The Role of Sucrose in Cariogenic Dental Biofilm Formation--New Insight

Faculty of Dentistry of Piracicaba, UNICAMP, Av. Limeira 901, CEP 13414-903 Piracicaba, São Paulo, Brazil.
Journal of Dental Research (Impact Factor: 4.14). 11/2006; 85(10):878-87. DOI: 10.1177/154405910608501002
Source: PubMed


Dental caries is a biofilm-dependent oral disease, and fermentable dietary carbohydrates are the key environmental factors involved in its initiation and development. However, among the carbohydrates, sucrose is considered the most cariogenic, because, in addition to being fermented by oral bacteria, it is a substrate for the synthesis of extracellular (EPS) and intracellular (IPS) polysaccharides. Therefore, while the low pH environment triggers the shift of the resident plaque microflora to a more cariogenic one, EPS promote changes in the composition of the biofilms' matrix. Furthermore, it has recently been shown that the biofilm formed in the presence of sucrose presents low concentrations of Ca, P(i), and F, which are critical ions involved in de- and remineralization of enamel and dentin in the oral environment. Thus, the aim of this review is to explore the broad role of sucrose in the cariogenicity of biofilms, and to present a new insight into its influence on the pathogenesis of dental caries.

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Available from: Adriana Franco Paes Leme, Oct 01, 2015
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    • "sucrose and are considered virulence factors (Paes Leme et al., 2006). Exopolysaccharide synthesis is catalyzed by a group of bacterial enzymes termed glycosyltransferases (GTF) and fructosyltransferases (FTF), encoded by the genes gtf and ftf, respectively, which under certain conditions can be strongly associated with cell surfaces and which apparently mediate glucan induced agglutination (Li and Burne, 2001). "
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    DESCRIPTION: Expression of adherence genes of Streptococcus mutans in the presence ofLactobacillus acidophilus and glucose
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    • "In this way, repeated conditions of low pH select a more cariogenic microflora (Marsh 1991, 1994), and the extracellular polysaccharides promote changes in the composition of the biofilm matrix (Ribeiro et al. 2005; Paes Leme et al. 2006). The biofilm formed in the presence of sucrose has low concentrations of Ca, Pi, and F, which are critical ions involved in the de-and remineralization of enamel and dentine (Paes Leme et al. 2006). Extracellular polysaccharides also promote bacterial adherence to tooth surfaces (Rölla 1989) and contribute to the structural integrity of dental biofilms while increasing the porosity of the biofilm formed, thereby allowing different sugars to diffuse into the deepest parts of the biofilm, resulting in low plaque pH values due to microbial catabolism (Zero et al. 1986). "
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    ABSTRACT: The importance of sugars as a cause of caries is underemphasized and not prominent in preventive strategies. This is despite overwhelming evidence of its unique role in causing a worldwide caries epidemic. Why this neglect? One reason is that researchers mistakenly consider caries to be a multifactorial disease; they also concentrate mainly on mitigating factors, particularly fluoride. However, this is to misunderstand that the only cause of caries is dietary sugars. These provide a substrate for cariogenic oral bacteria to flourish and to generate enamel-demineralizing acids. Modifying factors such as fluoride and dental hygiene would not be needed if we tackled the single cause-sugars. In this article, we demonstrate the sensitivity of cariogenesis to even very low sugars intakes. Quantitative analyses show a log-linear dose-response relationship between the sucrose or its monosaccharide intakes and the progressive lifelong development of caries. This results in a substantial dental health burden throughout life. Processed starches have cariogenic potential when accompanying sucrose, but human studies do not provide unequivocal data of their cariogenicity. The long-standing failure to identify the need for drastic national reductions in sugars intakes reflects scientific confusion partly induced by pressure from major industrial sugar interests. © International & American Associations for Dental Research 2015.
    Journal of dental research 08/2015; DOI:10.1177/0022034515590377 · 4.14 Impact Factor
    • "This bacterial pathogen can rapidly orchestrate the assembly of cariogenic biofilms when frequently exposed to sucrose. Sucrose is utilized by S. mutans–derived exoenzymes (e.g., glucosyltransferases ) to produce extracellular glucans, which enhance local accumulation of microbes and facilitate the buildup of cariogenic biofilms on the tooth surface (Paes Leme et al. 2006; Bowen and Koo 2011). However, S. mutans may not act alone in ECC, as other organisms contribute to caries pathogenesis (Takahashi and Nyvad 2011). "
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    ABSTRACT: Candida albicans cells are often detected with Streptococcus mutans in plaque biofilms from children affected with early childhood caries. The coadhesion between these 2 organisms appears to be largely mediated by the S. mutans-derived exoenzyme glucosyltransferase B (GtfB); GtfB readily binds to C. albicans cells in an active form, producing glucans locally that provide enhanced binding sites for S. mutans. However, knowledge is limited about the mechanisms by which the bacterial exoenzyme binds to and functions on the fungal surface to promote this unique cross-kingdom interaction. In this study, we use atomic force microscopy to understand the strength and binding dynamics modulating GtfB-C. albicans adhesive interactions in situ. Single-molecule force spectroscopy with GtfB-functionalized atomic force microscopy tips demonstrated that the enzyme binds with remarkable strength to the C. albicans cell surface (~2 nN) and showed a low dissociation rate, suggesting a highly stable bond. Strikingly, the binding strength of GtfB to the C. albicans surface was ~2.5-fold higher and the binding stability, ~20 times higher, as compared with the enzyme adhesion to S. mutans. Furthermore, adhesion force maps showed an intriguing pattern of GtfB binding. GtfB adhered heterogeneously on the surface of C. albicans, showing a higher frequency of adhesion failure but large sections of remarkably strong binding forces, suggesting the presence of GtfB binding domains unevenly distributed on the fungal surface. In contrast, GtfB bound uniformly across the S. mutans cell surface with less adhesion failure and a narrower range of binding forces (vs. the C. albicans surface). The data provide the first insights into the mechanisms underlying the adhesive and mechanical properties governing GtfB interactions with C. albicans. The strong and highly stable GtfB binding to C. albicans could explain, at least in part, why this bacterially derived exoenzyme effectively modulates this virulent cross-kingdom interaction. © International & American Associations for Dental Research 2015.
    Journal of dental research 07/2015; 94(9). DOI:10.1177/0022034515592859 · 4.14 Impact Factor
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