Resin-Composite Biodegradation By-products Modulate Streptococcus mutans Growth and Gene Expression

One of the major reasons for resin composite restoration failure is related to secondary caries. Streptococcus mutans is a primary species associated with the initiation and progression of caries. Breakdown of the resin-dentin interface results in the generation of biodegradation by-products (BBPs) such as methacrylic acid (MA) and triethyleneglycol (TEG). It was previously demonstrated that BBPs affect the metabolism and gene expression of S. mutans.

Objectives: To further assess the effects of resin composite BBPs, MA and TEG, on 1) S. mutans growth and 2) expression of virulence genes directly involved in pathogenesis of this bacterium.

Methods: Bacterial growth was assessed by optical density changes following the incubation of S. mutans with a range of concentrations of  MA and TEG corresponding with in vivo conditions, (0, 0.5, 1, 5 and 10 mM), at normal (pH=7.0) or pathogenic (pH=5.5) conditions. Gene expression was measured by quantitative real-time polymerase chain reaction (qRT-PCR) for both planktonic and biofilm cultures of S. mutans UA159 in the presence of different concentrations of TEG (0.00, 0.001, 0.01 and 0.1mM) at pH 5.5.

Results: MA inhibited S. mutans growth in a dose dependent manner at both pathogenic and physiological pH, whereas TEG stimulated the bacterial growth in the concentration range of 1-10 mM at pH 5.5, which is the optimum pH for development of dental caries. qRT-PCR results identified the up-regulation of seven virulence genes including Glucosyltransferases B and C, Glucan binding protein-B, ComCDE and F1-F0-ATPase in the presence of 0.01 and 0.1 mM concentration of TEG at pH 5.5.The changes were more pronounced in biofilm growth condition compared with planktonic cells.

Conclusions: Biodegradation by-products of resin composite modulate S. mutans growth and can up-regulate the expression of several virulence genes in a concentration- and pH-dependent manner. These processes may contribute to the progression of secondary caries.