Stephan Curve Research Articles

Effect of composite resin containing antibacterial filler on sugar-induced pH drop caused by whole saliva bacteria

Secondary caries around restorations is a major problem and can be attributed to bacteria invading microgaps formed at the tooth-restoration interface. An antibacterial composite resin containing quaternary ammonium silica (QASi) filler has been reported to inhibit enamel demineralization in situ. However, whether the prevention of enamel demineralization by QASi-containing composite resin is because of the reduced metabolic activity of acid-producing saliva bacteria is unclear. The purpose of this study was to compare the effects of QASi-containing composite resin and 2 other restorative materials on the viability of salivary bacteria and sugar-induced acid production. Whole saliva from each of the 30 study participants, 14 at high risk and 16 at low risk for caries, was brought into contact with quadruplicate specimens of 3 restorative materials, Infinix Flowable Composite, an anti-bacterial composite resin containing 1.5% QASi filler (Nobio), Filtek Supreme Flowable Restorative (3M), a conventional flowable composite resin, and dental amalgam (Silmet). Bacterial growth and sugar-induced acid production on each restorative material were measured every 20 minutes for 18 hours. Caries risk groups were compared using the t test and repeated measures analysis of variance (α=.05). When significant, Bonferroni multiple comparisons were used. On average, the saliva with the QASi-containing composite resin specimens maintained a near-neutral pH, not dropping below pH 6.0. The saliva associated with both conventional restorative materials exhibited a pH drop below 5.5 (P<.001), the critical threshold for tooth demineralization according to the Stephan curve. Virtually no growth was measured on the surface of the antibacterial composite resin, whereas bacteria grew on the conventional composite resin and dental amalgam (P<.001). No differences were observed between participants at high and low risk of caries. Unlike amalgam and conventional composite resin, the QASi-containing composite resin showed a near-complete shutdown of the metabolic activity of salivary bacteria upon contact and virtually no bacterial viability. This suggests that the prevention of tooth demineralization by QASi-containing restoratives is associated with a significant reduction in bacterial metabolic activity.

Pre-treatment oral microbiome analysis and salivary Stephan curve kinetics in white spot lesion development in orthodontic patients wearing fixed appliances. A pilot study

BackgroundWhite spot lesions (WSLs) are a formidable challenge during orthodontic treatment, affecting patients regardless of oral hygiene. Multifactorial in nature, amongst potential contributors to their development are the microbiome and salivary pH. The aim of our pilot study is to determine if pre-treatment differences in salivary Stephan curve kinetics and salivary microbiome features correlate with WSL development in orthodontic patients with fixed appliances. We hypothesize that non-oral hygiene determined differences in saliva could be predictive of WSL formation in this patient population through analysis of salivary Stephan curve kinetics, and that these differences would further manifest as changes in the oral microbiome.MethodsIn this prospective cohort study, twenty patients with initial simplified oral hygiene index scores of “good” that were planning to undergo orthodontic treatment with self-ligating fixed appliances for at least 12 months were enrolled. At pre-treatment stage, saliva was collected for microbiome analysis, and at 15-minute intervals after a sucrose rinse over 45 min for Stephan curve kinetics.Results50% of patients developed a mean 5.7 (SEM: 1.2) WSLs. There were no differences in saliva microbiome species richness, Shannon alpha diversity or beta diversity between the groups. Capnocytophaga sputigena exclusively and Prevotella melaninogenica predominantly were found in WSL patients, while Streptococcus australis was negatively correlated with WSL development. Streptococcus mitis and Streptococcus anginosus were primarily present in healthy patients. There was no evidence to support the primary hypothesis.ConclusionsWhile there were no differences in salivary pH or restitution kinetics following a sucrose challenge and no global microbial differences in WSL developers, our data showed change in salivary pH at 5 min associated with an abundance of acid-producing bacteria in saliva. The results suggest salivary pH modulation as a management strategy to inhibit the abundance of caries initiators. Our study may have uncovered the earliest predecessors to WSL/caries development.

