Roncari Rocha Guilherme, Sims Kenneth R, Xiao Baixue, Klein Marlise I, Benoit Danielle S W
Department of Dental Materials and Prosthodontics, São Paulo State University, São Paulo, Brazil.
Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
J Oral Microbiol. 2021 Nov 25;14(1):1997230. doi: 10.1080/20002297.2021.1997230. eCollection 2022.
Dental caries is a multifactorial disease caused by pathogenic biofilm. In particular, synthesizes biofilm exopolysaccharides, while is associated with the development of severe carious lesions.
This study aimed to prevent the formation of and biofilms by exploiting pH-sensitive nanoparticle carriers (NPCs) with high affinity to exopolysaccharides to increase the substantivity of multi-targeted antibiofilm drugs introduced topically .
Dual-species biofilms were grown on saliva-coated hydroxyapatite discs with sucrose. Twice-daily, 1.5 min topical treatment regimens of unloaded and drug-loaded NPC were used. Drugs included combinations of two or three compounds with distinct, complementary antibiofilm targets: -farnesol (terpenoid; bacterial acid tolerance, fungal quorum sensing), myricetin (flavonoid; exopolysaccharides inhibitor), and 1771 (lipoteichoic acid inhibitor; bacterial adhesion and co-aggregation). Biofilms were evaluated for biomass, microbial population, and architecture.
NPC delivering -farnesol and 1771 with or without myricetin completely prevented biofilm formation by impeding biomass accumulation, bacterial and fungal population growth, and exopolysaccharide matrix deposition (. control unloaded NPC). Both formulations hindered acid production, maintaining the pH of spent media above the threshold for enamel demineralization. However, treatments had no effect on pre-established dual-species biofilms.
Complementary antibiofilm drug-NPC treatments prevented biofilm formation by targeting critical virulence factors of acidogenicity and exopolysaccharides synthesis.
龋齿是一种由致病性生物膜引起的多因素疾病。特别是，[具体细菌名称1]合成生物膜胞外多糖，而[具体细菌名称2]与严重龋损的发展有关。
本研究旨在通过利用对胞外多糖具有高亲和力的pH敏感纳米颗粒载体（NPCs）来防止[具体细菌名称1]和[具体细菌名称2]生物膜的形成，以增加局部引入的多靶点抗生物膜药物的黏附性。
在涂有唾液的羟基磷灰石圆盘上用蔗糖培养双物种生物膜。采用每日两次、每次1.5分钟的空载和载药NPC局部治疗方案。药物包括两种或三种具有不同互补抗生物膜靶点的化合物组合：β-法尼醇（萜类化合物；细菌耐酸性、真菌群体感应）、杨梅素（黄酮类化合物；胞外多糖抑制剂）和1771（脂磷壁酸抑制剂；细菌黏附和共聚）。对生物膜的生物量、微生物群落和结构进行评估。
递送β-法尼醇和1771（有无杨梅素）的NPC通过阻碍生物量积累、细菌和真菌群体生长以及胞外多糖基质沉积，完全防止了生物膜形成（与空载NPC对照相比）。两种制剂均阻碍了酸的产生，使用过的培养基的pH值维持在釉质脱矿阈值以上。然而，这些处理对预先形成的双物种生物膜没有影响。
互补的抗生物膜药物-NPC治疗通过靶向产酸和胞外多糖合成的关键毒力因子来防止生物膜形成。
