Journal
JOURNAL OF ORAL MICROBIOLOGY
Volume 14, Issue 1, Pages -Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/20002297.2021.1997230
Keywords
Biofilm; treatment; dental caries; Streptococcus mutans; Candida albicans
Categories
Funding
- National Institutes of Health [R01 DE018023, F31 DE026944]
- National Science Foundation [DMR 1206219, DMR 2103553]
- Sao Paulo Research Foundation (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo - FAPESP) [2018/01429-4, 2019/22316-6]
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This study aimed to prevent the formation of dental caries by using pH-sensitive nanoparticle carriers (NPCs) to target critical virulence factors. The results showed that the NPC delivering specific drugs could completely prevent biofilm formation and hinder acid production, maintaining the pH above the threshold for enamel demineralization.
Background Dental caries is a multifactorial disease caused by pathogenic biofilm. In particular, Streptococcus mutans synthesizes biofilm exopolysaccharides, while Candida albicans is associated with the development of severe carious lesions. Aim This study aimed to prevent the formation of S. mutans and C. albicans biofilms by exploiting pH-sensitive nanoparticle carriers (NPCs) with high affinity to exopolysaccharides to increase the substantivity of multi-targeted antibiofilm drugs introduced topically in vitro. Methods 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: tt-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. Results NPC delivering tt-farnesol and 1771 with or without myricetin completely prevented biofilm formation by impeding biomass accumulation, bacterial and fungal population growth, and exopolysaccharide matrix deposition (vs. 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. Conclusion Complementary antibiofilm drug-NPC treatments prevented biofilm formation by targeting critical virulence factors of acidogenicity and exopolysaccharides synthesis.
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