A MATHEMATICAL-MODEL OF THE INFLUENCE OF SALIVARY UREA ON THE PH OF FASTED DENTAL PLAQUE AND ON THE CHANGES OCCURRING DURING A CARIOGENIC CHALLENGE

Urea diffusing from saliva into dental plaque is converted to ammonia and carbon dioxide by bacterial ureases, The influence of normal saliv ary urea levels on the pH of fasted plaque and on the depth and durati on of a Stephan curve is uncertain, A numerical model which simulates a cariogenic challenge (a 10% sucrose rinse alone or one followed by u se of chewing-gum with or without sugar) was modified to include saliv ary urea levels hom 0 to 30 mmol/l, It incorporated: site-dependent ex change between bulk saliva and plaque surfaces via a salivary film sug ar and urea diffusion into plaque, pf-l-dependent rates of acid format ion and urea breakdown: diffusion and dissociation of end-products and other buffers (acetate: lactate, phosphate, ammonia and carbonate); d iffusion of protons and other ions; equilibration with fixed and mobil e buffers, and charge-coupling between ionic flows. The K-m (2.12 mmol /l) and V-max (0.11 mu mol urea/ min/mg dry weight) values for urease activity and the pH dependence of V-max were taken from the literature , From the results, it is predicted that urea concentrations normally present in saliva (3-5 mmol/l) will increase the pH at the base of a 0 .5-mm-thick fasted plaque by up to 1 pH unit, and raise the pH minimum after a sucrose rinse or sugar-containing chewing-gum by at least hal f pH unit, The results suggest that plaque cariogenicity may be invers ely related to salivary urea concentrations, not only when the latter are elevated because of disease, but even when they are in the normal range.