Effects of Lactobacillus casei Shirota intake on caries risk in children

Background/purposeYakult is a well-known probiotic beverage consisting of a single live bacterial species, Lactobacillus casei Shirota. However, the potential cariogenic/cariostatic effects of Yakult intake among children have not been studied yet. Hence, this study aimed to investigate the clinical effects of short-term Yakult intake on oral biofilm acidogenicity, cariogenic bacterial counts, and caries risk in children. Materials and methodsEighteen children, 7–11 years of age, consumed standard Yakult daily for 7 days. Prior to and after intervention, functional oral biofilm acidogenicity characterized by the Stephan curve, Lactobacillus and Streptococcus mutans counts, and caries risk were determined. ResultsProbiotic intervention demonstrated significant increase in minimum pH from 4.88 to 5.14 (P=0.02), 18.2% reduction in area under the Stephen curve [area under the curve (AUC)], and 29.3% decrease in pH recovery time, although these two differences were not statistically significant. No difference was observed in S. mutans and Lactobacillus counts or caries risk after intervention (all P>0.05). However, on subgroup analysis using “reduction of AUC” to separate “responders” from the “nonresponders”, the significant cariostatic effects on oral biofilm acidogenicity, among “responders”, were revealed by an increase in minimum pH (P=0.005) and a reduction in pH recovery time (P=0.003). ConclusionThere may be a potential cariostatic effect of short-term Yakult intake in reducing functional biofilm acidogenicity in children with certain oral biofilm and risk profile. Further studies may be needed to validate this probiotic effect. Quality risk assessment may be critical prior to prescribing/recommending Yakult as an adjunct caries-preventive treatment for children.

A microfluidic platform with pH imaging for chemical and hydrodynamic stimulation of intact oral biofilms.

A microfluidic platform with a fluorescent nanoparticle-based sensor is demonstrated for real-time, ratiometric pH imaging of biofilms. Sensing is accomplished by a thin patterned layer of covalently bonded Ag@SiO2+FiTC nanoparticles on an embedded planar glass substrate. The system is designed to be sensitive, responsive and give sufficient spatial resolution to enable new micro-scale studies of the dynamic response of oral biofilms to well-controlled chemical and hydrodynamic stimulation. Performance under challenging operational conditions is demonstrated, which include long-duration exposure to sheer stresses, photoexcitation and pH sensor biofouling. After comprehensive validation, the device was used to monitor pH changes at the attachment surface of a biofilm of the oral bacteria, Streptococcus salivarius. By controlling flow and chemical concentration conditions in the microchannel, biochemical and mass transport contributions to the Stephan curve could be probed individually. This opens the way for the analysis of separate contributions to dental caries due to localized acidification directly at the biofilm tooth interface.

The Stephan Curve revisited

The Stephan Curve has played a dominant role in caries research over the past several decades. What is so remarkable about the Stephan Curve is the plethora of interactions it illustrates and yet acid production remains the dominant focus. Using sophisticated technology, it is possible to measure pH changes in plaque; however, these observations may carry a false sense of accuracy. Recent observations have shown that there may be multiple pH values within the plaque matrix, thus emphasizing the importance of the milieu within which acid is formed. Although acid production is indeed the immediate proximate cause of tooth dissolution, the influence of alkali production within plaque has received relative scant attention. Excessive reliance on Stephan Curve leads to describing foods as "safe" if they do not lower the pH below the so-called "critical pH" at which point it is postulated enamel dissolves. Acid production is just one of many biological processes that occur within plaque when exposed to sugar. Exploration of methods to enhance alkali production could produce rich research dividends.

