Accumulation of methylglyoxal in the gingival crevicular fluid of chronic periodontitis patients.

BACKGROUND, AIMS: Methylglyoxal (MG), a toxic product of cellular metabolism, is elevated in tissues and fluids in a number of human diseases. A cross-sectional study was undertaken to determine whether MG accumulates in the gingival crevicular fluid (GCF) of chronic periodontitis patients. METHODS: GCF samples were collected for 30 s each from three teeth with pocket depths greater than 3 mm (DD sites), from 14 chronic periodontitis patients. Control samples were taken from three healthy sites (DH sites) in the same patients, as well as from seven subjects who were periodontally healthy (HH sites). Fluid volumes were determined and the strips were placed in 0.5 N perchloric acid. Subsequently, samples were derivatized with o-phenylenediamine and the resulting methylquinoxaline was assayed by high-performance liquid chromatography on Lichrospher(R)-100 RP-18, with UV detection. RESULTS: Mean pocket depths were 5.7+/-0.7, 2.7+/-0.6 and 2.7+/-0.5 mm (mean+/-SD) for the DD, DH and HH sites, respectively. Mean MG levels were found to be 208.7+/-241.7 and 142.9+/-235.7 pmol/site in the GCF from DD and DH sites, respectively (p=0.0023), but only 11.5+/-4.4 pmol/site for the HH sites. Bacteroides forsythus has been found to accumulate high levels of MG in culture (unpublished data) and, consistent with this, the sampled diseased sites contained higher levels of B. forsythus than the corresponding healthy sites (2.7+/-4.2 x 10(5) versus 0.7+/-1.1 x 10(5), respectively; p=0.022). Total "red complex" microorganisms were significantly elevated in the DD sites. CONCLUSIONS: In view of the known protein- and DNA-modifying effects of MG, the finding of elevated levels of MG in the GCF from chronic periodontitis patients supports the hypothesis that MG may contribute to destructive tissue damage in this disease.

Clostridium beijerinckii and Clostridium difficile detoxify methylglyoxal by a novel mechanism involving glycerol dehydrogenase.

In contrast to gram-negative bacteria, little is known about the mechanisms by which gram-positive bacteria degrade the toxic metabolic intermediate methylglyoxal (MG). Clostridium beijerinckii BR54, a Tn1545 insertion mutant of the NCIMB 8052 strain, formed cultures that contained significantly more (free) MG than wild-type cultures. Moreover, BR54 was more sensitive to growth inhibition by added MG than the wild type, suggesting that it has a reduced ability to degrade MG. The single copy of Tn1545 in this strain lies just downstream from gldA, encoding glycerol dehydrogenase. As a result of antisense RNA production, cell extracts of BR54 possess significantly less glycerol dehydrogenase activity than wild-type cell extracts (H. Liyanage, M. Young, and E. R. Kashket, J. Mol. Microbiol. Biotechnol. 2:87-93, 2000). Inactivation of gldA in both C. beijerinckii and Clostridium difficile gave rise to pinpoint colonies that could not be subcultured, indicating that glycerol dehydrogenase performs an essential function in both organisms. We propose that this role is detoxification of MG. To our knowledge, this is the first report of targeted gene disruption in the C. difficile chromosome.

Food starches and dental caries.

