Abstract

The objectives were to: (1) determine the salivary concentrations of urea during 20 min chewing of a sugar–free gum containing 30 mg of urea; (2) measure the degree to which this urea would diffuse into a gel–stabilized plaque; (3) study the effect of the urea on the fall and subsequent rise in pH (Stephan curve) on exposure to 10% sucrose for 1 min; (4) model the measurements 2 and 3 mathematically. In point 1, the salivary urea concentration of the 12 subjects peaked at 47 mmol/l in the first 2 min of gum chewing, falling within 15 min to the unstimulated salivary concentration of 3.4 mmol/l. Recovery of urea from the saliva averaged 81.5%. ‘Plaques’ of 1% agarose or 67% dead bacteria in agarose accumulated urea from the saliva roughly as expected, whereas those plaques containing 8% live and 59% dead Streptococcus vestibularis showed negligible accumulation. Computer modelling showed this difference to be due to urease of live bacteria breaking down the urea as rapidly as it entered the plaque. Simulation of the effect of gum chewing subsequent to initiation of a Stephan curve in the latter type of plaque showed a rapid rise in pH but then a fall again on return to unstimulated conditions. This fall had not been seen in previous studies, with Streptococcus oralis, nor was it predicted by the computer modelling. Neither experimental simulation nor computer modelling suggested that chewing urea–containing gum before exposure to sucrose would have any effect on a subsequent Stephan curve. Thus chewing gum is only likely to inhibit caries when it is chewed after consumption of fermentable carbohydrate, rather than before.

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