Search

The aim of this research was to evaluate the resorption and osseointegration of an autogenous bone ring, which was grafted in a local vertical alveolar defect with simultaneous implant placement. Six Beagle dogs were enrolled in the study; their 4 nonadjacent mandibular premolars were extracted, and the buccal plate was removed to create bone defects in 2 of the 4 sites. Three months after extraction, Straumann implants (Ø 3.3 mm, length of 8 mm) were placed in the bone defect sites with simultaneous autogenous bone ring grafting and in the conventional extraction sites. After a 3-month healing period and a 3-month loading period, the animals were euthanized. The harvested samples were analyzed using micro-computed tomography (CT) scanning and histological analysis. From the micro-CT measurements, the average vertical bone resorption of the bone ring was 0.23 ± 0.03 mm, which was not significantly different from that around the conventional implant, 0.24 ± 0.12 mm (P >.05). The ratio of the bone volume to the total volume of the bone ring group was 91.11 ± 0.02, which was higher than that of the control group, 88.38 ± 2.34 (P <.05). From the hard tissue section, the bone rings developed fine osseointegration with the implants and the base alveolar bone. The results suggest autogenous bone ring grafting with simultaneous implant placement can survive in a local vertical bone defect with little bone resorption and good osseointegration in dogs with strict management. A bone ring graft must be compared with guided bone regeneration, and a larger and longer observation must be confirmed in clinical patients. [ABSTRACT FROM AUTHOR]

Objective: To explore the potential osteogenic induction mechanism of enamel matrix derivatives (EMDs) on bone marrow mesenchymal stem cell (BMSC) sheets with different titanium surface morphologies., Methods: The BMSCs were inoculated on the surfaces of titanium alloys with different morphologies: anodic oxidation (AO), sand-blasted, large grit and acid-etched, and no treatment (control). The proliferation and osteogenic differentiation of BMSCs on the different surface morphologies were observed with the same concentration of EMDs. To further understand the osteogenic mechanism of EMDs on BMSC sheets with different morphologies, a real-time RT-PCR and a western blot were used to detect the overall levels of osteogenic genes and osteogenic proteins. Finally, to verify the osteogenic effect of BMSC sheets stimulated by EMDs in vivo, BMSC sheets with different morphologies were implanted into the subcutaneous tissue of the back of nude mice, and the bone formation was detected by HE staining., Results: The EMDs and surface morphology in the AO group synergically increased the expression levels of osteogenic active factors (RUNX2, OSX and OCN) and enhanced the osteogenic differentiation effect of BMSCs. The in vivo experiments showed that the BMSC sheets in the AO group were rich in osteogenic active factors, and promoted the formation of ectopic bone tissue after implantation into the subcutaneous tissue of the back of nude mice., Conclusion: EMDs and AO morphology synergically enhance the secretion of bone osteogenic active factors of BMSCs and promote the formation of heterotopic bone., Competing Interests: None., (AJTR Copyright © 2023.)

To study the effect of miR-153-3p on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) in a high glucose environment and its potential mechanism. The results showed that high glucose inhibited the osteogenic differentiation of BMSCs, and the expression of miR-153-3p increased during osteogenic differentiation. Further experiments found that in BMSCs induced by high glucose, overexpression of miR-153-3p inhibited the osteogenic differentiation of BMSCs, and the expressions of osteogenesis-related genes bone sialoprotein, Collagen I and alkaline phosphatase were down-regulated, while silencing of miR-153-3p alleviated the inhibition effect. The dual-luciferase reporter gene assay confirmed that the 3'-untranslated region (3'-UTR) of runt related transcription factor 2 (RUNX2) had a targeted binding site with miR-153-3p and a negative regulatory effect. Molecular studies further confirmed that miR-153-3p inhibited the osteogenic differentiation of BMSCs by targeting the 3'-UTR of RUNX2. In conclusion, our study found that as one key regulator of high glucose affecting the osteogenic differentiation of BMSCs, miR-153-3p may play a negative regulatory role by inhibiting the expression of RUNX2., Competing Interests: None., (AJTR Copyright © 2022.)

Lysophosphatidic acid (LPA) is a multifunctional phospholipid. Osteocytes are the most abundant cells in bone and can orchestrate bone formation and resorption, in part by producing cytokines that regulate osteoblast and osteoclast differentiation and activity. Interleukin (IL)-6 and IL-8 are two important cytokines that have potent effects on bone fracture healing. Previous studies suggest that platelet-derived LPA may influence fracture healing by inducing osteocyte dendrite outgrowth. However, the biological mechanism through which LPA induces cytokine production in osteocytes is poorly understood. In this study, we report that LPA markedly enhanced IL-6 and CXCL15 (mouse homologue of human IL-8) production in MLO-Y4 cells and that this enhancement was suppressed by the LPA 1/3 -selective antagonist Ki16425, the G i/o protein inhibitor PTX or the protein kinase C (PKC) inhibitor sotrastaurin. We also observed that of all the PKC isoform targets of sotrastaurin, only PKCθ was activated by LPA in MLO-Y4 cells and that this activation was blocked by sotrastaurin, Ki16425 or PTX. Taken together, the results of the present study demonstrate that LPA may be a potent inducer of IL-6 and CXCL15 production in MLO-Y4 cells and that this induction is associated with the activation of LPA 1 , G i/o protein and the PKCθ pathway. These findings may help us better understand the mechanism of fracture healing and contribute to the treatment of bone damage., (Copyright © 2019 Elsevier B.V. All rights reserved.)