Caries Susceptibility of Endodontically versus Nonendodontically Treated Teeth

Introduction The aim of the present investigation was to evaluate the caries susceptibility of endodontically versus nonendodontically treated teeth in relation to dental plaque–related factors. Methods Twenty patients with 2 endodontically treated teeth (ETT) each were examined regarding cariogenic microflora of proximal plaque, in situ plaque pH drop after a sucrose rinse (Stephan curve), and de novo plaque formation. Recurrent caries and the quality of the coronal fillings/crowns of these teeth were also evaluated. ETT were compared with contralateral, nonendodontically treated teeth (NETT). Results Irrespective to the type of restoration, Streptococcus mutans count, de novo plaque formation, and recurrent caries were higher on the surface of ETT compared with NETT ( P < .05). Moreover, the initial (resting) pH in plaque was significantly lower ( P < 0.05) in ETT. Conclusions ETT showed an increased susceptibility to caries as a result of either alteration in their biological environment or inadequacy of the marginal fit of the dental restoration. Clinicians should be aware of this risk.

A clinical study on the effect of the prebiotic inulin in the control of oral malodour

The aim of this clinical study was to evaluate the potential of an inulin mouth rinse to reduce the proportions of tongue bacteria associated with oral malodour. Thirteen panellists rinsed with either 10% sucrose or a 10% inulin mouth rinse twice daily for 21 days. Breath odour levels were assessed using a Halimeter† and organoleptic assessment, both before and after sucrose, inulin or water rinses. Tongue pH was registered and the tongue flora was cultured on media selective for total and obligate anaerobes, streptococci and inulin fermenters. There were no differences in baseline Halimeter† levels over the 21 day period, but a slight decrease in organoleptic scores was noted. A reduction in odour levels assessed by Halimeter† and organoleptically was observed immediately after rinsing. The effect was greater by the end of the 21 day regime. Microbial counts remained high, and no significant differences were observed, but there was a trend towards increased streptococcal counts by the end of the 21 day period. Tongue pH baseline levels were approximately neutral, but immediately after carbohydrate rinses a typical Stephan curve was observed. There is some indication that the use of twicedaily carbohydrate mouth rinses (sucrose or the prebiotic inulin) can reduce oral malodour by encouraging the growth of acidogenic bacteria and inhibiting the obligate anaerobes associated with malodour. Inulin is a less cariogenic substrate, and inulin mouth rinsing may provide a novel method for the control of oral malodour. Key words: oral malodour, volatile sulphur compounds, prebiotic, inulin, oral bacteria

A role of salivary carbonic anhydrase VI in dental plaque

Carbonic anhydrase (CA) VI is a unique secreted isozyme of CA, which catalyzes the reversible reaction CO2 +H2O<-->H+ +HCO3-. CA VI has been thought to provide a greater buffering capacity to fluids into which it is secreted. This study was performed to confirm this in saliva. Nine healthy subjects participated in the study. The pH of the dental plaque from each subject was monitored after a mouth rinse with 10% sucrose with or without 10(-5)M acetazolamide, a specific inhibitor of CA. Also CA was examined in plaque by enzyme histochemistry, immunohistochemistry and Western blot analysis. Though sucrose and sucrose plus inhibitor yielded Stephan curves with a similar temporal pattern, the pH values of the latter were significantly lower than those of the former. Plaque exhibited CA activity by enzyme histochemistry. Immunohistochemistry and Western analysis demonstrated that the activity was due to CA VI but not to CA I or CA II. The results indicate that CA VI in saliva penetrates plaque and facilitates acid neutralization by salivary bicarbonate. Therefore, CA VI may be considered an anti-caries protein in saliva.

Demineralization of Dentin by Streptococcus mutans Biofilms Grown in the Constant Depth Film Fermentor

To develop a bacterial demineralization model, we grew Streptococcus mutans biofilms in a constant depth film fermentor (CDFF) and studied the effects of sucrose pulsing frequency (SPF) in time on dentin demineralization. S. mutans biofilms were grown in dentin specimens with grooves and on dentin surface specimens for 20 days. During the experiments, 2% sucrose was pulsed either 4 or 8 times per day for periods of 30 min. Diluted brain-heart infusion medium containing 25 mM PIPES buffer and 1.5 mM CaCl₂ was pulsed as the alternative growth medium. Specimens with intact biofilms were taken out on days 5, 12 and 20. The model was assessed by viable counts of the biofilm, mineral loss and lesion depth in the dentin specimens (by transversal microradiography) and pH measurements in the groove (by pH microelectrode). The results showed that biofilms formed on the dentin surface specimens were constant in viable counts for the low SPF, while this parameter tended to increase with time under the high SPF. Lesions with intact surfaces were formed and the lesion size increased significantly over time and increased significantly with increasing SPF. Typical Stephan curves were found after sucrose pulsing. The pH inside the groove returned to neutral under low SPF, but remained below 6.5 under high SPF. With the CDFF S. mutans biofilm model, lesions can be created in dentin within reasonable experimental time periods, as a result of the presence of a biofilm and in response to carbohydrate challenges.

