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Amelogenesis is a complicated process that concerns the interaction between growing hydroxyapatite crystals and extracellular proteins, which requires the tight regulation of pH. In dental fluorosis, the balance of pH regulation is broken, leading to abnormal mineralization. The current review focuses on the electrolyte transport processes associated with pH homeostasis, particularly regarding the changes in ion transporters that occur during amelogenesis, following exposure to excessive fluoride. Furthermore, the possible mechanism of fluorosis is discussed on the basis of acid hypothesis. There are two main methods by which F− accelerates crystal formation in ameloblasts. Firstly, it induces the release of protons, lowering the pH of the cell microenvironment. The decreased pH stimulates the upregulation of ion transporters, which attenuates further declines in the pH. Secondly, F− triggers an unknown signaling pathway, causing changes in the transcription of ion transporters and upregulating the expression of bicarbonate transporters. This results in the release of a large amount of bicarbonate from ameloblasts, which may neutralize the pH to form a microenvironment that favors crystal nucleation. The decreased pH stimulates the diffusion of F− into the cytoplasm of amelobalsts along the concentration gradient formed by the release of protons. The retention of F− causes a series of pathological changes, including oxidative and endoplasmic reticulum stress. If the buffering capacity of ameloblasts facing F− toxicity holds, normal mineralization occurs; however, if F− levels are high enough to overwhelm the buffering capacity of ameloblasts, abnormal mineralization occurs, leading to dental fluorosis. [ABSTRACT FROM AUTHOR]

Dental fluorosis is a global issue. Although there are multiple causes of dental fluorosis, the precise mechanism remains controversial. Previous studies have demonstrated that extracellular fluoride may promote an accumulation of fluoride ions in ameloblasts, which may induce oxidative and endoplasmic reticulum stresses, leading to dental fluorosis. However, the exact process by which fluoride ions enter cells has not been determined. In the present study, intracellular fluoride concentration was determined using a newly developed specific fluorescent probe called probe 1. Under high extracellular fluoride concentrations, the fluorescence intensity of the ameloblasts increased, however, exogenous transforming growth factor-β1 (TGF-β1) was able to inhibit the increase. Furthermore, changes in the expression of the voltage-gated chloride channels 5 and 7 (ClC5 and ClC-7), which are responsible for the transport of fluoride were investigated. The results indicated that fluoride reduced the expression of endogenous TGF-β1 and increased the expression of ClC-5 and ClC-7. Additionally, exogenous TGF-β1 reduced the expression of ClC-5 and ClC-7. The results of the present study indicate that exogenous TGF-β1 may prevent accumulation of fluoride in ameloblasts through the regulation of ClC-5 and ClC-7 under high extracellular fluoride concentrations. [ABSTRACT FROM AUTHOR]

The present study aimed to evaluate the impact of total extracorporeal circulation on hemodynamics and placental function in an ovine fetal model. Mid-term ovine fetuses (n=6) underwent extracorporeal circulation (30 min), cardioplegic arrest (20 min) and monitoring (120 min). The ascending aorta and umbilical cords of the fetuses were occluded during the bypass and an extracorporeal membrane oxygenator was used as the oxygen source. Biventricular intracardiac pressures, echocardiographic data, blood gas levels and placental function variables were recorded, and statistical analysis was performed using the repeated-measure analysis of variance test. The data indicated that fetal heart rate and blood pressure at 30, 60, 90 and 120 min following the bypass were stable relative to pre-arrest baseline (pre-bypass) values (P>0.05). However, end diastolic pressures in the ovine right ventricles post-bypass were significantly increased at 30, 60, 90 and 120 min relative to pre-bypass pressures (P<0.05). The pulsatility index also increased at 30 min post-bypass relative to the pre-bypass score (0.91±0.06 vs. 0.61±0.14; P=0.007). The mean resistivity index at all time points post-bypass was consistent with the pre-bypass score (P>0.05), while the mean Tei index values for the left and right ventricles post-bypass were significantly higher at all time points relative to pre-bypass values (P<0.05). The pre-bypass fetal blood pH, SaO2, base excess and lactate values were maintained during arrest (P>0.05). Fetal hemodynamics and placental function additionally remained stable for up to 2 h upon reperfusion following total extracorporeal circulation and cardioplegic arrest. Collectively these data suggest that the reproducible ovine fetal model may be useful in the evaluation of fetal cardiac surgery. [ABSTRACT FROM AUTHOR]