Effects of acidification on growth and glycolysis of Streptococcus sanguis and Streptococcus mutans

After carbohydrate intake, pH in dental plaque decreases rapidly and reaches about 4 within a few minutes. The acidification not only promotes demineralization of tooth surface but can also cause damage to bacteria in dental plaque. We, therefore, investigated the effect of acidification on the dental plaque bacteria Streptococcus sanguis and Streptococcus mutans. At pH 4.0 and 4.2, both growth and glycolytic activities in these streptococci were repressed. Prolonged acidification (for 60 min at pH 4.0) not only repressed both growth and glycolytic activities but also impaired them in S. sanguis cells with concomitant inactivation of the glycolytic enzymes, hexokinase, phosphofructokinase, glyceraldehyde-phosphate dehydrogenase and enolase. The impaired abilities of glycolysis and growth recovered following incubation at pH 7.0 for 80–90 min, and this was accompanied by reactivation of the glycolytic enzymes. On the other hand, these impairments were not observed in S. mutans cells exposed to prolonged acidification. These results indicate that the low pH frequently occurring in dental plaque may transiently impair streptococcal glycolysis and growth and that S. mutans is more durable to the acidification than S. sanguis.     

Physiologic actions of zinc related to inhibition of acid and alkali production by oral streptococci in suspensions and biofilms

Zinc is a known inhibitor of acid production by mutans streptococci. Our primary objective was to extend current knowledge of the physiologic bases for this inhibition and also for zinc inhibition of alkali production by Streptococcus rattus FA-1 and Streptococcus salivarius ATCC 13419. Zinc at concentrations as low as 0.01-0.1 mm not only inhibited acid production by cells of Streptococcus mutans GS-5 in suspensions or in biofilms but also sensitized glycolysis by intact cells to acidification. Zinc reversibly inhibited the F-ATPase of permeabilized cells of S. mutans with a 50% inhibitory concentration of about 1 mm for cells in suspensions. Zinc reversibly inhibited the phosphoenolpyruvate: sugar phosphotransferase system with 50% inhibition at about 0.3 mm ZnSO4, or about half that concentration when the zinc-citrate chelate was used. The reversibility of these inhibitory actions of zinc correlates with findings that it is mainly bacteriostatic rather than bactericidal. Zinc inhibited alkali production from arginine or urea and was a potent enzyme inhibitor for arginine deiminase of S. rattus FA-1 and for urease of S. salivarius. In addition, zinc citrate at high levels of 10-20 mm was weakly bactericidal.     

Mutans streptococci and non-mutans streptococci acidogenic at low pH, and in vitro acidogenic potential of dental plaque in two different areas of the human dentition.

Samples of human dental plaque were obtained from sound tooth surfaces in the lower anterior and upper posterior areas of each of 11 subjects with various degrees of caries experience. Both types of plaque were compared for: (1) their pH-lowering potential [pH at 10 and 60 min after sugar addition and the pH drop between 0 and 10 min (delta pH)] with an in vitro method involving dispersed plaque suspensions and excess glucose supply; (2) the proportions of mutans streptococci; and (3) the distribution of the predominant non-mutans streptococci according to their final pH in glucose broth. Compared with plaque from the lower anterior area, plaque from the upper posterior area exhibited a significantly higher pH-lowering potential, i.e., a lower pH at 10 and 60 min and a greater delta pH and significantly higher levels of mutans streptococci. The final pH values for the non-mutans streptococci exhibited a wide range from about 4.4 to over 5.0. The proportions of such organisms designated as capable of acidogenesis at low pH (final pH less than 4.6), whether expressed as a percentage of the total non-mutans streptococci or of the total plaque flora, were significantly increased in plaque from the upper posterior area. The proportions of non-mutans streptococci capable of acidogenesis at low pH in plaque from the upper posterior area were also significantly increased, with decreasing pH values at 10 and 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Membrane locus and pH sensitivity of paraben inhibition of alkali production by oral streptococci

