Abstract
Modification of oral biofilms adhering to dental hard tissues could lead to new treatment approaches in cariology and periodontology. In this study the impact of DNase I and/or proteinase K on the formation of a simulated supragingival biofilm was investigated in vitro. Six-species biofilms were grown anaerobically in the presence of DNase I and proteinase K. After 64 h biofilms were either harvested and quantified by culture analysis or proceeded to staining followed by confocal laser scanning microscopy. Microbial cells were stained using DNA-dyes or fluorescent in situ hybridization. Exopolysaccharides, eDNA and exoproteins were stained with Calcofluor, anti-DNA-antibody, and SyproTM Ruby, respectively. Overall, results showed that neither DNase I nor proteinase K had an impact on total colony-forming units (CFUs) compared to the control without enzymes. However, DNase I significantly suppressed the growth of Actinomyces oris, Fusobacterium nucleatum, Streptococcus mutans, Streptococcus oralis and Candida albicans. Proteinase K treatment induced significant increase in S. mutans and S. oralis CFUs (p < 0.001), whereas C. albicans and V. dispar showed lower CFUs compared to the control. Interestingly, confocal images visualized the biofilm degradation caused by DNase I and proteinase K. Thus, enzymatic treatment should be combined with conventional antimicrobial agents aiming at both bactericidal effectiveness and biofilm dispersal.
Highlights
Oral infectious diseases display the consequences of dynamic interactions between microorganisms, their host and the host’s diet, leading to microbial colonization of oral surfaces and the establishment of pathogenic biofilms [1]
The log10 counts of five individual microbial species decreased significantly in a dose-independent manner after DNase I treatment
A. oris exhibited means of 6.45 ± 0.27 colony-forming units (CFUs) (0.001 mg/mL DNase I, p = 0.002) and 6.58 ± 0.26 CFU (0.002 mg/mL DNase I, p = 0.026) in the log10 scale, which is a slightly, yet significantly reduced microbial growth compared with the untreated negative control
Summary
Oral infectious diseases display the consequences of dynamic interactions between microorganisms, their host and the host’s diet, leading to microbial colonization of oral surfaces and the establishment of pathogenic biofilms [1]. Biofilms formed on either tooth or dental material surfaces are known as oral biofilms and have been clearly recognized as a virulence factor in several oral infectious diseases, including dental caries, periodontitis and endodontic infections [2]. Biofilms are defined as “aggregates of micro-organisms in which the associated cells are frequently embedded in a self-produced matrix of extracellular polymeric substances (EPS) that are adherent to each other and/or a surface [3]. The composition and structure of EPS varies according to the host, presence of nutrients/substrates, type of microorganisms, and local mechanical factors e.g., shear stress [4]. The EPS promotes microbial adhesion on biotic and abiotic surfaces
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