Promotional Effect and Molecular Mechanism of Synthesized Zinc Oxide Nanocrystal on Zirconia Abutment Surface for Soft Tissue Sealing.

Studies have confirmed that tooth loss is closely related to systemic diseases, such as obesity, diabetes, cardiovascular diseases, some types of tumors, and Alzheimer's disease. Among many methods for tooth restoration, implant restoration is the most commonly used method. After implantation, long-term stability of implants requires not only good bone bonding but also good soft tissue sealing between implants and surrounding soft tissues. The zirconia abutment is used in clinical implant restoration treatment, but due to the strong biological inertia of zirconia, it is difficult to form stable chemical or biological bonds with surrounding tissues. In this study, we investigated synthesized zinc oxide (ZnO) nanocrystal on the zirconia abutment surface by the hydrothermal method to make it more beneficial for soft tissue early sealing and the molecular mechanism. In vitro experiments found that different hydrothermal treatment temperatures affect the formation of ZnO crystals. The crystal diameter of ZnO changes from micron to nanometer at different temperatures, and the crystal morphology also changes. In vitro, scanning electron microscopy, energy dispersive spectrometry, and real-time polymerase chain reaction results show that ZnO nanocrystal can promote the attachment and proliferation of oral epithelial cells on the surface of zirconia by promoting the binding of laminin 332 and integrin ß4, regulating the PI3K/AKT pathway. In vivo, ZnO nanocrystal ultimately promotes the formation of soft tissue seals. Collectively, ZnO nanocrystal can be synthesized on a zirconia surface by hydrothermal treatment. It can help to form a seal between the implant abutment and surrounding soft tissue. This method is beneficial to the long-term stability of the implant and also can be applied to other medical fields.

Simvastatin enhances bone formation around titanium implants in rat tibiae.

Statins are cholesterol-lowering drugs that have been reported to promote bone formation. The purpose of this study was to investigate the effect of simvastatin on the enhancement of bone formation around titanium implants. Thirty-week-old female rats received pure titanium implants in both tibiae. The animals were intra-peritoneally administered 0, 0.125, 1, 5 or 10 mg kg(-1) of simvastatin daily. After 30 days, the animals were sacrificed, and specimens were prepared. The bone contact ratio of the implant, bone density in the medullary canal and percentage of cortical bone were obtained. Markers for bone turnover were also measured using sera collected at the time of euthanasia. In the medullary canal, a scanty amount of bone was observed in the 0, 0.125 and 1 mg kg(-1) groups. In contrast, in both the 5 and 10 mg kg(-1) groups, thicker bone trabeculae were abundant. Histometric observations showed that the bone contact ratio and the bone density of both groups were significantly greater than those of the other groups (anova, P < 0.01). However, no significant difference in the percentage of cortical bone was found between groups. Serum chemistry showed that statin increased bone formation markers and decreased bone resorption markers. In conclusion, although the dose equivalent to that used in human patients with hypercholesterolemia was not effective, a simvastatin dose of 5 mg kg(-1) or higher increased medullary bone formation around the titanium. In contrast, no effect of simvastatin on pre-existing cortical bone was indicated.

Platelet-rich plasma suppresses osteoclastogenesis by promoting the secretion of osteoprotegerin.

BACKGROUND AND OBJECTIVE: Platelet-rich plasma is characterized by containing fundamental protein growth factors. Although many in vitro studies have documented the capability of platelet-rich plasma to induce the growth of osteoblasts or osteoblast-like cells, the effect of platelet-rich plasma on osteoclastogenesis has not yet been studied. The aim of the present study was to evaluate the effects of platelet-rich plasma and platelet-poor plasma on osteoclastogenesis with rat bone marrow cell culture. MATERIAL AND METHODS: Platelet-rich plasma and platelet-poor plasma were produced from the whole blood of rat. For cell culture, rat bone marrow cells were isolated from rat tibiae and then treated with 1,25alpha dihydroxy vitamin D(3) and with different concentrations of platelet-rich plasma or platelet-poor plasma. After 4 d of culture, rat bone marrow cells were stained with tartrate-resistant acid phosphatase (TRAP), and TRAP-positive cells that had more than three nuclei (TRAP-positive multinucleated cells) were counted as osteoclast-like cells. Osteoprotegerin, known as an osteoclastogenesis-related factor, cells was quantified using an enzyme-linked immunosorbent assay (ELISA). RESULTS: Although platelet-poor plasma had no effect on the formation of TRAP-positive multinucleated cells, platelet-rich plasma decreased the number of TRAP-positive multinucleated cells in a dose-dependent manner. The amount of osteoprotegerin produced from rat bone marrow cells and from MC3T3-E1 cells was enhanced in platelet-rich plasma-treated groups. CONCLUSION: Under our experimental conditions, platelet-rich plasma decreased the formation of TRAP-positive multinucleated cells and increased the secretion of osteoprotegerin. This study suggests that platelet-rich plasma suppresses osteoclastogenesis, therefore inhibiting bone resorption. In addition we also demonstrated that platelet-rich plasma increased the secretion of osteoprotegerin, an inhibitor for osteoclast formation, thus suggesting that the enhancement of osteoprotegerin secretion induces this inhibitory effect.

Oxidative stress-induced DNA damage in the synovial cells of the temporomandibular joint in the rat.

Synovial hyperplasia is a feature of degenerative temporomandibular joint (TMJ) disease. However, the mechanism by which hyperplasia progresses in the TMJ is unknown. Based on the hypothesis that the oxidative stress generated by mechanical loading causes degenerative changes in the TMJ synovium, we investigated the generation of the highly reactive species, peroxynitrite, and the occurrence of DNA damage in the synovium. After condylar hypermobility of rat TMJs, a marker of peroxynitrite, nitrotyrosine, was localized to the nuclei and cytoplasm of the synovial lining cells and fibroblasts in synovitis-induced TMJ. DNA single-strand breaks were found in the nuclei of the synovial cells only after enzyme treatment, whereas DNA double-strand breaks were not detected. These findings indicate that condylar hypermovement induces the proliferation of synovial cells, and suggest that oxidative stress leads to the progression of synovial hyperplasia via DNA damage of the synovial cells in TMJs after mechanical loading.