Sucrose and starches are the predominant dietary carbohydrates in modern societies. While the causal relationship between sucrose and dental caries development is indisputable, the relationship between food starch and dental caries continues to be debated and is the topic of this review. The current view of dental caries etiology suggests that in-depth evaluation of the starch-caries relationship requires the consideration of several critical cariogenic determinants: (1) the intensity (i.e., the amount and frequency) of exposure of tooth surfaces to both sugars and starches, (2) the bioavailability of the starches, (3) the nature of the microbial flora of dental plaque, (4) the pH-lowering capacity of dental plaque, and (5) the flow rate of saliva. Studies of caries in animals, human plaque pH response, and enamel/dentin demineralization leave no doubt that processed food starches in modern human diets possess a significant cariogenic potential. However, the available studies with humans do not provide unequivocal data on their actual cariogenicity. In this regard, we found it helpful to distinguish between two types of situations. The first, exemplified by our forebears, people in developing countries, and special subject groups in more modern countries, is characterized by starch consumption in combination with a low sugar intake, an eating frequency which is essentially limited to two or three meals per day, and a low-to-negligible caries activity. The second, exemplified by people in the more modern societies, e.g., urban populations, is characterized by starch consumption in combination with significantly increased sugar consumption, an eating frequency of three or more times per day, and a significantly elevated caries activity. It is in the first situation that food starches do not appear to be particularly caries-inducive. However, their contribution to caries development in the second situation is uncertain and requires further clarification. Although food starches do not appear to be particularly caries inducive in the first situation, the possibility cannot be excluded that they contribute significantly to caries activity in modern human populations. The commonly used term "dietary starch content" is misleading, since it represents a large array of single manufactured and processed foods of widely varying composition and potential cariogenicity. Hence, increased focus on the cariogenicity of single starchy foods is warranted. Other aspects of starchy foods consumption, deserving greater attention, include the bioavailability of starches in processed foods, their retentive properties, also in relation to sugars present (starches as co-cariogens), their consumption frequency, the effect of hyposalivation on their cariogenicity, and their impact on root caries. The starch-caries issue is a very complex problem, and much remains uncertain. More focused studies are needed. At present, it appears premature to consider or promote food starches in modern diets as safe for teeth.

IL-8 degradation by Porphyromonas gingivalis proteases.

Gingival epithelial cells are the primary barrier to infection by periodontal pathogens. The production of chemotactic cytokines, including interleukin-8 (IL-8), is one mechanism the host uses in response to infection. In this study it was found that both gingival and oral epithelial cells produced IL-8, but after infection with the periodontal pathogen Porphyromonas gingivalis, accumulation of the cytokine could not be detected. Northern analysis established that infected epithelial cells still expressed IL-8 mRNA, suggesting that the cytokine was destroyed after secretion. Incubation of IL-8 with P. gingivalis cells resulted in rapid loss of the cytokine; however, in the presence of a protease inhibitor the loss was significantly retarded, indicating that IL-8 was degraded by P. gingivalis proteases.

Inhibition of salivary amylase by black and green teas and their effects on the intraoral hydrolysis of starch.

Tea decoctions prepared from a number of black and green teas inhibited amylase in human saliva. Black teas gave higher levels of inhibition than green teas, and removal of tea tannins with gelatin led to the loss of inhibitory activity from all decoctions. Streptococcal amylase was similarly inhibited by tea decoctions. Fluoride was without effect on amylase. Since salivary amylase hydrolyzes food starch to low molecular weight fermentable carbohydrates, experiments were carried out to determine whether tea decoctions would interfere with the release of maltose in food particles that became entrapped on the dentition. Subjects consumed salted crackers and rinsed subsequently for 30 s with black or green tea decoctions, or water. Maltose release was reduced by up to about 70% after rinsing with the teas. Black tea decoction was significantly more effective than green tea, in agreement with the in vitro data. The observations supported the hypothesis that tea consumption can be effective in reducing the cariogenic potential of starch-containing foods such as crackers and cakes. Tea may reduce the tendency for these foods to serve as slow-release sources of fermentable carbohydrate.

Gingival inflammation induced by food and short-chain carboxylic acids.

Earlier studies in our laboratories demonstrated that particles of a number of snack foods that are retained on the dentition accumulate fermentable sugars and short-chain carboxylic acids (SCCA; acetic, formic, lactic, and propionic) to different degrees. The present study was undertaken to test the hypothesis that the accumulated SCCA can induce a gingival inflammatory response. Five periodontally and medically healthy subjects were given portions of plain doughnuts (high SCCA levels) or oatmeal cookie (low SCCA), or had the SCCA applied directly to the gingival margins of designated teeth. Subjects were given wax to chew, or nothing, as controls. Inflammation was assessed by measurements of subgingival temperature, flow rates of gingival crevicular fluid (GCF), and neutrophil emigration into GCF. Subgingival temperatures of the maxillary gingiva rose by 1.32 +/- 0.30 degrees C (mean +/- SE) 5 min after the subjects consumed the doughnuts and remained elevated for at least 1 hr. These values were significantly higher than those obtained from subjects after ingestion of oatmeal cookies (0.63 +/- 0.17 degree C; p < 0.01), consistent with the low levels of SCCA in the retained cookie particles. Wax chewing elicited a similar response, indicating a masticatory effect on the gingiva. Gingival temperatures in the unchallenged controls remained unchanged. Neutrophil emigration into the GCF was significantly elevated in subjects after doughnut consumption. Rinses with a solution of SCCA, or application of the SCCA to the gingiva, also brought about significant elevations in subgingival temperature and neutrophil emigration. The findings describe the inflammatory effects of food ingestion on the gingiva of healthy human subjects, and support the hypothesis that SCCA in the particles of retained food are at least partly responsible for the observed responses.