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

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.

Plaque pH and Associated Parameters in Relation to Caries

Intensified plaque acidogenicity in caries–prone subjects was reported many years ago, but emerging evidence has suggested that the relationship may not be as strong as once thought. We have now determined a range of acidogenicity variables in subjects having both caries prevalence and incidence data, and have included plaque mineral data in the analysis. pH measurements were made in 20 randomly selected subjects from a high–caries group (mean DMFS = 8.95) and 20 from a caries–free group of Beijing children aged 12 years participating in a caries prediction study. Subgroups with a 12–month DMFS increment ≥2 or = 0 were also formed from the two groups, respectively. Measurements were made with an iridium oxide electrode inserted between teeth 13/14, 23/24, 34/35 and 44/45, before and every 5 min for 30 min after rinsing with 10% sucrose, and the 4 resulting ‘Stephan curves’ averaged using a plaque pH analysis program. Supragingival plaque was collected from buccal and lingual smooth surfaces of posterior and upper anterior teeth and its acid extract analysed for Ca, P and F. Caries–free subjects (based on past experience) had a significantly higher maximum plaque pH and pH value after 30 min (reflecting a faster return to resting pH), a lower minimum enamel dissolution capacity of plaque and recorded less time below pH 7.0 than did high–caries subjects. No other differences were significant, including those of the principal acidogenic parameters ‘minimum pH attained after a sugar rinse’, ‘curve area below the critical pH of 5.5’ and ‘time below the critical pH’. Selection of the caries groups on the basis of both experience and incidence did not reveal significant differences in more parameters. Upper arch plaque was significantly more acidogenic than lower arch plaque, and there was a consistently strong association between upper and lower arch values in individuals. Ca, P and F in the subjects’ plaque had little or no influence on the principal acidogenic parameters. Our failure to find a relationship between caries prevalence or activity and these principal acidogenicity parameters may be related to differences between fissure and smooth surface plaque, temporal variations in acidogenicity and/or to use of F toothpaste during the 1–year observation period. These results support the view that factors such as the frequency of acidogenic episodes may be more important in caries progression than the degree of acidogenicity during any one episode.

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 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.

The effect of different concentrations of sugars in two foods (yoghurts and baked beans) on plaque pH

The effect of different concentrations of sugars in two foods (strawberry yoghurt and baked beans) on plaque acidogenicity was investigated using plaque sampling with a 'Beetrode' electrode. Six varieties of yoghurt, four varieties of baked beans and positive and negative control solutions of 10 per cent sucrose and sorbitol, respectively, were tested on six volunteers, selected according to the guidelines agreed at the San Antonio Conference of 1985. Plaque was harvested immediately before a one minute challenge with the test condition and at 5, 10, 15, 20 and 30 minutes thereafter. Parameters investigated were minimum plaque pH reached after a one minute consumption/rinse of the test food or control solution, maximum drop in plaque pH and 'area of the Stephan curve below pH 6.5'. An Acidogenic Potential Index was calculated for each test food and the results did not suggest a linear relationship between sucrose concentration in a food and acidogenic potential.

Salivary factors in caries models.

