1 Oral Health Cooperative Research Centre, Melbourne Dental School, Bio21 Institute, University of Melbourne, Melbourne, Australia.
J Dent Res. 2019 Feb;98(2):218-224. doi: 10.1177/0022034518809088. Epub 2018 Nov 4.
Dental caries is associated with plaque dysbiosis, leading to an increase in the proportions of acidogenic and aciduric bacteria at the expense of alkali-generating commensal species. Stannous fluoride (SnF) slows the progression of caries by remineralization of early lesions but has also been suggested to inhibit glycolysis of aciduric bacteria. Casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) promotes fluoride remineralization by acting as a salivary biomimetic that releases bioavailable calcium and phosphate ions, and the peptide complex has also been suggested to modify plaque composition. We developed a polymicrobial biofilm model of caries using 6 bacterial species representative of supragingival plaque that were cultured on sound human enamel and pulsed with sucrose 4 times a day to produce a high cariogenic challenge. We used this model to explore the mechanisms of action of SnF and CPP-ACP. Bacterial species in the biofilms were enumerated with 16S rRNA gene sequence analyses, and mineral loss and lesion formation were determined in the enamel directly under the polymicrobial biofilms via transverse microradiography. The model tested the twice-daily addition of SnF, CPP-ACP, or both. SnF treatment reduced demineralization by 50% and had a slight effect on the composition of the polymicrobial biofilm. CPP-ACP treatment caused a similar inhibition of enamel demineralization (50%), a decrease in Actinomyces naeslundii and Lactobacillus casei abundance, and an increase in Streptococcus sanguinis and Fusobacterium nucleatum abundance in the polymicrobial biofilm. A combination of SnF and CPP-ACP resulted in a greater suppression of the acidogenic and aciduric bacteria and a significant 72% inhibition of enamel demineralization.
龋齿与牙菌斑失调有关,导致产酸和嗜酸菌的比例增加,而产生碱的共生种减少。氟化亚锡 (SnF) 通过早期病变的再矿化来减缓龋齿的进展,但也有人认为它可以抑制嗜酸菌的糖酵解。酪蛋白磷酸肽-无定形磷酸钙 (CPP-ACP) 通过作为一种唾液仿生物释放可利用的钙和磷酸盐离子来促进氟化物再矿化,并且该肽复合物也被认为可以改变菌斑组成。我们使用代表龈上菌斑的 6 种细菌开发了一种多微生物龋齿生物膜模型,这些细菌在健康的人牙釉质上培养,并每天脉冲 4 次蔗糖以产生高致龋挑战。我们使用该模型探索了 SnF 和 CPP-ACP 的作用机制。使用 16S rRNA 基因序列分析对生物膜中的细菌种类进行计数,并通过横向显微射线照相法直接在多微生物生物膜下的牙釉质中确定矿物质损失和病变形成。该模型测试了 SnF、CPP-ACP 或两者的每日两次添加。SnF 处理使脱矿化减少了 50%,并对多微生物生物膜的组成有轻微影响。CPP-ACP 处理导致牙釉质脱矿化(50%)相似的抑制,多微生物生物膜中放线菌和乳杆菌属的丰度降低,而链球菌和核梭杆菌的丰度增加。SnF 和 CPP-ACP 的组合导致产酸和嗜酸菌的抑制更为明显,牙釉质脱矿化抑制率高达 72%。