Effectiveness of calcium lactate added to food in reducing intraoral demineralization of enamel.

Following the demonstration that rinses with solutions of soluble calcium salts reduced sucrose-induced demineralization, a study was undertaken to determine whether a similar effect could be obtained by the supplementation of a solid food with calcium lactate (CL). Subjects wore palatal appliances containing blocks of bovine enamel that were coated with Streptococcus mutans IB 1600 and ate 5-gram portions of cookies made with defined levels of CL. Determinations were made of changes in iodide penetrability (delta Ip) of the enamel, as well as the pH, calcium and inorganic phosphate of the streptococcal plaque. CL at 3.2% (w/w) reduced delta Ip from 12.9 +/- 1.7 to 6.1 +/- 0.9 units, i.e. by 52.7%. Plaque pH was not affected. Demineralization was reduced progressively with increasing concentrations of added CL, and CL was most effective with increasingly sweet cookies. Plaque contained 32.4 +/- 6.0 and 17.1 +/- 4.2 mM calcium after 1 and 5 min, respectively. Calculations showed that the plaque was saturated with respect to enamel during the first 5-10 minutes after food ingestion, in spite of the progressive drop in plaque pH. In conclusion, the present study demonstrated the reduction of the cariogenic potential of solid food by relatively low concentrations of CL. The effect appeared to be related to the ability of the food to maintain high levels of calcium in the streptococcal plaque during the period of active acidogenesis.

Short-chain carboxylic-acid-stimulated, PMN-mediated gingival inflammation.

This communication reviews the effects of short-chain carboxylic acids on human cells of importance to the periodontium. The central hypothesis is that these acids can alter both cell function and gene expression, and thus contribute to the initiation and prolongation of gingival inflammation. Short-chain carboxylic acids [CH3-(CH2)x-COOH, x < 3] are metabolic intermediates with a broad range of apparently paradoxical biological effects. For example, lactic acid (CH3-CHOH-COOH), a 3-carbon alpha-hydroxy-substituted acid, is widely recognized for its cariogenicity. Lactic acid, however, also occurs in tropical fruits, and is the active ingredient in a variety of anti-wrinkle creams developed by dermatologists. In marked contrast, the unsubstituted 3-carbon propionic acid (CH3-CH2-COOH) is used as a food preservative and is the active principle for one class of non-steroidal anti-inflammatory agents. Interestingly, the addition of one carbon to propionic acid dramatically changes the biological effects. The unsubstituted 4-carbon butyric acid (CH3-CH2-CH2-COOH) is used by hematologists as a de-differentiating agent for the treatment of sickle cell anemia, but by oncologists as a differentiating agent for cancer chemotherapy. Finally, acting either individually or in concert, these acids can increase vascular dilation. Clearly, these acids, while metabolically derived, have a number of very divergent activities which are cell-type-specific (Fig. 1). It may be telling that periodontal bacteria produce these acids in millimolar concentrations, and that these bacteria can be characterized by their acid production profiles. It is no less interesting that these acids occur in the gingival crevices of human subjects with severe periodontal disease at millimolar levels which are > 10-fold higher than those found in mildly diseased subjects, and are undetectable in healthy subjects. Further, when applied directly to healthy human gingiva, short-chain carboxylic acids stimulate a gingival inflammatory response and inflammatory cytokine release. At the cellular level, these acids inhibit proliferation of gingival epithelial and endothelial cells, and inhibit leukocyte apoptosis and function, but can stimulate leukocyte cytokine release. At the molecular level, these acids can stimulate neutrophil gene transcription, translation, and protein expression. Thus, the likelihood is high that these acids, in addition to their cariogenic activity, can promote and prolong gingival inflammation. Our challenge will be to identify the cell or cells of the periodontium which respond to short-chain carboxylic acids, to delineate their responses and the molecular mechanism(s) of these effects, and to categorize the aspects of the inflammatory components which damage and those which protect the host. With this information, it may be possible to begin to rationally identify and test pharmaceutical agents which diminish the harmful aspects, while enhancing the beneficial components, of the inflammatory response.

