Effects of salivary film velocity on pH changes in an artificial plaque containing Streptococcus oralis, after exposure to sucrose

Results from a computer model suggest that following exposure of dental plaque to sucrose, the rate of clearance of acids from plaque into the overlying salivary film will be greatly retarded at low film velocities. This was investigated with an in vitro technique in which artificial plaque containing S. oralis cells was exposed to 10% sucrose for one min. The pH at the proximal (P) and distal (D) undersurfaces of the plaque (0.5 or 1.5 mm thick) was then monitored during the passage of a 0.1-mm-thick film of a sucrose-free solution over the surface. Over the range of salivary film velocities that have been estimated to occur in vivo (0.8-8 mm/min), lower minimum pH values and increased times for the pH to recover toward neutrality occurred at the lower salivary film velocity. Lower pH values were also reached with the 0.5- than with the 1.5-mm-thick plaque. P/D pH gradients, with a lower pH distally, developed at film velocities of 0.8 and 8 mm/min, and the gradients were much more pronounced at the lower velocity. No P/D pH gradients developed when the film velocity was 86.2 mm/min. Incorporation of dead S. oralis cells into the plaque at percentages up to 57% reduced the extent of the pH fall and prolonged the recovery of the pH toward neutrality. The results support the prediction that, other factors being equal, plaque located in regions of the mouth with low salivary film velocity will achieve pH values lower than those of plaque of identical dimensions and microbial composition located in areas where salivary film velocity is high.     

Effects of salivary bicarbonate content and film velocity on pH changes in an artificial plaque containing Streptococcus oralis, after exposure to sucrose

Chewing-gum stimulation of salivary flow (at the time of the pH minimum following exposure of plaque to carbohydrate) has been shown to cause a rapid increase in plaque pH. The objective of this study was to determine whether the rise in plaque pH is primarily due to the increased buffering capacity of stimulated saliva, or to the fact that an increased flow rate increases the concentration gradient for acid to diffuse from the plaque into the overlying salivary film, which will be moving at a higher velocity. This was investigated with an in vitro technique in which artificial plaque (0.5 or 1.5 mm deep) containing S. oralis cells was exposed to 10% sucrose for one min. The pH values at the proximal and distal undersurfaces of the plaque were then monitored during the passage of a 0.1-mm-thick film of a sucrose-free artificial saliva over the surface, at a range of film velocities (0.8-8 mm/min) that have been estimated to occur in vivo. When a minimum plaque pH had been achieved, the salivary film velocity was either (a) kept the same, with or without 15 mmol/L HCO3 (the concentration measured in chewing-gum-stimulated saliva), (b) increased to 86.2 mm/min, or (c) increased to 86.2 mm/min with 15 mmol/L HCO3 added to the artificial saliva. The findings suggest that after sucrose ingestion, the rapid rise from minimum plaque pH values, which can occur with gum-chewing stimulation of salivary flow, is due to the combined effects of the increase in salivary film velocity, and of a greater availability of bicarbonate.(ABSTRACT TRUNCATED AT 250 WORDS)     

Human dental plaque pH, and the organic acid and free amino acid profiles in plaque fluid, after sucrose rinsing

The relationship between these factors was studied in plaque and plaque fluid samples taken at intervals during the Stephan pH curve following a sucrose mouth rinse. Levels of lactate rose after the rinse, then fell during the pH recovery phase. Levels of acetate, propionate and phosphate fell after rinsing, then rose again. Amino acid concentrations also changed, with many showing a fall followed by a rise; others rising then falling; and some showing a more variable or complex pattern. In resting plaque fluid, only alanine, proline, glutamic acid, glycine and ammonia were present at concentrations above 1 mmol/l. Delta-aminovaleric acid was detected at levels below those that have been found in monkeys. Hydroxyproline and hydroxylysine were consistently detected, levels of arginine were generally low, and those of cystine consistently very low. The results may provide a basis for understanding the complex metabolic interrelations that occur in the course of the Stephan curve and which may reflect or produce the observed pH changes. They suggest that besides the amount of acid produced, the type of acid, buffering power and base production should be considered as determinants of plaque 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

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.     

pH responses to sucrose and the formation of pH gradients in thick 'artificial mouth' microcosm plaques.

