In order to endow environmental protection features to dentifrice, hydroxyapatite (HA) was added to ordinary dentifrice. The effects on dentinal tubule occlusion and surface mineralization were compared after brushing dentine discs with dentifrice with or without HA. The two types of dentifrice were then added to 100 µg/ml of hexavalent chromium cation (Cr6+) solution in order to evaluate their capacities of adsorbing Cr6+ from water. Our results showed that the dentifrice containing HA was significantly better than the ordinary dentifrice in occluding the dentinal tubules with a plugging rate greater than 90%. Moreover, the effect of the HA dentifrice was persistent and energy-dispersive spectrometer (EDS) revealed that the atomic percentages of calcium and phosphorus on the surface of dentine discs increased significantly. Adding HA to ordinary dentifrice significantly enhanced the ability of dentifrice to adsorb Cr6+ from water with the removal rate up to 52.36%. In addition, the sorption was stable. Our study suggests that HA can be added to ordinary dentifrice to obtain dentifrice that has both relieving dentin hypersensitivity benefits and also helps to control environmental pollution.
Cleidocranial dysplasia (CCD) is an autosomal-dominant disorder caused by a lack of function of one or more alleles of the RUNX2 gene. Mutations of the RUNX2 gene were analyzed in a family with CCD, and a novel nonsense mutation was identified, c. 1096G > T, p.E366X, which was predicted to cause a number of potential dysfunctions. Western blot analysis showed that the novel mutation created a shortened protein product, which lost 155 aa in the C-terminal domain. The mutant protein was detected to be localized mostly in the cytoplasm, not in the nucleus, which demonstrated that transport of the RUNX2 protein into the nucleus was disturbed by the p.E366X mutation. For the first time, RUNX2(+/m) dental pulp cells (DPCs) were isolated from two permanent incisors of the CCD patient. Compared to RUNX2(+/+) controls, RUNX2(+/m) DPCs presented an impeded progression from the G1 to the S phase in the cell cycle, a lower rate of proliferation, weaker ability of calcification, and distinct ultrastructure. More interestingly, the ultrastructural analysis and energy dispersive X-ray spectrometry (EDS) analysis showed that the CCD tooth exhibited insufficient mineralization of enamel and dentin. This study suggests that the truncated RUNX2 mutant protein may be responsible for the alterations of RUNX2(+/m) DPCs, and RUNX2 gene may be involved in dental development by affecting the cell growth and differentiation, which provides new insights into understanding of dental abnormalities in CCD patients.
Background Dentin hypersensitivity is a common negative oral condition that can be treated with dentifrice containing hydroxyapatite (HA). The study evaluated the effect of nano-HA dentifrice on plugging the dentinal tubules for an anti-sensitivity reaction compared to a dentifrice containing common-sized particles. Also, the adsorption capacity of different particle sizes of HA mixed in a dentifrice and which is the optimal particle size was considered. Methods Fourty premolar dentine discs and fourty molar dentine discs were randomly divided into 4 groups: distilled water group, ordinary dentifrice group and 80, 300 nm HA dentifrice group. Each dentin disc was brushed with a dentifrice twice daily at 7600 rpm under 100 g force for 2 mins for 7 consecutive days and divided into two parts, half of the dentin disc was detected by the scanning electron microscope (SEM) and energy dispersive spectrometer (EDS), the other half was brushed with distilled water and observed by SEM. One milliliter dentifrice solution (80 nm HA dentifrice, 300 nm HA dentifrice, ordinary dentifrice) was added to 50 ml potassium dichromate solution for 1, 14, and 28 d. The residual Chromium (Cr 6+ ) concentration in the supernatant was measured by the diphenylcarbon phthalocyanine hydrazine method. The elemental constitution in the precipitate was detected by EDS. The Kruskal-Wallis test was used to analyze surface mineralization and different plugging rates of dentinal tubules. The absorption capacity of dentifrices were also evaluated by the Kruskal-Wallis test. Results The plugging rate in the HA dentifrice group was higher than that in the ordinary dentifrice group, and the 80 nm HA dentifrice group showed the best result. The atomic percentages of Ca and P of 80 nm dentifrice group on the surface of dentinal tubules were the highest. The 80 nm HA dentifrice group showed the best adsorption and stable effect of Cr 6+ , followed by the 300 nm HA dentifrice group. The 300 nm HA dentifrice and the ordinary dentifrice showed desorption phenomenon. Conclusions The dentifrice containing HA, especially the 80 nm HA dentifrice, exerts good dentinal tubule occlusion and surface mineralization effect. This dentifrice was also a good adsorbent of Cr 6+ .
Background: MKPs are critical regulators of innate immunity, and yet their regulation remains poorly understood. Results: Upon LPS stimulation, macrophage MKP-1/2 underwent robust phosphorylation on C-terminal serine residues. Mutating the serine residues to alanine decreased their stabilities while mutating them to aspartate dramatically increased their stabilities. Conclusion: ERK plays a critical role in MKP-1/2 accumulation. Significance: MAPKs cross-talk via MKPs to shape inflammatory responses.
The present study aimed to investigate the role of magnitude in adaptive response of osteoblasts exposed to compressive stress. Murine primary osteoblasts and MC3T3-E1 cells were exposed to compressive stress (0, 1, 2, 3, 4, and 5 g/cm2) in 3D culture. Cell viability was evaluated, and expression levels of Runx2, Alp, Ocn, Rankl, and Opg were examined. ALP activity in osteoblasts and TRAP activity in RAW264.7 cells co-cultured with MC3T3-E1 cells were assayed. Results showed that compressive stress within 5.0 g/cm2 did not influence cell viability. Both osteoblastic and osteoblast-regulated osteoclastic differentiation were enhanced at 2 g/cm2. An increase in stress above 2 g/cm2 did not enhance osteoblastic differentiation further but significantly inhibited osteoblast-regualted osteoclastic differentiation. This study suggested that compressive stress regulates osteoblastic and osteoclastic differentiation through osteoblasts in a magnitude-dependent manner.
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