Division of Oral Microbiology and Immunology, Clinic of Preventive Dentistry, Periodontology and Cariology, Center of Dental Medicine, University of Zürich, Zürich, Switzerland.
Division of Oral Diseases, Department of Dental Medicine, Karolinska Institutet, Stockholm, Sweden.
Arch Oral Biol. 2018 May;89:77-83. doi: 10.1016/j.archoralbio.2018.02.010. Epub 2018 Feb 20.
Fluoride is widely used as an anti-caries agent, e.g. in toothpastes and mouth rinses. However, the nature of the anti-caries action is not entirely clear. Mechanisms suspected to explain the cariostatic effect include inhibitory effects on acid formation by bacteria, inhibition of extracellular polysaccharide (EPS) production, inhibition of enamel demineralization and enhancement of remineralizaton or combination thereof. The aim of this study was to examine with the supragingival Zurich in vitro biofilm model the effect of fluoride in NaF formulation, on the microbiota and on demineralization.
Biofilms consisting of Actinomyces oris, Candida albicans, Fusobacterium nucleatum, Streptococcus oralis, Veillonella dispar and Streptococcus sobrinus, were grown anaerobically on sintered hydroxyapatite or bovine enamel disks, exposed to 200, 400, and 1400 ppm of NaF, or 0.1% chlorhexidine (positive control). The biofilms were harvested after 64 h and CFUs were assessed for total bacteria. Demineralization of enamel disks was measured by quantitative light-induced fluorescence.
NaF did not affect the bacterial numbers. No enamel mineral loss was observed at 1400 and 400 ppm of fluoride, whereas the pH of the surrounding medium was increased to 5.5 and 5.0, respectively, compared to the untreated control (pH 4.5 and mineral loss ΔF of -32%). At 1400 ppm NaF the biofilm's EPS volume was also significantly reduced.
Administration of NaF completely prevented demineralization without affecting biofilm composition and growth. This protective effect may be attributed to the observed decrease in acid production or EPS volume, or to a shift in the de/remineralization balance.
氟化物被广泛用作抗龋剂,例如在牙膏和漱口水中。然而,抗龋作用的性质尚不完全清楚。被认为可以解释其抗龋作用的机制包括抑制细菌产酸、抑制细胞外多糖(EPS)的产生、抑制牙釉质脱矿以及增强再矿化或其组合。本研究的目的是使用龈上苏黎世体外生物膜模型,研究 NaF 配方中的氟化物对微生物群和脱矿的影响。
在烧结羟基磷灰石或牛牙釉质盘上,厌氧培养包含黏性放线菌、白色念珠菌、核梭杆菌、口腔链球菌、变异韦荣球菌和变形链球菌的生物膜,然后将其暴露于 200、400 和 1400ppm 的 NaF 或 0.1%洗必泰(阳性对照)。64 小时后收获生物膜,评估总细菌的 CFU。通过定量光诱导荧光法测量牙釉质盘的脱矿情况。
氟化物对细菌数量没有影响。在 1400 和 400ppm 的氟化物条件下,没有观察到牙釉质的矿物质损失,而周围介质的 pH 值分别升高到 5.5 和 5.0,与未处理的对照组(pH 4.5 和矿物质损失ΔF 为-32%)相比。在 1400ppm 的 NaF 条件下,生物膜的 EPS 体积也显著减少。
给予 NaF 完全可以预防脱矿,而不会影响生物膜的组成和生长。这种保护作用可能归因于观察到的酸产量或 EPS 体积减少,或者脱矿/再矿化平衡的变化。