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      Changes in the salivary electrolytic dynamic after sucrose exposure in children with Early Childhood Caries

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          Abstract

          This study sought to explore if the effect of 20% sucrose rinse (SR) on the salivary electrolytic concentration of calcium (Ca 2+), phosphate (Pi) and fluoride (F ) in children with Early Childhood Caries (ECC) is different from healthy children. Here, fifty-eight  preschoolers aged 3 to 5 years were divided into 2 groups: caries-free (CF) and with ECC. Changes in saliva flow rate, pH and buffering capacity (BC), as well as in concentrations of Ca 2+, Pi, and F , and the degree of saturation in relation to hydroxyapatite (DSS HAp) and fluorapatite (DSS FAp) were evaluated. The pre-rinse [Ca 2+] was higher in the ECC group in the CF group. A significant increase in [Ca 2+] was demonstrated after SR in the CF group (p = 0.05). The [Pi] was reduced by 18% after SR in the ECC group (p = 0.007). The [F -] reduced in both groups after SR (p < 0.000). There was a moderate positive correlation between [Ca 2+] and the DSS HAp and DSS FAp. Multivariate analysis showed that children with a higher [Ca 2+] in pre-rinse saliva are more likely to have ECC. In conclusion, the effect of a 20% sucrose rinse on the electrolytic concentration of Ca 2+, Pi and F - was different when children with ECC were compared with CF children.

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          The exopolysaccharide matrix: a virulence determinant of cariogenic biofilm.

          Many infectious diseases in humans are caused or exacerbated by biofilms. Dental caries is a prime example of a biofilm-dependent disease, resulting from interactions of microorganisms, host factors, and diet (sugars), which modulate the dynamic formation of biofilms on tooth surfaces. All biofilms have a microbial-derived extracellular matrix as an essential constituent. The exopolysaccharides formed through interactions between sucrose- (and starch-) and Streptococcus mutans-derived exoenzymes present in the pellicle and on microbial surfaces (including non-mutans) provide binding sites for cariogenic and other organisms. The polymers formed in situ enmesh the microorganisms while forming a matrix facilitating the assembly of three-dimensional (3D) multicellular structures that encompass a series of microenvironments and are firmly attached to teeth. The metabolic activity of microbes embedded in this exopolysaccharide-rich and diffusion-limiting matrix leads to acidification of the milieu and, eventually, acid-dissolution of enamel. Here, we discuss recent advances concerning spatio-temporal development of the exopolysaccharide matrix and its essential role in the pathogenesis of dental caries. We focus on how the matrix serves as a 3D scaffold for biofilm assembly while creating spatial heterogeneities and low-pH microenvironments/niches. Further understanding on how the matrix modulates microbial activity and virulence expression could lead to new approaches to control cariogenic biofilms.
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            Oral Microbiome Metabolism: From "Who Are They?" to "What Are They Doing?".

            Recent advances in molecular biology have facilitated analyses of the oral microbiome ("Who are they?"); however, its functions (e.g., metabolic activities) are poorly understood ("What are they doing?"). This review aims to summarize our current understanding of the metabolism of the oral microbiome. Saccharolytic bacteria-including Streptococcus, Actinomyces, and Lactobacillus species-degrade carbohydrates into organic acids via the Embden-Meyerhof-Parnas pathway and several of its branch pathways, resulting in dental caries, while alkalization and acid neutralization via the arginine deiminase system, urease, and so on, counteract acidification. Proteolytic/amino acid-degrading bacteria, including Prevotella and Porphyromonas species, break down proteins and peptides into amino acids and degrade them further via specific pathways to produce short-chain fatty acids, ammonia, sulfur compounds, and indole/skatole, which act as virulent and modifying factors in periodontitis and oral malodor. Furthermore, it is suggested that ethanol-derived acetaldehyde can cause oral cancer, while nitrate-derived nitrite can aid caries prevention and systemic health. Microbial metabolic activity is influenced by the oral environment; however, it can also modify the oral environment, enhance the pathogenicity of bacteria, and induce microbial selection to create more pathogenic microbiome. Taking a metabolomic approach to analyzing the oral microbiome is crucial to improving our understanding of the functions of the oral microbiome.
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              Saliva and dental caries.

              Caries is a unique multifactorial infectious disease. Our understanding of etiological factors, the progress of the disease, and the effectiveness of prophylactic procedures have led us to believe that we understand the disease. However, we still have too few answers to many questions: "Why can we not predict who will get the disease?" "Why do we not become immunized?" "How much saliva is enough?" or "Which salivary components are protective?" and "Which salivary components predispose for caries?" It is generally accepted, however, that saliva secretion and salivary components secreted in saliva are important for dental health. The final result, "caries to be or not to be", is a complex phenomenon involving internal defense factors, such as saliva, tooth surface morphology, general health, and nutritional and hormonal status, and a number of external factors-for example, diet, the microbial flora colonizing the teeth, oral hygiene, and fluoride availability. In this article, our aim is to focus on the effects of saliva and salivary constituents on cariogenic bacteria and the subsequent development of dental caries.
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                Author and article information

                Contributors
                nobre@fop.unicamp.br
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                5 March 2020
                5 March 2020
                2020
                : 10
                : 4146
                Affiliations
                ISNI 0000 0001 0723 2494, GRID grid.411087.b, Department of Health Sciences and Pediatric Dentistry, Piracicaba Dental School, , University of Campinas-UNICAMP, ; Av. Limeira 901, Piracicaba, SP CEP 13414-903 Brazil
                Author information
                http://orcid.org/0000-0002-2120-3187
                Article
                61128
                10.1038/s41598-020-61128-6
                7057989
                32139791
                fa643c43-0e1d-4b95-b4f1-53cc22e7c40e
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 9 October 2019
                : 18 February 2020
                Funding
                Funded by: The work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) [Grant. No. 2017/17630-8] and Fundação de Desenvolvimento da Unicamp (FUNCAMP) [Grant. No. 45631-18].
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                © The Author(s) 2020

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                diagnostic markers,risk factors
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                diagnostic markers, risk factors

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