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Tea catechin epigallocatechin gallate inhibits Streptococcus mutans biofilm formation by suppressing gtf genes

Department of Pediatric Dentistry, College of Dentistry, University of Illinois at Chicago, Chicago, IL 60612, USA.
Archives of oral biology (Impact Factor: 1.88). 12/2011; 57(6):678-83. DOI: 10.1016/j.archoralbio.2011.10.021
Source: PubMed

ABSTRACT The anti-cariogenic properties of tea have been suggested for decades. Tea polyphenols, especially epigallocatechin gallate (EGCG), have been shown to inhibit dental plaque accumulation, but the exact mechanisms are not clear at present. We hypothesise that EGCG suppresses gtf genes in Streptococcus mutans at the transcriptional level disrupting the initial attachment of S. mutans and thus the formation of mature biofilms.
In this study, the effect of EGCG on the sucrose-dependent initial attachment of S. mutans UA159 in a chemically defined medium was monitored over 4 h using a chamber slide model. The effects of EGCG on the aggregation and gtf B, C, D gene expression of S. mutans UA159 were also examined.
It was found that EGCG (7.8-31.25 μg/ml) exhibited dose-dependent inhibition of the initial attachment of S. mutans UA159. EGCG did not induce cellular aggregation of S. mutans UA159 at concentrations less than 78.125 μg/ml. Analysis of data obtained from real-time PCR showed that EGCG at sub-MIC level (15.6 μg/ml) significantly suppressed the gtf B, C, D genes of S. mutans UA159 compared with the non-treated control (p < 0.05).
These findings suggest that EGCG may represent a novel, natural anti-plaque agent that inhibits the specific genes associated with bacterial biofilm formation without necessarily affecting the growth of oral bacteria.

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Available from: Xin Xu, Aug 08, 2015
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    • "gtfBgtfCgtfD pH [13] gtfBgtfC pH [14] Koo [15] gtfBgtfC gtfDgtfBgtfC gtfBgtfC gtfD gtfBgtfC [] [1] Cummins D. Dentin hypersensitivity: from diagnosis to a breakthrough therapy for everyday sensitivity relief[J]. J "
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    • "Interestingly, a study by Xu, et al.34 (2011) demonstrated that EGCg inhibited biofilm formation of S. mutans which could be attributed to the interactions of EGCg with glucosyltransferase enzymes, thus disrupting the formation and integrity of the oral biofilm. More recently, Xu, et al.35 (2012) also demonstrated that EGCg suppresses the gtfB, gtfC, gtfD genes associated with extracellular polysaccharide formation of S. mutans. The potential anticariogenic activity of EGCg in clinical service clearly requires more research, since EGCg has been shown to interact with salivary proteins. "
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