Parabens were found to be potent inhibitors of alkali production from arginine by oral streptococci such as Streptococcus rattus, Streptococcus sanguis and Streptococcus gordonii. For example, 2 mumol butylparaben per ml completely and irreversibly inhibited arginolysis by intact cells of S. rattus FA-1 and was lethal for the organism. In contrast, butylparaben was not a very effective inhibitor of ureolysis by intact cells of Streptococcus salivarius 57.I, although it did kill the cells. Butylparaben irreversibly inhibited the cytoplasmic enzymes arginine deiminase, carbamate kinase and urease in permeabilized cells or isolated form. However, inhibition of arginolysis by intact cells appeared to be due primarily to irreversible inhibition of transport systems for arginine uptake, because butylparaben added to intact cells did not reduce levels of arginine deiminase when the cells were subsequently permeabilized after washing. The insensitivity of ureolysis by intact cells to butylparaben can be related to the known high permeability of cell membranes to urea and the cytoplasmic location of urease. The potency of butylparaben as an inhibitior of arginolysis or glycolysis and as a lethal agent was found to be greater at acid pH that at neutral or alkaline pH.     

Fluoride, triclosan and organic weak acids as modulators of the arginine deiminase system in biofilms and suspension cells of oral streptococci

Introduction:  The arginine deiminase system (ADS) of oral bacteria is a major generator of alkali (ammonia) in dental plaque and is considered to have anticaries effects. However, many of the antimicrobial agents used in oral care products may reduce alkali production by the ADS. The objective of our work was to assess the sensitivity of the ADS of oral streptococci to commonly used antimicrobials, fluoride, triclosan and organic weak acids.
Methods:  Streptococcus sanguinis NCTC 10904 and Streptococcus ratti FA-1 were grown in suspension cultures and mono-organism biofilms. ADS activity at pH values of 4, 5 and 6 was assessed, and the actions of the agents was determined in terms of reduced production of alkali from arginine, inhibition of ADS enzymes and changes in uptake of arginine.
Results:  ADS activity was not greatly affected by pH changes between 4 and 6 and was greater per unit of biomass for cell suspensions than for biofilms. NaF was a poor inhibitor, while triclosan was highly effective with a 50% inhibitory dose for the two organisms between 0.03 and 0.05 and between 0.10 and 0.15 m m -h for suspension cells and biofilms, respectively. The weak acid indomethacin was nearly as potent at pH 4.0 as triclosan, while capric and lauric acids were less potent, especially for biofilms. The methyl ester of lauric acid was slightly stimulatory. The major targets for the inhibitors appeared to be transport systems for arginine uptake, although carbamate kinase was a secondary target.
Conclusion:  Triclosan, indomethacin, caprate and laurate can reduce ADS activity in dental plaque.     

Transient acid-impairment of growth ability of oral Streptococcus, Actinomyces, and Lactobacillus: a possible ecological determinant in dental plaque

Introduction:  Dental plaque pH decreases to about 4 through bacterial fermentation of carbohydrates and this low pH is maintained for from several minutes to about an hour. Repeated acidification causes demineralization of the tooth surface, resulting in caries formation. The acidification also influences plaque bacteria. Severe acidification kills bacteria efficiently, while physiological acidification, the condition occurring in plaque, kills bacteria partially and may impair growth ability. We, therefore, investigated the effects of physiological acidification on representative caries-related bacteria.
Methods:  Streptococcus mutans , Streptococcus sobrinus , Streptococcus sanguinis , Streptococcus oralis , Lactobacillus paracasei , and Actinomyces naeslundii were used. Effects of physiological acidification at pH 4.0 on cell viability and growth ability, as well as the growth rate of these bacteria at pH 4.0–7.0, were investigated.
Results:  Mutans streptococci and Lactobacillus grew at pH 4.0 but the growth of S. sanguinis and S. oralis ceased below pH 4.2 and pH 4.2–4.4, respectively. Acidification at pH 4.0 for 1 h killed 43–89%, 45% and 35–76% of S. sanguinis , S. oralis , and Actinomyces , respectively. Furthermore, assessment of bacterial growth curves revealed that the growth ability of the surviving cells of S. sanguinis , S. oralis and Actinomyces was impaired, but it was recovered within 2–5 h after the environmental pH had returned to 7.0. The acidification neither killed nor impaired the growth of mutans streptococci and Lactobacillus .
Conclusions:  These results indicate that physiological and transient acidification is not sufficient to kill bacteria, but it causes a temporary acid-impairment of their growth ability, which may function as an ecological determinant for microbial composition in dental plaque.     