Effects of a high-bicarbonate dentifrice on intraoral demineralization.

Dentifrices available on the market today contain sodium bicarbonate in a wide range of concentrations. Anticaries efficacy has been demonstrated for these dentifrices in a variety of tests. New insights were gained in the present study in which the effect of a high-bicarbonate dentifrice on the sucrose-induced demineralization of tooth enamel in situ was examined. With the intraoral Delta Ip system it is possible to follow the minute changes in tooth enamel that essentially model the daily episodes of demineralization accompanying the ingestion of various foods. The results revealed a pronounced effect on the pH of the test plaque and a considerable reduction in mineral loss from the enamel. The effect persisted for more than 1 hour and, during that time, appeared to predominate over the effect of fluoride. These findings suggest that bicarbonate may provide additional protection against the loss of tooth enamel. Such effects may be significant for the design of new high-bicarbonate products.

Cytotoxic effects of short-chain carboxylic acids on human gingival epithelial cells.

Previous studies showed that foods that are retained on the dentition can accumulate high levels of short-chain carboxylic acids (acetic, formic, lactic and propionic). Since gingival epithelium is the first periodontal tissue to be challenged by oral factors, a study was undertaken to determine whether short-chain carboxylic acids can affect epithelial cells in vitro. Immortalized human oral epithelial cells were grown in supplemented keratinocyte growth medium at 37 degrees C, and the effects of short-chain carboxylic acids were determined with tetrazolium-based and trypan blue exclusion assays. Low concentrations of short-chain carboxylic acids inhibited the growth of human oral epithelial cells, while higher concentrations led to cell death. The effects of short-chain carboxylic acids on the cells were dose-dependent and varied among the individual acids (propionate > formate > lactate > acetate). Growth inhibition was partly reversible and growth resumed after removal of the acids. However, the time needed for recovery of the cells increased with short-chain carboxylic acids concentration, consistent with progressively greater damage to the cells at higher short-chain carboxylic acids concentrations. The observed effects of short-chain carboxylic acids on gingival cells in vitro supported our hypothesis that short-chain carboxylic acids can damage the integrity of gingival epithelium in situ.

Accumulation of fermentable sugars and metabolic acids in food particles that become entrapped on the dentition.

Earlier studies (Kashket et al., 1991) showed that particles of high-starch snack foods remained longer on the teeth than those of high-sucrose, low-starch foods. The question arose whether the prolonged presence of food particles enhances cariogenicity. A study was undertaken to measure sugars, starches, and metabolic acids in retained food particles. Subjects consumed portions of different foods, and particles were removed from all bicuspids and first molars at defined times after swallowing. Dry weights, sugars, and short-chain carboxylic acids were determined. High-sucrose foods were cleared rapidly from the teeth, while high-starch foods were retained for up to 20 min. Sucrose, glucose, and fructose persisted in the retained particles. Particles of high-starch foods accumulated maltose and maltotriose, presumably from the breakdown of starch by salivary amylase. At maximum, maltose plus maltotriose constituted 94% of total sugars in particles of potato chips; corresponding values in doughnuts, peanut butter cookies, and salted crackers were 43, 51, and 61%, respectively. Total fermentable sugars in the particles of high-starch foods were similar to those for the high-sucrose confectionery products. Carboxylic acids accumulated within the particles, presumably due to the fermentation of the sugars by entrapped salivary micro-organisms. At maximum (5 to 7 min), acetic, formic, lactic, and propionic acids rose 17-, 30-, 15-, and 1.3-fold, respectively, in doughnuts, and to smaller degrees in potato chips, salted crackers, and chocolate-caramel-peanut bars. In summary, the study demonstrated the persistence of sugars, the progressive accumulation of starch breakdown products, and the fermentation of the accumulated sugars in retained food particles. The findings support the view that high-starch foods contribute to the development of caries lesions.

