Department of Preventive and Community Dentistry, Oral Health Research Institute, Indiana University School of Dentistry, Indianapolis, IN 46202, USA.
Caries Res. 2012;46(1):62-8. doi: 10.1159/000335573. Epub 2012 Jan 28.
The present mechanistic in vitro study aimed to investigate dose-response effects of zinc and fluoride on caries lesion remineralization and subsequent protection from demineralization. Artificial caries lesions were created using a methylcellulose acid gel system. Lesions were remineralized for 2 weeks using citrate-containing artificial saliva which was supplemented with zinc (0-153 μmol/l) and fluoride (1.1 or 52.6 μmol/l) in a 7 × 2 factorial design. Lesions were also remineralized in the absence of zinc and citrate, but in the presence of fluoride. After remineralization, all lesions were demineralized for 1 day under identical conditions. Changes in mineral distribution characteristics of caries lesions after remineralization and secondary demineralization were studied using transverse microradiography. At 1.1 μmol/l fluoride, zinc exhibited detrimental effects on remineralization in a dose-response manner and mainly by preventing remineralization near the lesion surface. At 52.6 μmol/l fluoride, zinc retarded remineralization only at the highest concentration tested. Zinc enhanced overall remineralization at 3.8-15.3 μmol/l. At 76.5 and less so at 153 μmol/l, zinc showed extensive remineralization of deeper parts within the lesions at the expense of remineralization near the surface. Citrate did not interfere with remineralization at 1.1 μmol/l fluoride, but enhanced remineralization at 52.6 μmol/l fluoride. Lesions exhibiting preferential remineralization in deeper parts showed higher mineral loss after secondary demineralization, suggesting the formation of more soluble mineral phases during remineralization. In summary, zinc and fluoride showed synergistic effects in enhancing lesion remineralization, however only at elevated fluoride concentrations.
本体外机制研究旨在探讨锌和氟化物对龋齿病变再矿化的剂量反应效应，以及随后对脱矿的保护作用。使用甲基纤维素酸凝胶系统创建人工龋齿病变。使用含有柠檬酸盐的人工唾液对病变进行 2 周的再矿化，该唾液补充有锌（0-153 μmol/l）和氟化物（1.1 或 52.6 μmol/l），采用 7×2 析因设计。在没有锌和柠檬酸盐但存在氟化物的情况下，病变也进行再矿化。再矿化后，所有病变在相同条件下进行 1 天的脱矿处理。使用横向显微 X 射线摄影术研究再矿化和二次脱矿后龋齿病变的矿物质分布特征变化。在 1.1 μmol/l 氟化物的情况下，锌以剂量反应的方式对再矿化产生有害影响，主要通过防止病变表面附近的再矿化。在 52.6 μmol/l 氟化物的情况下，锌仅在测试的最高浓度下延缓再矿化。锌在 3.8-15.3 μmol/l 时增强了整体再矿化。在 76.5 μmol/l 及以下，在 153 μmol/l 时，锌以牺牲表面附近的再矿化为代价，在病变的较深部位广泛再矿化。在 1.1 μmol/l 氟化物的情况下，柠檬酸盐不干扰再矿化，但在 52.6 μmol/l 氟化物时增强了再矿化。表现出在深部优先再矿化的病变在二次脱矿后表现出更高的矿物质损失，表明在再矿化过程中形成了更易溶解的矿物质相。总之，锌和氟化物在增强病变再矿化方面表现出协同作用，但仅在氟化物浓度升高时才如此。
