Anion Translocation Through the Enamel Organ

Abstract

The objective of this study was to determine whether cells of the secretory- and maturation-stage enamel organ of rats contain anion translocation mechanisms similar to those found in other ion-regulating epithelia. Sodium bromide (Br) was used to localize the distribution of anions in the enamel organ. Furosemide, an inhibitor of the Na-K-2C1 co-transporter and other anion transporters, was administered with NaBr or sodium fluoride (F) to investigate if halogens other than Cl can use these transport mechanisms. We obtained the data by using freeze-fracture and freeze-drying methodology in conjunction with scanning and transmission electron microscopy (SEM, TEM) and energy-dispersive x-ray spectroscopy (EDS). The secretory- and maturation-stage enamel organ prevented Br from entering the enamel matrix. Br was localized in the Tomes' processes, but not in the enamel matrix, strongly suggesting that the distal intercellular junctions of ameloblasts are "tight". Furosemide disrupted anion transport to allow not only Cl but also Br to enter the forming enamel matrix. Periodic administration of high F doses promoted the formation of bands of disrupted enamel, reflecting the periodicity of F administration. The same concentration of F administered with furosemide increased the severity of disrupted enamel, resulting in "blisters" and pits in the maturing enamel. The enamel "blisters" contained pools of small, disorganized enamel crystallites. The group receiving furosemide only displayed normal enamel structure but had increased C1 in the enamel matrix. This study provides evidence that anion transporters, possibly the Na-K-2CI co-transporter, function to regulate anion translocation, including F, to the enamel matrix in secretory- and maturation-stage enamel organ. These mechanisms may explain why the ionic composition on the cellular side of the anion barrier is different from that of the enamel matrix.