The pH of plaque and concentration of lactic and volatile acids present before and after exposure in vivo to sugar has been investigated. Plaque was weighed and the acids quantitatively extracted, volatiles were estimated by GLC and the lactate isomers enzymically. All samples contained acetate, propionate, n-butyrate, L(+) and D(––) lactate. Total acid (mostly volatile) in plaque after overnight fasting and 2.5 h after breakfast was similar (3.0 ×10––5 mmol/mg wet weight). 5 min after exposure to one sugar lump (= 40% w/w sucrose/saliva), at the pH minimum, the concentration was 5 × 10––5 mmol/mg wet weight, the major change being an 8-fold rise in L(+), a 5-fold rise in D(––) lactate and a halving of volatiles. Increased sugar exposure (five successive lumps) did not immediately produce more acid than one lump, but, after 30 min, more L(+) lactate was present from the increased sugar and the pH recovery was slower. Plaque before or 60 min after sugar had more total volatiles than lactate. The mean values for total and individual acids produced from glucose and sucrose did not differ significantly (p > 0.5). Although the volatiles are the dominant acid radicals around neutral pH the ‘Stephan curve’ is due to production of L(+) and to a lesser extent D(––) lactic acid.
Two independent cross-over studies investigated the possibility of enhanced early enamel lesion remineralization with the use of chewing gum. The first study involved a sorbitol-containing chewing gum, and the second, which had an identical protocol, tested a sucrose-containing chewing gum. In each study, 12 volunteers wore in situ appliances on which were mounted enamel sections containing artificial caries lesions. Subjects brushed twice daily for two min with a 1100-ppm-F (NaF) dentifrice (control and test) and in the test phase chewed five sticks of gum per day for 20 min after meals and snacks. Microradiographs of the enamel lesions were made at baseline and at the end of the seven-week experimental period. In the sugar-free gum study, the weighted mean total mineral loss (delta z) difference [(wk7-wk0) x (-1)] was 788 vol.% min. x micron for the gum, corresponding to remineralization of 18.2%, vs. the control value of 526 vol.% min. x micron, 12.1% remineralization (p = 0.07). There were no significant differences for the surface-zone (p = 0.20) and lesion-body (p = 0.28) values. In the sucrose-containing gum study, the delta z difference was 743 vol.% min. x micron for the gum, corresponding to a remineralization of 18.3%, vs. the control value of 438 vol.% min. x micron, 10.8% remineralization (p = 0.08). The surface-zone values were not significantly different (p = 0.55). For the lesion body, however, the sucrose-containing gum value of 6.11 vol.% min. was significantly different (p = 0.01) from that of the control (2.81 vol.% min.).
Recent evidence of the actions of chewing gum on plaque pH needs to be assessed against the background of other evidence, including clinical data. 'Sugar-free' gums are non-cariogenic and potentially beneficial in reversing early caries, while the potential cariogenicity of sucrose-sweetened gums can be modified by additives or selected patterns of use.
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