Cariogenicity of Streptococcus mutans Strains with Defects in Fructan Metabolism Assessed in a Program-fed Specific-pathogen-free Rat Model

Abstract

To define the role of dental plaque fructans and the enzymes involved in their metabolism in the initiation and progression of dental caries, we constructed otherwise-isogenic mutants of Streptococcus mutans defective in the ability to synthesize fructans, to degrade fructans, or to do both. The cariogenic potential of these organisms was evaluated in a specific-pathogen-free rat model in which the feeding patterns of the animals were controlled by means of a König-Hofer programed feeder. Specifically, rats were infected with wild-type S. mutans UA159 or derivatives of this strain which contained an insertionally-inactivated fructanase (fruA) gene, fructosyltransferase (ftf) gene, or which had both genes inactivated. The animals were fed 17 meals per day of Diet 2000 containing 56% sucrose at 70-minute intervals for five weeks, and caries experience was evaluated. Animals infected with S. mutans with a mutated fruA gene only had statistically significant decreases in sulcal caries severity. Such a decrease was not observed in previous studies with ad libitum-fed animals (Wexler et al., 1992). The manifestation of diminished virulence in the programmed feeding model, but not in ad libitum-fed animals, supports the concept that the primary contribution of FruA to virulence is through the utilization of fructans storage polysaccharides. Animals infected with strains carrying the ftf mutation or simultaneous mutations in ftf and fruA did not display decreased virulence, perhaps indicating that sucrose utilization pathways may compete for substrate in vivo, or that accumulation of fructans may affect the ecology or the physicochemical characteristics of dental plaque in such a way as to reduce its cariogenic potential. The results of this study also emphasize that the contribution of a particular virulence determinant to the caries process may be highly dependent on the experimental design, feeding regimen and diet, and the presence or absence of other enzymatic activities.

The Streptococcus mutans vicX Gene Product Modulates gtfB / C Expression, Biofilm Formation, Genetic Competence, and Oxidative Stress Tolerance

“…The water-insoluble glucans produced by the gtfB/C-encoded enzymes are critical for sucrose-dependent colonization of smooth surfaces by the mutans streptococci (12,20). In fact, rats infected with S. mutans strains deficient in either of these genes had significantly reduced levels of dental caries (4,21,32,40), which emphasized the conclusion that the glucosyltransferases have an important role in caries etiology.…”

Inhibitory Effects of MoAbs against a Surface Protein Antigen in Real‐Time Adherence In vitro and Recolonization In vivo of Streptococcus mutans

“…Firstly, we performed a study in order to establish an experimental system of the adherence of S. mutans to rat teeth. Previous infection studies of S. mutans in the rat oral cavity have been performed using Diet 2000, which contains 50% or more sugar [33,34]. However, by this method, S. mutans produces a larger amount of insoluble glucan than it does in the human oral cavity.…”

Streptococcus mutans: a new Gram-positive paradigm?

“…In this regard, there are well-established in vivo models for S. mutans, including rat (Burne et al, 1996;Koo et al, 2005;Yamashita et al, 1993) and transgenic mouse caries models (Burne et al, 1996;Catalán et al, 2011;Culp et al, 2005;Yamashita et al, 1993), as well as rabbit and mouse models of infective endocarditis (Bahn et al, 1978;Paik et al, 2003). In fact, it was the pioneering work conducted in the 1950s and 60s using hamsters and gnotobiotic rats that established S. mutans as the principal aetiological agent of dental caries (Fitzgerald & Keyes, 1960;Orland et al, 1955;Zinner et al, 1965).…”