Artificial microcosm plaques were grown in a five-plaque culture system for up to 6 weeks, reaching a maximum depth of several mm. Procedures for long-term pH measurement with glass electrodes were established; they showed that the application of 5 or 10% sucrose for 6 min with a slow continuous flow of a basal medium containing mucin (BMM) generated the pH changes characteristic of in vivo Stephan curves. These pH responses were reproducible between plaques. Plaque mass and thickness were critical variables. Successive, sucrose-induced pH curves in plaques up to 4 mm thickness showed minor reductions only in the amplitude and rates of pH change. In plaques over 4 mm thick there was a pronounced reduction in pH response to successive sucrose applications, indicating increased diffusion limitations--a result of plaque growth to seal in the freshly-inserted pH electrode. In plaques of 6 mm maximum thickness, 10% sucrose induced a decrease to below pH 5.5 lasting 24 h, compared to the pH response in 2 mm thick plaque, which returned to the resting pH in 2 h. Differences in pH of up to 0.9 units were identified in thick plaques between inner and outer layers. The BMM flow rate was a critical determinant of the amplitude of the pH response to sucrose and subsequent return to resting pH. These results confirm, for microcosm plaque, the importance of clearance dynamics and diffusion-limited gradients in regulating plaque pH.     

An analysis of factors influencing diffusion from dental plaque into a moving film of saliva and the implications for caries

Recent studies have indicated that saliva in the mouth is present as a film only about 0.1 mm thick, and that this film moves at different rates (about 0.8 to 7.6 mm/min) in different regions of the oral cavity. The clearance rates of KCl, as a model diffusant, from agarose gels at different sites in the mouth have also been found to vary markedly, and it has been proposed that these variations are related to differences in the velocity of the salivary film. A computer model has been developed for prediction of clearance half-times for substances diffusing from plaque of variable dimensions into a film of fluid 0.1 mm thick, moving at different velocities. The results show that over the range of velocities calculated to occur in the mouth, the clearance half-times are directly related to the length of plaque over which the fluid passes, and inversely related to the salivary film velocity. The predictions of the model are in good agreement with experimental results from a physical model. Tests were made of the predicted effect of salivary film velocity on the shape of the pH curve initiated by exposure of plaque to a saturated sucrose solution, followed by normal salivary clearance. With a low salivary film velocity, the fall in pH was greater and more prolonged.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of 0.2 per cent (48 mM) NaF rinses daily on human plaque acidogenicity in situ (Stephan curve) and fluoride content

Plaque acidogenicity (Stephan curves) and fluoride concentrations were measured in 40 subjects before and during a 1–2 month period of daily mouth-rinsing with 48 mM NaF. Plaque-fluoride concentration increased on average 12-fold during the rinsing period and there was also a small, but statistically significant (p < 0.025), average increase of 0.11 units in the pH minimum of the Stephan curve. This increase was slightly larger (0.20 units) for the group of 27 subjects whose pH minima prior to fluoride-rinsing were 5.7 or lower. Inclusion of 48 mM NaF in the sucrose rinse used to induce the Stephan curve for 4 subjects raised the average pH minimum by 0.70 units. The effect of fluoride rinsing on plaque acidogenicity and fluoride concentration was lost within 4–10 days of withdrawal of the rinse. It is concluded that a reduction in plaque acidogenicity may supplement the cariostatic action of fluoride on enamel solubility.     

Clearance of glucose and sucrose from the saliva of human subjects

The ability of 20 healthy people to clear test solutions of sucrose (0.73 M) and glucose (1.4 M) from the mouth was examined. Both sugars were cleared within 20 min in a two-step manner. Rapid clearance occurred between 0 and 6 min; much slower clearance occurred thereafter. It took 7.2 min with glucose and 6.3 min with sucrose for the saliva-sugar concentration to fall to 1 mg/ml. Salivary flow, stimulated during sugar exposure, decreased in a two-step pattern similar to sugar clearance. Evidently, clearance was dependent on the rate of flow of saliva which took about 1 h to return to its resting flow level. Comparison of the pattern of sugar clearance to the Stephan curve (the rapid pH fall followed by a slow pH rise seen after rinsing with sugar solutions) indicated that the pH-fall phase of the curve occurs during the initial period of rapid sugar clearance and salivary flow, and the pH-rise phase occurs during the subsequent period of slower clearance and slow saliva flow. Comparison with the data of Swenander-Lanke (1957) [Acta odont. scand. 15, 3-156], indicated that the clearance of sugar solutions also reflects the clearance of sugar-containing solid foods from the mouth.     