Effects of a high-bicarbonate dentifrice on intraoral demineralization.

Dentifrices available on the market today contain sodium bicarbonate in a wide range of concentrations. Anticaries efficacy has been demonstrated for these dentifrices in a variety of tests. New insights were gained in the present study in which the effect of a high-bicarbonate dentifrice on the sucrose-induced demineralization of tooth enamel in situ was examined. With the intraoral Delta Ip system it is possible to follow the minute changes in tooth enamel that essentially model the daily episodes of demineralization accompanying the ingestion of various foods. The results revealed a pronounced effect on the pH of the test plaque and a considerable reduction in mineral loss from the enamel. The effect persisted from more than 1 hour and, during that time, appeared to predominate over the effect of fluoride. These findings suggest that bicarbonate may provide additional protection against the loss of tooth enamel. Such effects may be significant for the design of new high-bicarbonate products.

Enamel rehardening with cheese in irradiated patients.

Radiotherapy of head and neck malignancies results in severe xerostomia which induces radiation caries. Hard cheese has potent anti-cariogenic effects, even with minimal salivary gland function. Eight patients irradiated for neck cancer volunteered for this study. The saliva flow rate varied between 0.0-0.15 ml/minute. In vitro etched enamel slabs, prepared from human teeth, were exposed intraorally to parafilm stimulated salivary secretion for 5 minutes or, alternatively, to cheese compounds and saliva due to masticating 20 gm hard cheese for 5 minutes. Microhardness measurements were carried out on the enamel surface at start (baseline), after etching and after rehardening. Stimulated saliva or cheese compounds and saliva, due to mastication, induced rehardening of surface enamel in both, non-irradiated and irradiated subjects. The rehardening was significantly increased in the irradiated group consuming cheese as compared to rehardening by stimulated saliva only and not significantly less of that achieved in non-irradiated subjects. Rehardening achieved with stimulated saliva in irradiated patients was of a borderline-significant lower degree in comparison to non-irradiated subjects. The reduced rehardening capacity of a decreased saliva flow in irradiated patients may be complemented by cheese compounds. For xerostomic patients, hard cheese consumption may be regarded as effective to keep initial caries under control.

Delayed effect of wheat starch in foods on the intraoral demineralization of enamel.

There is considerable evidence for an association between dental caries and food starches. However, the intraoral utilization of starch may be quite complex, giving rise to conflicting results. Demineralization induced by unsweetened cookies was examined in an intraoral model system that utilized palatal appliances containing blocks of bovine enamel. The enamel surfaces were covered with either a filter paper disc to trap sugars or a layer of Streptococcus mutans to metabolize the sugars and bring about enamel demineralization. Demineralization was determined as an increase in porosity with respect to iodide ions (delta Ip). Measurements revealed a rapid elevation and maintenance of high levels of maltose in the plaque space after ingestion of the unsweetened or sweet cookies. Entrapped food particles appeared to serve as a reservoir of maltose. Unsweetened cookies brought about enamel demineralization, but the pH of the streptococcal plaque fell slowly, and the initiation of demineralization was delayed. Thus, delta Ip and plaque pH were -0.3 +/- 1.3 U and 6.1 +/- 0.3, respectively, after 15 min. The delay was shown to be related to the need to induce the acidogenic streptococci to metabolize maltose. Once induced, delta Ip rose rapidly and reached a maximum at 45 min. Sweet cookies released sucrose and maltose and brought about a rapid onset of demineralization. In summary, the data demonstrated (1) that maltose was released rapidly from unsweetened cookie particles and diffused into the plaque space of the model system and (2) that maltose-dependent demineralization of enamel required time for the induction of the streptococcal cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Validation of the intraoral delta Ip system and use of the system to test the efficacy of Mentadent dentifrice.

