Dimethacrylate Monomers and Photoinitiators Alter Streptococcus mutans Biofilms

Objectives:   Monomers and photoinitiators can elute from dimethacrylate-based dental materials, but their effects on oral bacteria, including pathogenic strains, are not known.  Our objective was to determine effects of common monomers and photoinitiators on metabolic activity and overall biomass of acidogenic Streptococcus mutans (S. mutans) biofilms. 

Methods: S. mutans biofilms were formed in 25 % THYE (Todd Hewitt Broth + 5 mg/mL yeast extract) with 30 mmol/L sucrose and varying concentrations of bisphenol A glycerolate dimethacrylate (BisGMA), triethyleneglycol dimethacrylate (TEGDMA), camphorquinone (CQ), or ethyl 4-N,N-dimethylaminobenzoate (4E).  Controls were grown without additives.  At 4 h and 24 h, biofilms were evaluated for metabolic activity (MTT assay-3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), overall biomass (crystal violet), and growth medium pH.  Three experiments (each with n=4) were performed. Viability analysis was performed on select samples using laser scanning confocal microscopy.  One-way analysis of variance was applied with Tukey-Kramer multiple comparisons (P<0.05 indicates significance). 

Results: TEGDMA (500 µg/mL) significantly reduced metabolic activity but not biomass at 24 h.  BisGMA (50 µg/mL) significantly reduced biofilm metabolic activity and biomass at 24 h.  CQ (100 µg/mL) had the opposite effect, with significantly reduced metabolic activity and biomass at 4 h followed by significantly higher metabolic activity at 24 h, suggesting a delay in biofilm growth. 4E (up to 10 µg/mL) had no detectable effect.  Viability staining at 24 h supported these results, with an increase in membrane-compromised cells with 50 µg/mL BisGMA and an increase in live cells for 100 µg/mL CQ.     

Conclusions: Monomers and photoinitiators that can leach from dental polymeric materials can alter oral biofilm growth.  These material-directed changes in biofilm activity may play an important role in the formation of pathogenic oral biofilms and the development of recurrent caries.

Acknowledgements: Interagency Agreement between the National Institute of Dental and Craniofacial Research and NIST [Y1-DE-7005-01].