The effects of different concentrations of sucrose, fructose, and glucose on pH changes by Streptococcus mitior in an artificial mouth

The aim of this study was to determine the effects of the initial sucrose (S) concentration, as well as those of fructose (F), glucose (G), and invert sugar (F/G), on the pH developed by a layer of S. mitior, to represent dental plaque, in an artificial mouth which simulates the process of oral sugar clearance. At S, F. G, and F/G concentrations of 2% and with normal oral sugar clearance rates, the bacteria produced a smaller pH fall from S than from the other sugars; at initial concentrations of 20%, however, the differences were not significant. With constant S concentrations of 0.5-35%, the minimum pH reached was 4.03 +/- 0.14 (S.D.); with S concentrations of 50% and above, slightly but significantly higher values (4.41 +/- 0.34) occurred. However, with normal sugar clearance, the pH fall was much less than with a constant concentration and was dependent on the S concentration over the range of 0-10%, but was independent at higher concentrations. Exposure of the bacteria to S for as short a period as two min during normal sugar clearance gave a nearly maximum pH fall. This suggests that rinsing the mouth with water more than two min after consumption of sucrose in liquid form will have very little effect in reducing the pH fall in dental plaque. A more appropriate method for reducing acid formation by dental plaque would be consumption of a salivary stimulant which would increase the flow rate and buffer capacity of the saliva.     

Why does supragingival calculus form preferentially on the lingual surface of the 6 lower anterior teeth?

Many authors have assumed that the reason supragingival calculus tends to form preferentially on the lingual surface of the 6 lower anterior teeth is because saliva from the adjacent submandibular ducts is a source of calcium and phosphate ions and because loss of CO2 as the saliva enters the mouth increases the local pH. However, the fluid phase of plaque in all locations is supersaturated with respect to the calcium phosphates in calculus and there is always a tendency for calculus to deposit, except after sugar consumption, when plaque pH may fall below the critical level and the plaque fluid becomes unsaturated. pH is least likely to fall below the critical level in plaque lingual to the lower anterior teeth, as this plaque is very thin, sugar concentration after sugar intake is lowest in that area and its clearance rate is fastest, and the high salivary film velocity there promotes loss of any acid formed in plaque. A high salivary film velocity also brings more salivary urea to the site, which facilitates plaque alkalinization. These factors all contribute to the development of shallow Stephan curves of short duration and together provide a more reasonable explanation for the fact that supragingival calculus deposition progresses most easily on the lingual surface of the lower anterior teeth.     

Changes in lactate and other ions in plaque and saliva after a fluoride rinse and subsequent sucrose administration

The purpose of this study was to examine plaque and saliva composition after a fluoride rinse and subsequent sucrose application. Fifteen subjects accumulated plaque for 48 h, and then rinsed with a fluoride rinse based on 228 microg/g (ppm) Na2SiF6 and some received no rinse. After 60 min, upper and lower buccal molar plaque samples and 1-min saliva samples were collected. The subjects then rinsed with 10% g/g sucrose solution, and 7 and 15 min later, a second and a third set of samples were collected. Plaque fluid and clarified saliva were then recovered from these samples by centrifugation, and the remaining plaque acid extracted. The plaque fluid, centrifuged saliva, and plaque extract samples were then analyzed using micro techniques for pH, free calcium, phosphate, organic acids (plaque fluid and saliva only) and fluoride. Considering both the fluoride rinse and no-rinse groups, the most notable compositional changes in saliva 7 min after the sucrose rinse were pH -0.40 unit, free calcium 0.42 mM, lactate 5.2 mM, phosphate -1.3 mM, and fluoride 2.8 microM; while in plaque fluid, the corresponding changes were pH -1.59 unit, free calcium 1.5 mM, lactate 35 mM, phosphate -1.6 mM and fluoride -26 microM. After sucrose rinsing, undersaturation was found with respect to dicalcium phosphate dihydrate in saliva and plaque fluid and with respect to tooth enamel in some plaque fluid samples. Plaque fluid composition appeared to be strongly influenced by salivary clearance, diffusive loss of ions into the water phase of the rinse, and lower jaw pooling of the sucrose and fluoride components of the rinses. After the experimental rinse, the fluoride concentration in plaque fluid [86 +/- 22 mM (upper molar site), 162 +/- 150 mM (lower molar site)], saliva (26 +/- 18 mM), and whole plaque [99 +/- 97 microg/g (upper molar site), 197 +/- 412 microg/g (lower molar site)] was comparable to the values in previous studies using this rinse. These very high plaque fluid fluoride concentrations, compared with the 'no-rinse' samples, induced an approximately 0.3-unit increase in the plaque fluid pH 7 min after the sucrose rinse, a small decrease (approximately 20%) in lactate production and a modest increase in enamel saturation. Although these changes were all statistically significant, no correlation was found between the decrease in lactate concentration and plaque fluid fluoride, pH or whole plaque fluoride.     