Ongoing efforts within the oral care industry to improve dentifrices by the addition of anti-tartar compounds, bicarbonate and other agents, have necessitated the continuing evaluation of new products in order to assure their anti-caries effectiveness. However, clinical evaluation of new products is time consuming, prohibitively expensive and ethically questionable. Recently, a number of intraoral models have been developed that appear to be well-suited to evaluate new products. In the present study, an intraoral system was used that monitors short-term demineralization of surface enamel. Subjects wore appliances that contained Streptococcus mutans-coated blocks of bovine enamel and rinsed first with 15 ml of a 20% slurry of dentifrice and, after 30 minutes, with a 10% sucrose solution. Iodide penetrability (Ip) was determined before and after each intraoral exposure, and the difference, or delta Ip, was taken as the measure of demineralization. The model system responded linearly to increasing concentrations of fluoride in a series of standard dentifrice preparations. Mentadent, a fluoride toothpaste with baking soda and peroxide, was shown to reduce enamel demineralization and to provide protection comparable to a clinically tested dentifrice (Crest Regular). These results established the validity of the delta Ip method, and demonstrated the efficacy of Mentadent according to the criteria established at the ADA Consensus Conference on Intraoral Models in 1990.

Reduction of intra-oral demineralization of enamel after single exposures to sodium fluoride.

Studies demonstrated the effects of single rinses with low concentrations of NaF on the intra-oral demineralization of enamel. Blocks of bovine enamel were covered with Streptococcus mutans IB1600, mounted in palatal appliances, and worn in the mouths of volunteers for specified times. Subjects rinsed with solutions of NaF, with or without sucrose. Demineralization was determined as changes in iodide penetrability (delta Ip) of the enamel, while the pH and F of the streptococcal plaque, and enamel F, were determined with ion-specific electrodes. Delta Ip was reduced by about 80% (from 14.5 +/- 2.7 to 2.8 +/- 2.3 units) when 250 micrograms F/mL was added to the sucrose rinse. Corresponding plaque pH's were 4.1 +/- 0.5 and 4.2 +/- 0.3, consistent with a lack of effect on bacterial acidogenesis. Protection against mineral loss was concentration-dependent. Administration of sucrose at different times after NaF revealed that the effect of F persisted for at least 60 min. Analyses of plaque F demonstrated an initial elevation and concentration within the cells, followed by a drop to stable, baseline values. Enamel F increased slowly to almost 500 micrograms/g enamel after 105 min. The protective effect of F appeared to be manifested in two stages, the first related to a high plaque F and the second to F that became incorporated into the enamel. Analysis of the data suggested that F was transferred from plaque to enamel during the experimental period.

Effect of timing of administered calcium lactate on the sucrose-induced intraoral demineralization of bovine enamel.

A number of soluble calcium salts are known to reduce the demineralization of enamel in the mouth. The present study was undertaken to examine the effects of rinses containing different concentrations of calcium lactate, and the time of giving the rinses with respect to sucrose challenges. Subjects wore palatal appliances containing blocks of bovine enamel whose surfaces were covered with Streptococcus mutans IB 1600, and rinsed with 10% sucrose for 1 min. Changes in iodide penetrability of the enamel, and the pH and extracellular ion concentrations of the streptococcal plaque were determined. When added to the sucrose rinse, 100 or 150 mM calcium lactate reduced demineralization by about 35%, although the plaque pH was not affected. Plaque calcium was elevated but diffused away rapidly so that concentrations after 45 min were close to control values. Plaque inorganic phosphate and lactate were not affected. Ongoing demineralization appeared to be stopped when 100 mM calcium lactate was given 15 min after the sucrose rinse. When the lactate was given 15 min before the sucrose rinse, demineralization was reduced by only about 25%, consistent with the rapid diffusion of plaque calcium. The combination of (i) pretreatment with calcium lactate and (ii) admixture of calcium lactate with sucrose was most effective. Demineralization was reduced about 55% with 100 mM calcium lactate under these conditions, and protective effects were seen with as little as 25 mM. In summary, the findings demonstrate the enamel-protective effect of relatively low concentrations of calcium lactate, and point to the need to sustain a high plaque calcium during periods of maximum acidogenicity.

