In vitro demineralization of artificial large-scale hydroxyapatite single crystal: Implications of fluoridized tooth enamel for acid resistance

Fluoride treatment has been well known to improve acid resistance of tooth enamel, leading to the widespread use of fluoride therapies in dentistry such as fluoride rinse and fluoridereleasing dental materials. The effect of fluoridation is likely based on the chemical properties of fluoridized hydroxyapatite; however, nanoscale tiny hydroxyapatite crystals in tooth enamel make it difficult to observe the demineralization pattern of fluoridated enamel versus the untreated enamel at a single crystal level. The purpose of this study was to mimic the demineralization patterns of fluoridated and untreated enamel by means of the newly developed hydrothermally enlarged enamel-like hydroxyapatite single crystals at Showa University. Largescale hydroxyapatite single crystals were hydrothermally produced from polyphosphoric acid and calcium oxide. The crystals were stored in sodium fluoride solutions with four different concentrations for 30 days, then exposed to 3% citric acid solution for up to 60 min. The degradation patterns of each sample were observed using a conventional scanning electron microscope and were analyzed using F K-edge X-ray absorption near edge structure spectra. The surfaces of the hydroxyapatite crystals treated by relatively low concentrations of fluoride showed degradation in citric acid as well as in the untreated control. The hydroxyapatite crystals treated with 1,500 and 9,000 ppm F revealed that the fluoridated outer pillar of the crystals remained mostly intact which made calcium fluoride detectable. Fluoridization of tooth enamel might be preventive of an early acid erosion at a crystal level with a caution of sufficient fluoride concentration and exposure over time. The remaining substantial portion of the crystal pillar implies of highly fluoridized crystals, and a possible remineralization occurs as long as saliva provides minerals required for enamel remineralization by in vivo regulation.