The acid-tolerant microbiota associated with plaque from initial caries and healthy tooth surfaces

The intent of this study was to compare the inherent acid tolerance of bacteria in samples of dental plaque from tooth sites in subjects with and without initial caries. Plaque was collected from approximal surfaces showing early enamel caries and from healthy tooth surfaces in the same subjects, as well as from enamel surfaces of caries-free individuals. In addition to plating on blood agar, the plaque samples were plated directly on non-selective solid agar medium buffered to pH 7.0, 6.0, 5.5, 5.0, 4.5 and 4.0 to avoid any loss of adaptation to acid during primary isolation of plaque bacteria. The results showed that approximately 50% of the total cultivable plaque microbiota from caries, as well as healthy tooth sites, was able to grow at pH 5.5 and 1% at pH 5.0, pH values regarded as critical for the demineralization of tooth enamel. At pH 5.0, members of the genus Streptococcus were the dominant group, but mutans streptococci accounted for less than half of the streptococcal viable count. The other acid-tolerant streptococcal isolates included Streptococcus anginosus, Streptococcus constellatus, Streptococcus gordinii, Streptococcus intermedius, Streptococcus mitis, Streptococcus oralis, Streptococcus salivarius and SStreptococcus sanguis. Analysis of the results indicated that the mutans streptococci in dental plaque were highly variable with respect to acid tolerance, and that both caries and healthy sites harboured significant numbers of mutans streptococci that were not acid-tolerant.     

Non-mutans streptococci in patients receiving radiotherapy in the head and neck area

OBJECTIVE: To study mutans and non-mutans streptococci in patients after radiotherapy of the head and neck. METHODS: Oral rinse samples collected from nasopharyngeal carcinoma patients before and after radiotherapy were diluted and cultured on nonselective and selective media for enumeration of total cultivable plaque flora, mutans and non-mutans streptococci and lactobacilli. Non-mutans streptococci were identified biochemically and by 16S rDNA sequence homology analysis. RESULTS: After irradiation, mutans streptococci were not isolated; the levels of Streptococcus mitis and lactobacilli increased significantly. The level of Streptococcus salivarius increased, but the significance was the borderline. The level of Streptococcus sanguis decreased significantly after irradiation. The abundance of other oral streptococci species showed no significant changes. CONCLUSIONS: S. mitis and S. salivarius are the predominant non-mutans streptococci in the high-caries-risk oral flora following radiotherapy.     

The complex oral microflora of high-risk individuals and groups and its role in the caries process

The involvement of the oral biofilm in the caries process requires re-evaluation. The essential role of mutans streptococci (Streptococcus mutans and Streptococcus sobrinus) in the caries process is not proven. Acid production by dental plaque is not dependent upon the presence of mutans streptococci; caries occurs in the absence of these species and their presence does not necessarily indicate caries activity. Other oral bacteria, non-mutans streptococci, Actinomyces spp. and Bifidobacterium spp., are acidogenic and aciduric. They outnumber mutans streptococci in dental plaque, and there are data which support a role for these bacteria in the initiation and progression of caries. Molecular studies demonstrate the great diversity and complexity of the flora associated with caries. Many taxa identified have not been cultured and the role of these taxa is not known. We have, in mutans streptococci, good markers of disease but not necessarily the aetiological agents of the disease. Considerably more research is required to investigate the transition of tooth surfaces from being intact and sound to the white spot lesion stage. A combination of conventional and molecular approaches are required to elucidate the involvement of an individual taxon and of microbial populations with particular traits in the caries process.     

