Platelet-derived growth factor (PDGF) stimulates chemotaxis and proliferation of osteoblasts, and induces bone formation in vivo. To determine how PDGF might regulate these cells, the effect of PDGF on long-term mineralizing cultures of fetal rat osteoblastic cells was examined. Although PDGF increased cell proliferation in these cultures, continuous treatment with PDGF caused a dose-dependent decrease in mineralized nodule formation. When cells were treated with multiple, brief (1 day) exposures to PDGF at the osteoblast differentiation stage, there was a significant 50% increase in mineralized nodule area. Based on modulation of alkaline phosphatase activity it appears that longer-term exposure to PDGF reduces mineralized nodule formation largely by inhibiting differentiated osteoblast function, while short-term exposure enhances proliferation without inhibiting the differentiated phenotype. Thus, the ultimate affect of PDGF on bone formation is likely to reflect two processes: a positive effect through enhancing cell number or a negative effect by inhibiting differentiated function. The inhibitory effect of PDGF on formation of a mineralized matrix is unlikely to be simply a result of enhanced proliferation of "fibroblastic" cells since cultures treated with PDGF for 3 days and then transferred to new plastic dishes exhibited a 70% increase in mineralized nodule area compared to controls. These results would predict that multiple, brief exposures to PDGF would enhance bone formation in vivo, while prolonged exposure to PDGF, which is likely to occur in chronic inflammation, would inhibit differentiated osteoblast function and limit bone regeneration.

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Platelet-derived growth factor (PDGF) is mitogenic and chemotactic for osteoblastic cells in vitro. It is expressed during osseous wound healing and stimulates formation of new bone in vivo. PDGF stimulates cells by binding to specific cell surface receptors. The purpose of this study was to examine the effects of PDGF on osteoblastic proliferation and differentiation in long-term mineralizing cultures. Utilizing Northern blot analysis, we found that continuous PDGF treatment increased histone expression, indicative of enhanced proliferation, but suppressed osteoblast differentiation, demonstrated by inhibition of alkaline phosphatase, type I collagen, and osteocalcin expression. The inhibitory effect of PDGF on the differentiated function of osteoblasts was further established by findings that PDGF significantly inhibited nodule formation. The expression of PDGF receptors varied at different stages of culture. PDGF receptor mRNA expression increased when the cells had achieved a mature phenotype, during the stage of matrix maturation, and then decreased. However, as demonstrated by thymidine incorporation assays, the capacity of PDGF to stimulate DNA synthesis actually decreased during osteoblast maturation, as receptor expression increased. To investigate this apparent contradiction, tyrosyl phosphorylation and immunoblot assays were performed to assess changes in PDGF activation of their cognate receptors. The pattern of PDGF-induced tyrosyl phosphorylation remained relatively constant. This suggests that the diminished mitogenic activity of PDGF that occurs after osteoblast differentiation is regulated at a postreceptor level.

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The aim of this study was to explore the biophysical effects of static magnetic field on osteoblastic cells. MG63 cells were exposed to 0.25 and 0.4-T static magnetic fields (SMF). The cell cycle effects were tested by flow cytometry. The differentiation of the cells was assessed by detecting the changes in prostaglandin E2, osteocalcin, and extracellular matrix expression. Membrane fluidity was used to evaluate the alterations in the biophysical properties of cellular membranes after the SMF simulations. Our results show that SMF exposure increases prostaglandin E2 level and extracellular matrix express in MG63 cells. On the other hand, MG63 cells exposed to 0.4-T SMF exhibited a significant decrease in membrane fluidity at 8 h. Based on these findings, it appears reasonable to suggest that SMF affect osteoblastic maturation by increasing membrane rigidity and then inducing differentiation pathway.

The objective of this study was to evaluate the antibacterial efficacy against Enterococcus faecalis and Streptococcus mutans and in vivo toxicity using embryonic zebrafish assays of sodium hypochlorite (NaOCl) and electrolyzed oxidizing (EO) water (containing hypochlorous acid (HOCl))-based root canal irrigating solutions. Methodology: Using 100 µL microbial count of 1 × 10 8 cfu/mL Enterococcus faecalis to mix with each 10 mL specimen of NaOCl or HOCl for designed time periods. The above protocol was also repeated for Streptococcus mutans. The concentration of viable microorganisms was estimated based on each standardized inoculum using a plate-count method. Zebrafish embryo assays were used to evaluate acute toxicity. Results: All the HOCl or NaOCl treatment groups showed > 99.9% antibacterial efficacy against Enterococcus faecalis and Streptococcus mutans. Zebrafish embryos showed almost complete dissolution in 1.5% NaOCl within 5 min. Both survival rates after being treated with 0.0125% and 0.0250% HOCl for 0.5 min or 1.0 min were similar to that of E3 medium. Conclusions: Both NaOCl and HOCl revealed similar antibacterial efficacy (> 99.9%) against Enterococcus faecalis and Streptococcus mutans. While 1.5% NaOCl fully dissolved the Zebrafish embryos, both 0.0125% and 0.0250% HOCl showed little in vivo toxicity, affirming its potential as an alternative irrigation solution for vital pulp therapy.

Nickel-titanium (NiTi) instruments are extensively used in endodontic treatment because of their outstanding mechanical properties. However, unexpected fracture of NiTi rotary instruments occurs during endodontic procedures. Therefore, a reliable method to detect the structural status of a used NiTi instrument is needed. The aim of this study is to use natural frequency for monitoring structural changes of a NiTi instrument during and after the instrumentation process. In this study, laboratory modal testing experiments were performed on cyclic fatigue-loaded NiTi rotary instruments with a natural frequency detecting device. In addition, three-dimensional finite element (FE) models were established for assessing the structural changes that take place in repeatedly loaded NiTi instruments. Repeated rotational loading resulted in a significant decrease (p < 0.05) in natural frequency (with a decreasing ratio of 5.6%) when the tested instruments reached 77-85% of their total life limit. In FE analysis, a strong correlation between natural frequency and change in elastic modulus of the NiTi instrument was found. These findings indicated that natural frequency may represent an effective parameter for evaluating the micro-structural status of NiTi rotary instruments subjected to fatigue loadings.

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