A role of salivary carbonic anhydrase VI in dental plaque

OBJECTIVE: 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. DESIGN: 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. RESULTS: 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. CONCLUSIONS: 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.     

The effect of chewing sorbitol-sweetened gum on salivary flow and cemental plaque pH in subjects with low salivary flow

The purpose of this work was to study the effect of chewing a sorbitol-sweetened gum on whole and parotid salivary flow rates, and on the cemental plaque pH response to a sucrose rinse challenge, in subjects with low salivary flow. The results show that chewing a flavored sugarless gum significantly increases salivary flow rates in individuals with dry mouth. Additionally, chewing the sorbitol-sweetened gum effectively prevents the fall in cemental plaque pH generally seen in response to a sucrose challenge. This indicates that chewing a sorbitol-sweetened gum provides a palliative and possibly a protective benefit for people who suffer from dry mouth.     

Effect on a cariogenic challenge of saliva/plaque exchange via a thin salivary film studied by mathematical modelling

Computer models can be powerful tools for studying complex interacting processes. The computer model of events in dental plaque during a cariogenic challenge described here simulates diffusion and metabolism of substrate, plus coupled diffusion/reaction of fourteen other species, charged and uncharged, including acidic metabolic products and fixed buffers. Its extension to deal with the effects of poor contact with bulk saliva when the plaque is presumed covered by a thin salivary film is here considered. Site-specific mixing rates between film and salivary pool were modelled phenomenologically, using data from the literature. Fast mixing was assumed during an initial carbohydrate intake phase (2 min sugar rinse), followed by site-dependent mixing and logarithmic clearance. The analysis also suggested a possible way of estimating local salivary film thickness. Increasing the halving time for exchange between film and bulk saliva was shown to prolong the pH minimum greatly, and to increase mineral loss. The respective roles of fixed buffers as stores of protons and of mobile buffers (especially bicarbonate) as exporters of protons from the inner plaque were emphasised.     

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)     

The influence of salivary flow rate on diffusion of potassium chloride from artificial plaque at different sites in the mouth

The rate at which substances diffuse from dental plaque influences the rate of clearance of acid and bacterial toxins from plaque into saliva. The aim of this study was to compare the rates of clearance of potassium chloride, as a model substance, from artificial plaque of 3-, 4-, and 6-mm-diameter, positioned bilaterally at different locations in the mouth. The diffusant was KCl (1 mol/L) in a 1.0% agarose matrix, placed in wells 1.5 mm deep, in small acrylic devices 3 mm thick, which could be fastened to the teeth with dental floss and removed after different time periods. The half-time for clearance was determined from the best-fitting least-squares line of the potassium concentration remaining in the gel plotted against the square root of time. For 14 subjects, half-times for the lower anterior lingual and upper posterior lingual regions averaged about 2.5 times greater than those for clearance into a large, stirred volume in vitro, whereas those for the upper and lower anterior buccal regions averaged about 12.8 times greater. This difference may be due to the fact that anterior buccal sites are exposed only to minor rather than to major salivary gland secretions. When salivary flow was stimulated by the sucking of sour lemon drops, all in vivo half-times were reduced by about one-half. The half-times were also directly related to the surface areas of the chambers, which implies that rates of diffusion from plaque of substances such as acid or bacterial toxins are inversely related to the surface area of the plaque at a particular site.     