Consideration of salivary factors in caries models rarely extends beyond viewing saliva as a sink or diluent for plaque metabolic products, or as a source of buffering, for neutralizing plaque acids. In reality, saliva has a complex chemistry and a wide range of biochemical activities that may significantly affect plaque chemistry and microbiology. Thus, saliva is a major source of microbial nutrients, without which bacterial acid production is diminished. Buffering by salivary bicarbonate, and base production from urea and basic amino acids and peptides, significantly affect Stephan curves. Saliva is supersaturated with respect to basic calcium phosphate salts and contains novel inhibitors of calcium phosphate precipitation, while specific salivary proteins bind calcium. It seems important to consider if this system is reflected in plaque. Saliva, with contributions from serum and bacterial constituents, provides most of the precursors for the acquired enamel pellicle, which acts to slow demineralization during caries attack. Pellicle constituents appear to influence initial bacterial colonization of tooth surfaces and, therefore, may affect the microbial composition of plaque, but their detailed effects on plaque are poorly understood. Microbial adaptations to the anti-bacterial systems also seem important but are poorly investigated. Thus, saliva possesses an array of activities that have substantial actual or potential impact on plaque and, therefore, merit consideration for inclusion in systems intended to model dental caries.

Role of Saliva in Caries Models

The crucial role played by the actions of saliva in controlling the equilibrium between de- and remineralization in a cariogenic environment is demonstrated by the effects on caries incidence of salivary dysfunction and by the distribution of sites of caries predilection to those were salivary effects are restricted. However, of the several properties of saliva which may confer protective effects, it is not certain which are most important. A distinction can be made between static protective effects, which act continuously, and dynamic effects, which act during the time-course of the Stephan curve. Evidence implicates salivary buffering and sugar clearance as important dynamic effects of saliva to prevent demineralization; of these, the buffering of plaque acids may predominate. Enhanced remineralization of white spot lesions may also be regarded as dynamic protective effects of saliva. Fluoride in saliva (from dentifrices, ingesta, etc.) may promote remineralization and (especially fluoride in plaque) inhibit demineralization. The design of experiments using caries models must take into account the static and dynamic effects of saliva. Some models admit a full expression of these effects, while others may exclude them, restricting the range of investigations possible. The possibility is raised that protective effects of saliva and therapeutic agents may act cooperatively.

Distribution of sucrose around the mouth and its clearance after a sucrose mouthrinse or consumption of three different foods.

The distribution of sucrose in whole saliva and in saliva from seven different regions of the mouth was determined in 10 subjects over the 10-min period following the chewing of a doughnut, sucking on a mint candy, the drinking of orange juice, or use of a 10% sucrose mouthrinse. With all products, the sucrose was distributed non-uniformly, with particularly low concentrations on the lingual surfaces of the lower incisors and the facial surfaces of the upper molars. Clearance was also most rapid from these sites. Since the depth and duration of a Stephan curve in dental plaque is influenced by the sugar concentration to which the plaque is exposed, the results, together with previous results on salivary film velocity in different regions of the mouth, help to provide an explanation for the site-specificity of smooth-surface caries and of supragingival calculus deposition.

Influence of constant fluoride levels in solution on root hard tissue de- and remineralization measured by 125I absorptiometry.

To study the effect of fluoride on de- and remineralization of root hard tissue, an automatic pH-cycling caries model, simulating Stephan curves, was used for 21 days. From each of 13 unexposed human roots, four cementum/dentin blocks were prepared. Four experiments were carried out: one block from each tooth as subjected to pH cycling without and with fluoride at the concentrations of 0.02 ppm (1.0 mumol/l), 0.20 ppm (10.5 mumol/l) and 2.00 ppm (105.3 mumol/l) in the de- and remineralizing solutions, respectively. Mineral change in the specimens was monitored by 125I absorptiometry. When no fluoride was added to the solutions the change in transmission (delta T) increased continuously over 21 days, indicating loss of mineral. In the 0.02-ppm F experiment, there was a marked decrease in delta T, but almost no change in the 0.20-ppm F experiment. pH cycling with 2.00 ppm F in the solutions resulted in a gain of mineral in or most likely on the surface of the cementum/dentin blocks, indicated by a continuously decreasing delta T. The fluoride level in the solution significantly influenced the change in the mineral content of the specimens. Microradiographs of the sectioned blocks showed radiodense surface zones, varying degrees of subsurface demineralization and signs of remineralization or mineral deposition.

