PCR. Also, histochemical analysis was carried out to detect TRAP positive cells. All quantitative data were obtained in triplicate (n=3) and compared by t-test (P≤0.05). Among 250 evaluated miRs, miR-34a, -10a and -133b were simultaneously upregulated (>2 fold) at 4 and 8 weeks. At 8 weeks, the expression of miR-34a was higher (P=0.016) in the bone grown on PVDF compared with PTFE, followed by a downregulation of the RANKL expression (P=0.004). In addition, more TRAP positive cells were observed on new-formed bone grown on PTFE compared with PVDF membrane in both periods. In conclusion, PVDF membrane induces higher bone repair, at least in part, by triggering an intracellular mechanism of miR-34a upregulation/RANKL dowregulation loop, which inhibits osteoclastic activity.
14 May 2016 - 17 May 2016