Abstract
The deterioration of human oral microbiota is known to not only cause oral diseases but also to affect systemic health. Various environmental factors are thought to influence the disruption and restoration of the oral ecosystem. In this study, we focused on the effect of nitric oxide (NO) produced by denitrification and NO synthase enzymes on dental plaque microbiota. Interdental plaques collected from 10 subjects were exposed to NO donor sodium nitroprusside (SNP) and then cultured in a specialized growth medium. Depending on the concentration of exposed SNP, a decrease in α-diversity and a continuous change in β-diversity in the dental plaque community were shown by sequencing bacterial 16S rRNA genes. We also identified eight operational taxonomic units that were significantly altered by NO exposure. Among them, the exposure of NO donors to Fusobacterium nucleatum cells showed a decrease in survival rate consistent with the results of microbiota analysis. Meanwhile, in addition to NO tolerance, an increase in the tetrazolium salt-reducing activity of Campylobacter concisus cells was confirmed by exposure to SNP. This study provides an overview of how oral plaque microbiota shifts with exposure to NO and may contribute to the development of a method for adjusting the balance of the oral microbiome.
Highlights
The human oral microbiota consists of more than 700 species of bacteria, with more than 100 species present in each individual [1,2,3]
We investigated the effect of nitric oxide (NO), which is known to occur in the oral cavity and is one of the environmental factors that may shift the oral microbiota, on dental plaque using a simple system for in vitro culture
This study showed that dental plaque is composed of bacterial groups differing in NO sensitivity, and that the microbiota structure may change depending on NO concentration
Summary
The human oral microbiota consists of more than 700 species of bacteria, with more than 100 species present in each individual [1,2,3]. Excessive plaque accumulation is known to increase the risk of periodontal disease through changes to the microbiota that are dominated by anaerobic species that can cause inflammation [7,11,12]. Due to the complexity of the microbial community and various environmental factors affecting the microbiota, it is very difficult to identify the individual species responsible for the observed physiological and pathological changes. For this reason, the mechanisms that disrupt the microbiota caused by various stressors and the nature of the oral ecosystem that leads to recovery from the disorder remain poorly understood
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