Use of palladium touch microelectrodes under field conditions for in vivo assessment of dental plaque pH in children.

The aim of this study was to assess the applicability of palladium touch microelectrodes, connected to battery-run pH meters, for in vivo plaque pH measurements in children. The pH was assessed in 20 7-year-old and in 19 14-year-old caries-active and caries-inactive rural Kenyan children. The resting pH was measured at non-carious interproximal and occlusal sites and in open dentine cavities. Independent repeated measurements were performed at given sites at intervals of 15 s and 5 min and on different days. The resting plaque pH varied widely among the children, and there was no significant difference between caries-active and caries-inactive groups. The most striking feature was the considerable erratic fluctuations of pH at a given site with time, both in resting and in sucrose-challenged plaque. These fluctuations were sensitively recorded by palladium touch microelectrodes. After a sucrose rinse, not all sites in the same mouth behaved in a similar fashion, and thus the classical 'Stephan curve' was not always apparent. In conclusion, the palladium touch microelectrodes are highly applicable for plaque pH measurements in children, even under extreme field conditions.

The Effect of Sucrose on Plaque pH in the Primary and Permanent Dentition of Caries-inactive and -active Kenyan Children

The hypothesis that the Stephan pH responses of dental plaque would be different in caries-active and -inactive individuals was tested in 20 seven-year-old and 19 14-year-old Kenyan children. In each age group, half the children had greater than or equal to 2 dentin cavities; the other half had no such lesions. With a palladium-touch microelectrode, interdental plaque pH was monitored between m1/m2 in each quadrant in the primary dentition and in the four molar/premolar regions in the permanent dentition. pH was also monitored in caries cavities in the occlusal surfaces of lower first molars and on the tongue. pH was measured before and up to 60 min after the children rinsed with 10 mL of 10% sucrose. Caries status of the individual was unrelated to plaque pH in comparable non-carious sites in both of the age groups. The pH minimum in the maxilla was about 0.5 pH units lower than that in the mandible. Active occlusal caries lesions had a resting pH value of about 5.5, about 1 pH unit lower than that of sound surfaces. The pH dropped to about 4.5 in caries lesions and recovered slowly. In sound occlusal sites, a pH drop to about 6.0 was followed by a relatively rapid return to the resting value. Thus, when the mean values were considered, the classic Stephan curve response was evident. However, when the pH changes at single sites were considered at various time intervals, a substantial, erratic fluctuation was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Plaque Fluid and Diffusion: Study of the Cariogenic Challenge by Computer Modeling

Every cariogenic challenge involves a mixture of convective transport, diffusive transport, and biochemical reactions, plus physico-chemical reactions (including charge-coupling of diffusion), all of which together require numerical methods for their analysis. This presentation describes a one-dimensional finite-difference computer model of the cariogenic process, and some conclusions obtained from it. Sugar clearance from the mouth, together with site-dependent exchange between the bulk saliva and plaque surface via a salivary film, is combined with a finite-difference model of events occurring within the dental plaque. The latter includes: sugar diffusion and pH-dependent acid production; diffusion and dissociation equilibria for two acid end-products of fermentation and their anions (acetate and lactate); diffusion and dissociation equilibria of phosphate buffer; diffusion of potassium and chloride; diffusion of protons and simultaneous equilibration with fixed and mobile buffers. So that proper concentration distributions consistent with local charge neutrality can be ensured, an algorithm called Q-couple is used to impose charge-coupling between the fluxes of different ions including fixed charges. Mineral dissolution and precipitation are modeled as part of the same equilibrium calculations. The predictions of the model are compared with those of an earlier, much simpler one, in which fixed buffers were not included. It is shown that the known concentration of fixed buffer greatly extends the low pH of a Stephan curve. The isoelectric point of the plaque bacteria also appears to be of importance. The effects of various concentrations of mobile buffers, including acetate, are investigated. It is also shown that varying plaque/saliva contact over the known range derived from published studies has a profound effect on the modeled cariogenic challenge.