Limitations in the intraoral demineralization of bovine enamel.

A model system was used to examine the relation between the duration of plaque pH fall and enamel demineralization following the intake of dietary carbohydrate in humans. Subjects wore palatal appliances containing blocks of bovine enamel covered with Streptococcus mutans IB 1600, and rinsed with 5 or 10% sucrose. Changes in iodide penetrability (delta Ip) of the enamel, and the pH and extracellular calcium and inorganic phosphate (Pi) concentrations of the streptococcal plaque were determined. Following rinses with 5% sucrose, delta Ip increased with time and reached a maximum (11.2 +/- 2.2 units) at 45-60 min although the S. mutans plaque remained acidic (pH = 4.8 +/- 0.6). After 10% sucrose, the maximum (14.7 +/- 3.1 units) was reached while the plaque pH was 4.0 +/- 0.3. Second rinses with sucrose increased delta Ip at most by 30%. Thus, demineralization did not persist throughout the period of low plaque pH, but occurred primarily during the early phase of plaque acidogenesis. Enamel demineralization appeared to be limited by factors other than the pH of the streptococcal plaque. Calcium concentrations in the S. mutans plaque rose to a maximum of 10.9 +/- 2.8 mEq/l at 30 min after the 5% sucrose rinses, then fell; Pi reached a stable level of 12.2 +/- 2.3 mEq/l by 60 min. Calculations showed that conditions approached saturation with respect to enamel and dicalcium phosphate dihydrate as demineralization reached a maximum. Demineralization appeared to be limited at low plaque pH, therefore, by the accumulation of high levels of mineral ions in the streptococcal plaque.(ABSTRACT TRUNCATED AT 250 WORDS)

Lack of correlation between food retention on the human dentition and consumer perception of food stickiness.

When dental health professionals advise that sticky foods be avoided, it is left to the consumer to choose correctly among different foods. In this study, comparisons were made among consumer ratings of stickiness of 21 commercially available foods and objective measurements of tooth retention of each of the foods. No correlation was found between the two, and neither the rates of clearance of food particles from the teeth nor the rates of clearance of food-derived sugars from the saliva correlated with ratings of food stickiness. Cookies, crackers, and potato chips were most retentive, whereas caramels, jelly beans, raisins, and milk chocolate bars were among those poorly retained. Clearance rates appeared to vary inversely with initial retention. However, chocolate-caramel bars exhibited high initial retention and a very rapid rate of clearance from the teeth. The findings show that consumers cannot accurately assess the retentiveness of foods and, thus, the advise simply to avoid sticky ones is inadequate.

The effect of sucrose and fat in cookies on salivation and oral retention in humans.

Six adults were served accurately weighed portions (about 5 g) of cookies varying in sucrose and fat content. The cookies were chewed and spat out at the time the subjects were ready to swallow. Additional spittings were collected at intervals up to two, three, and four min. Chewing time decreased with increase in sucrose, or with increase in fat. The volume of saliva in each spitting was calculated from its wet and dry weights, and it was assumed either (a) that saliva produced during chewing was not carried over in the retained food, or (b) that saliva was incorporated in the retained food in the same proportion as in the first spitting. Both approaches revealed that salivary flow rates were independent of cookie formulation, with two exceptions: (1) The cookie highest in sucrose produced a significantly higher flow rate during chewing, and (2) the fat-free cookie, which was hard to chew, elicited an elevated flow rate up to two min. The total volume of saliva for the entire experimental period was similar for all formulations, except the latter. Masticatory effects, therefore, appeared to predominate over sweetness stimulation, unless sugar content was very high. The volume of saliva in the food bolus at the time of swallowing correlated with chewing time. Oral clearance of the cookies did not give straight lines when logarithms of retained material were plotted against time. Initial clearance rates appeared to diminish with increasing sucrose and fat content of the cookies. Effects of sugar and fat on all parameters may reflect changes in cookie texture and the sizes of particles produced within the mouth.