Effects of processed cheese on human plaque pH and demineralization and remineralization

This two-part study was undertaken to examine the effects of processed cheese on human plaque pH and de- and remineralization of enamel and root lesions in a human in situ caries model system. In the first part of the study the selected processed cheese (Kraft American Singles Processed Cheese Food) was eaten alone and followed by a 10% sucrose rinse after the acidogenicity of the plaque was demonstrated. A 10% sucrose rinse alone resulted in a mean minimum pH of 4.26. The cheese alone showed a mean minimum pF of 6.32 and cheese followed by sucrose resulted in a mean minimum pH of 6.48. The plaque pH of cheese eaten alone stayed at pH above 5.7 (the "safe for teeth" level). Cheese consumption also prevented the acid challenge when followed by sucrose. The second part of the study utilized the thin-sections of artificially created caries-like lesions on enamel and root, and sound root sections. One-month periods were used in a cross-over design to examine the effect of eating the cheese q.i.d. Polarized light microscopy was used to determine changes in the size of lesion areas. The addition of the processed cheese to the diet resulted in statistically significant reductions in enamel lesion size as well as a reduction in progression of root lesions. Lesions created on the sound root surfaces were approximately one-third the size of those created during the control period. This study indicates that processed cheese is hypoacidogenic, anti-acidogenic, and prevents demineralization as well as enhances remineralization.     

Effect of a hydroxyl ion-releasing composite resin on plaque acidogenicity

The aim of this in vivo study was to evaluate the neutralizing capacity, registered as change of plaque acidogenicity, on aged proximal restorations of an ion-releasing composite resin (IRCR), which releases hydroxyl, calcium, and fluoride ions at low pH. Twenty patients, with a mean age of 63 years (range 43-85), participated. All had one aged proximal IRCR restoration (mean age 15 months) and one nonrestored enamel surface to make an intraindividual comparison possible. The neutralizing effect of the IRCR was evaluated by measuring plaque pH, using the microtouch method, after a mouthrinse with 10% sucrose. The plaque pH measurements were repeated 1.5 years later on the IRCR (mean age 34 months), the enamel surfaces and a universal hybrid composite resin (CR). At both 15 and 34 months, the plaque on the IRCR surfaces showed the least acidogenic potential for the whole 60-min time interval. The largest differences between the IRCR, CR and enamel were found during the first 15 min. At 15 months, the total areas under the plaque pH curve (AUC(5.7) and AUC(6.2)) differed significantly between the IRCR and enamel surfaces for the time periods 0-5 min and 5-15 min. At 34 months, significant differences were found between IRCR and CR at the 0- to 5-min time period. It can be concluded that IRCR restorations countered the plaque pH fall and maintained it at levels where less enamel and dentin demineralization can occur.     

A comparison of the acid-base metabolisms of pooled human dental plaque and salivary sediment

The acid-base metabolisms of the mixed bacteria in pooled dental plaque and salivary sediment sampled from the same subjects were compared in vitro. Plaque at a suspension concentration of 8.3 per cent (v/v) was found to produce pH responses like those of sediment at 16.7 per cent (v/v) with all substrates and under all incubation conditions tested. The substrates examined included several carbohydrates (glucose, sucrose and starch) and several nitrogenous substrates (urea, arginine and the arginine peptide glycyl-glycyl-lysyl-arginine also called sialin). Also examined were the effects of endogenous substrates and of salivary supernatant and fluoride. A difference in suspension concentration was necessary to achieve similarity in pH response which was attributed to the presence of more non-viable epithelial cells in sediment than in plaque. Under these conditions, salivary sediment showed a slightly greater buffering capacity than plaque, a difference that was not evident if salivary supernatant was present. It was clear from this study that salivary sediment and pooled dental plaque from the same subjects have similar acid-base metabolisms and that the more abundant and readily available sediment could be used to study such metabolism in dental plaque.     

Role of sucrose in plaque formation

Results are presented which support the concept that the bacterial enzyme glucosyltransferase (GTF) plays a crucial role in sucrose induced plaque formation. GTF was shown to adhere strongly to anionic, hydrophobic and polysaccharide solid materials, and to be able to produce glucans in the adsorbed state. It appears conceivable that GTF adsorb to teeth and produce glucans. Glucan chains on the surface of the bacteria and glucans on the tooth surfaces interact (pack) and form a strong binding mechanism. The rigid alpha 1,3 linked glucans produced by Streptococcus mutans are particularly suited for interaction of this kind. This mechanism could account for sucrose-induced binding of bacteria to enamel, pellicle covered enamel and preformed plaque. S. mutans would adhere particularly strongly to tooth surfaces in the presence of sucrose, according to this model.