A major reason for dental resin composite restoration replacement is related to secondary caries promoted by acid production from bacteria including Streptococcus mutans (S. mutans). We hypothesized that S. mutans has esterase activities that degrade dental resin composites and adhesives. Standardized specimens of resin composite (Z250), total-etch (Scotchbond Multipurpose, SB), and self-etch (Easybond, EB) adhesives were incubated with S. mutans UA159 or uninoculated culture medium (control) for up to 30 days. Quantification of the BisGMA-derived biodegradation by-product, bishydroxy-propoxy-phenyl-propane (BisHPPP), was performed by high-performance liquid chromatography. Surface analysis of the specimens was performed by scanning electron microscopy (SEM). S. mutans was shown to have esterase activities in levels comparable with those found in human saliva. A trend of increasing BisHPPP release throughout the incubation period was observed for all materials and was more elevated in the presence of bacteria vs. control medium for EB and Z250, but not for SB (p < .05). SEM confirmed the increased degradation of all materials with S. mutans UA159 vs. control. S. mutans has esterase activities at levels that degrade resin composites and adhesives; degree of degradation was dependent on the material's chemical formulation. This finding suggests that the resin-dentin interface could be compromised by oral bacteria that contribute to the progression of secondary caries.
Pseudocholinesterase (PCE) and cholesterol esterase (CE) can hydrolyze bisphenylglycidyl dimethacrylate (bisGMA) and triethylene glycol dimethacrylate (TEGDMA) monomers. This study will test the hypothesis that enzyme activities showing CE and PCE character are found in human saliva at levels sufficient to hydrolyze ester-containing composites important to restorative denstistry. The study also seeks to ask if the active sites of CE and PCE with respect to composite could be inhibited. Photo-polymerized model composite resin was incubated in PCE and CE solutions, in the presence and absence of a specific esterase inhibitor, phenylmethylsulfonyl fluoride (PMSF). Incubation solutions were analyzed for resin degradation products by high-performance liquid chromatography (HPLC), UV spectroscopy, and mass spectrometry. Saliva was found to contain both hydrolase activities at levels that could degrade composite resins. PMSF inhibited the composite degradation, indicating a material hydrolysis mechanism similar to the enzymes' common function.
Bis-GMA-containing resin composites and adhesives undergo biodegradation by human-saliva-derived esterases, yielding Bis-hydroxy-propoxy-phenylpropane (Bis-HPPP). The hypothesis of this study is that the exposure of dental restorations to salivalike esterase activities accelerates marginal bacterial microleakage. Resin composites (Scotchbond, Z250, 3M) bonded to human dentin were incubated in either buffer or dual-esterase media (pseudocholinesterase/cholesterol-esterase; PCE+CE), with activity levels simulating those of human saliva, for up to 90 days. Incubation solutions were analyzed for Bis-HPPP by high-performance liquid chromatography. Post-incubation, specimens were suspended in a chemostat-based biofilm fermentor cultivating Streptococcus mutans NG8, a primary species associated with dental caries, for 7 days. Bacterial microleakage was assessed by confocal laser scanning microscopy. Bis-HPPP production and depth and spatial volume of bacterial cell penetration within the interface increased with incubation time and were higher for 30-and 90-day PCE+CE vs. buffer-incubated groups, suggesting that biodegradation can contribute to the formation of recurrent decay.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.