Literature DB >> 32312765

Contribution of Severe Dental Caries Induced by Streptococcus mutans to the Pathogenicity of Infective Endocarditis.

Ryota Nomura1, Saaya Matayoshi2, Masatoshi Otsugu2, Takahiro Kitamura2, Noboru Teramoto3, Kazuhiko Nakano2.   

Abstract

Streptococcus mutans, a major pathogen of dental caries, is regarded as a causative agent of infective endocarditis (IE), which mainly occurs in patients with underlying heart disease. However, it remains unknown whether severe dental caries that extend to pulp space represent a possible route of infection. In the present study, we evaluated the virulence of S. mutans for IE development using rats with concurrent severe dental caries and heart valve injury. Dental caries was induced in rats through the combination of a caries-inducing diet and the administration of S. mutans into the oral cavity. Then, the heart valves of a subset of rats were injured using a sterile catheter and wire under general anesthesia. The rats were euthanized at various times with various stages of dental caries. The number of teeth affected by dental caries with pulp exposure was increased in the rats in a time-dependent manner. S. mutans was recovered from injured heart tissue, which was mainly observed in rats with higher number of S. mutans bacteria in mandibular bone and a larger number of teeth in which caries extended to pulp. Dental caries was more severe in rats with heart injury than in rats without heart injury. Sequencing analysis targeting 16S rRNA revealed that specific oral bacteria appeared only in rats with heart injury, which may be related to the development of dental caries. Our findings suggest that dental caries caused by the combination of S. mutans infection and sucrose intake may contribute to S. mutans colonization in injured heart tissue.
Copyright © 2020 American Society for Microbiology.

Entities:  

Keywords:  Streptococcus mutans; dental caries; dental pulp; heart valve; infective endocarditis; rat model

Year:  2020        PMID: 32312765      PMCID: PMC7309618          DOI: 10.1128/IAI.00897-19

Source DB:  PubMed          Journal:  Infect Immun        ISSN: 0019-9567            Impact factor:   3.441


  42 in total

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