Abstract

Streptococcus mutans, a major pathogen of dental caries, is also known as a causative agent of cardiovascular disease. A 120 kDa collagen-binding protein (Cnm) of S. mutans is an important contributor to the pathogenicity of cardiovascular disease. Although dead bacteria have been detected in cardiovascular specimens by molecular biological methods, the pathogenicity of the bacteria remains unknown. Here, we analyzed the pathogenicity of killed S. mutans by focusing on collagen-binding ability and the effects on silkworms. In live S. mutans, Cnm-positive S. mutans had high collagen-binding activity, while Cnm-negative S. mutans had no such activity. After treatment with killed Cnm-positive S. mutans, amoxicillin-treated bacteria still had collagen-binding ability, while lysozyme-treated bacteria lost this ability. When live and amoxicillin-treated S. mutans strains were administered to silkworms, the survival rates of the silkworms were reduced; this reduction was more pronounced in Cnm-positive S. mutans infection than in Cnm-negative S. mutans infection. However, the administration of any of the lysozyme-treated bacteria did not reduce the survival rate of the silkworms. These results suggest that amoxicillin-killed Cnm-positive S. mutans strains maintain collagen-binding properties and pathogenicity in the silkworm model, and are possibly associated with pathogenicity in cardiovascular diseases.

Highlights

  • The oral cavity contains live bacteria, and bacteria that have been killed by the administration of antibiotics or by antimicrobial substances in ­saliva[1,2]

  • Scanning electron microscopy (SEM) images showed slight damage in the cell surface layer of S. mutans treated with amoxicillin (Fig. 1A), and transmission electron microscopy (TEM) images showed abnormal changes in the cytoplasm of the bacteria (Fig. 1B)

  • S. mutans is involved in the development of cardiovascular diseases such as infective endocarditis (IE) and intracerebral hemorrhage, when they infiltrate into the bloodstream from the oral c­ avity[8,17]

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Summary

Introduction

The oral cavity contains live bacteria, and bacteria that have been killed by the administration of antibiotics or by antimicrobial substances in ­saliva[1,2]. Live and dead bacteria present in the oral cavity can infiltrate the bloodstream when bleeding occurs following invasive dental treatment or daily tooth b­ rushing[1] Such bacterial invasion into the blood can induce cardiovascular diseases such as infective endocarditis (IE) or arteriosclerosis when bacterial adhesion occurs because of bacterial infections on the vascular walls, especially under abnormal ­conditions[3,4]. Previous studies reported that bacterial DNA of S. mutans was frequently detected in extirpated heart valve specimens from patients with IE using molecular biological methods, even when no live S. mutans was isolated from the patients by the blood culture m­ ethod[14]. Genes encoding collagen-binding proteins were frequently detected in these S. mutans-positive heart valve s­ pecimens[15] These results led us to hypothesize that dead S. mutans may be a possible virulence factor for cardiovascular diseases. Used for the prevention of IE, and lysozyme, an antimicrobial substance in saliva and serum, using a collagenbinding assay and a silkworm model

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