Yamazaki Hajime, Litman Amy, Margolis Henry C
Health Care Products Research Laboratories, Kao Corporation, 1-3, Bunka 2 chome, Sumidaku, Tokyo 131-8501, Japan.
Arch Oral Biol. 2007 Feb;52(2):110-20. doi: 10.1016/j.archoralbio.2006.08.012. Epub 2006 Oct 16.
This study was carried out to determine in vitro the effect of fluoride on (1) the demineralization of sound human enamel and (2) the progression of artificial caries-like lesions, under relevant oral conditions.
Thin sections of sound human enamel were exposed to solutions undersaturated with respect to tooth enamel to a degree similar to that found in dental plaque fluid following sucrose exposure in vivo, containing fluoride concentrations (0-0.38ppm) found in plaque fluid. Mineral changes were monitored for 98 days, using quantitative microradiography. The effect of fluoride (1.0-25.0ppm) on the progression of artificial caries-like lesions was similarly studied.
Fluoride concentrations of 0.19ppm and greater were found to prevent the demineralization of sound enamel in vitro. However, significantly higher concentrations of fluoride (25.0ppm) were required to prevent further demineralization of artificial caries-like lesions. Demineralizing solutions with intermediate fluoride concentrations (2.1-10.1ppm) induced simultaneously remineralization in the outer portion of the lesion and demineralization in the inner portion. Simultaneous remineralization and demineralization were also observed in hydroxyapatite pellets.
Our results show that the observed effect of fluoride on enamel demineralization is not solely a function of bulk solution properties, but also depends on the caries-status of the enamel surface. A mechanistic model presented indicates that, in comparison to sound enamel surfaces, higher concentrations of fluoride are required to prevent the progression of artificial caries-like lesions under in vivo-like conditions since the diffusion of mineral ions that promote remineralization is rate-limiting.
本研究旨在体外确定在相关口腔条件下氟化物对(1)健康人牙釉质脱矿以及(2)人工龋样病变进展的影响。
将健康人牙釉质薄片暴露于相对于牙釉质不饱和的溶液中,不饱和程度类似于体内蔗糖暴露后牙菌斑液中的情况,溶液中氟化物浓度(0 - 0.38ppm)为菌斑液中所发现的浓度。使用定量显微放射照相术监测矿物质变化98天。同样研究了氟化物(1.0 - 25.0ppm)对人工龋样病变进展的影响。
发现0.19ppm及更高浓度的氟化物可在体外预防健康牙釉质脱矿。然而,需要显著更高浓度的氟化物(25.0ppm)来预防人工龋样病变的进一步脱矿。中等氟化物浓度(2.1 - 10.1ppm)的脱矿溶液在病变外层诱导再矿化,同时在病变内层诱导脱矿。在羟基磷灰石颗粒中也观察到了同时发生的再矿化和脱矿。
我们的结果表明,观察到的氟化物对牙釉质脱矿的影响不仅取决于总体溶液性质,还取决于牙釉质表面的龋病状态。所提出的机制模型表明,与健康牙釉质表面相比,在类似体内的条件下,需要更高浓度的氟化物来预防人工龋样病变的进展,因为促进再矿化的矿物质离子扩散是限速的。