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

Abstract

Urea diffusing from saliva into dental plaque is converted to ammonia and carbon dioxide by bacterial ureases. The influence of normal salivary urea levels on the pH of fasted plaque and on the depth and duration of a Stephan curve is uncertain. A numerical model which simulates a cariogenic challenge (a 10% sucrose rinse alone or one followed by use of chewing-gum with or without sugar) was modified to include salivary urea levels from 0 to 30 mmol/l. It incorporated: site-dependent exchange between bulk saliva and plaque surfaces via a salivary film; sugar and urea diffusion into plaque; pH-dependent rates of acid formation and urea breakdown; diffusion and dissociation of end-products and other buffers (acetate, lactate, phosphate, ammonia and carbonate); diffusion of protons and other ions; equilibration with fixed and mobile buffers; and charge-coupling between ionic flows. The K_m (2.12 mmol/l) and V_max (0.11 μmol 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 half a pH unit. The results suggest that plaque cariogenicity may be inversely related to salivary urea concentrations, not only when the latter are elevated because of disease, but even when they are in the normal range.

Effect of L-arginine dietary supplementation on salivary urea concentration and pH in physically active individuals

“…Other studies showed that salivary urea rapidly enters dental plaque where its hydrolysis causes a significant pH rise 23,24 and that the pH change positively correlates with the concentration of urea. 12,14,15,25,26 In addition, urea serves oral bacteria not only to regulate intra-and extracellular pH but also as a source of nitrogen for the synthesis of different compounds. 27 This could also determine the impact of ureolysis on both dental plaque pH and salivary pH.…”

Salivary Concentrations of Urea Released from a Chewing Gum Containing Urea and how These Affect the Urea Content of Gel–Stabilized Plaques and Their pH after Exposure to Sucrose

“…Initially, with the aim of simulating the bench top studies, these measurements were made, as in Dibdin et al [1995] and Dibdin and Dawes [1998], in a simple phosphate buffer instead of the richer peptone-containing medium used in most other studies (e.g. Dibdin [1990Dibdin [ , 1992).…”

“…A computer model of the effect of these concentrations of salivary urea on plaque pH suggested that the normal levels of urea in saliva are sufficient to increase significantly the resting plaque pH and reduce the depth and duration of a Stephan curve after exposure to fermentable carbohydrate [Dibdin and Dawes, 1998]. Stephan [1940Stephan [ , 1943, Frostell [1960] and Kleinberg [1967] have shown that exposure of plaque to additional urea causes an increase in plaque pH.…”

“…The objectives of the present study were to: (1) determine the change in salivary urea concentration with time during the chewing of a gum containing 30 mg of urea; (2) find the time to achieve steady state when gel-stabilized plaque, not previously exposed to urea, is in contact with the normal salivary urea concentration; (3) measure the urea concentrations in gel-stabilized plaque at different time points during exposure of the plaque to an artificial saliva in which the urea concentrations varied as during the chewing, for 20 min, of a gum containing 30 mg of urea; (4) study the effect of such higher salivary urea concentrations on the Stephan curve which develops after exposure of a gel-stabilized plaque to sucrose in vitro, and (5) study these situations mathematically, including ammonia production, by means of a computer model (Dibdin [1990], as modified [Dibdin and Dawes, 1998] to include urea metabolism) in order to gain greater insight into the underlying mechanisms.…”

Assessment of Salivary Urea in Different Stages of Chronic Renal Failure Patients

“…8 With growing awareness regarding the interrelationship between medical and dental problems, need was felt for a simple, noninvasive, rapid method for assessing urea levels in CRF patients. Monitoring of markers in saliva instead of serum is advantageous because saliva collection is a noninvasive, simple, and inexpensive approach with minimal infectious risk that can be performed by the patient with no need for involvement from medical personnel.…”