The role of bacteria in the caries process: ecological perspectives

Dental biofilms produce acids from carbohydrates that result in caries. According to the extended caries ecological hypothesis, the caries process consists of 3 reversible stages. The microflora on clinically sound enamel surfaces contains mainly non-mutans streptococci and Actinomyces, in which acidification is mild and infrequent. This is compatible with equilibrium of the demineralization/remineralization balance or shifts the mineral balance toward net mineral gain (dynamic stability stage). When sugar is supplied frequently, acidification becomes moderate and frequent. This may enhance the acidogenicity and acidurance of the non-mutans bacteria adaptively. In addition, more aciduric strains, such as 'low-pH' non-mutans streptococci, may increase selectively. These microbial acid-induced adaptation and selection processes may, over time, shift the demineralization/remineralization balance toward net mineral loss, leading to initiation/progression of dental caries (acidogenic stage). Under severe and prolonged acidic conditions, more aciduric bacteria become dominant through acid-induced selection by temporary acid-impairment and acid-inhibition of growth (aciduric stage). At this stage, mutans streptococci and lactobacilli as well as aciduric strains of non-mutans streptococci, Actinomyces, bifidobacteria, and yeasts may become dominant. Many acidogenic and aciduric bacteria are involved in caries. Environmental acidification is the main determinant of the phenotypic and genotypic changes that occur in the microflora during caries.     

Transient acid‐impairment of growth ability of oral Streptococcus,Actinomyces, and Lactobacillus: a possible ecological determinant in dental plaque

Introduction: Dental plaque pH decreases to about 4 through bacterial fermentation of carbohydrates and this low pH is maintained for from several minutes to about an hour. Repeated acidification causes demineralization of the tooth surface, resulting in caries formation. The acidification also influences plaque bacteria. Severe acidification kills bacteria efficiently, while physiological acidification, the condition occurring in plaque, kills bacteria partially and may impair growth ability. We, therefore, investigated the effects of physiological acidification on representative caries‐related bacteria. Methods: Streptococcus mutans, Streptococcus sobrinus, Streptococcus sanguinis, Streptococcus oralis, Lactobacillus paracasei, and Actinomyces naeslundii were used. Effects of physiological acidification at pH 4.0 on cell viability and growth ability, as well as the growth rate of these bacteria at pH 4.0–7.0, were investigated. Results: Mutans streptococci and Lactobacillus grew at pH 4.0 but the growth of S. sanguinis and S. oralis ceased below pH 4.2 and pH 4.2–4.4, respectively. Acidification at pH 4.0 for 1 h killed 43–89%, 45% and 35–76% of S. sanguinis, S. oralis, and Actinomyces, respectively. Furthermore, assessment of bacterial growth curves revealed that the growth ability of the surviving cells of S. sanguinis, S. oralis and Actinomyces was impaired, but it was recovered within 2–5 h after the environmental pH had returned to 7.0. The acidification neither killed nor impaired the growth of mutans streptococci and Lactobacillus. Conclusions: These results indicate that physiological and transient acidification is not sufficient to kill bacteria, but it causes a temporary acid‐impairment of their growth ability, which may function as an ecological determinant for microbial composition in dental plaque.     

A modified mitis salivarius medium for a caries diagnostic test

A new medium, MSKB, composed of mitis salivarius agar base, sorbitol, kanamycin sulfate and bachracin, has been developed that is more selective for recovery of mutans streptococci (mutans) than the so called mitis salivarius bacitracin (MSB) medium. MSB and MSKB were compared for recovery and selectivity of mutans by plating saliva samples as well as pure cultures on both media. Sixty saliva samples were plated and counted for mutans and non-mutans colonies. Thirty-six samples had greater numbers of non-mutans on MSB than on MSKB, and 14 of the 36 had non-mutans colonies that could be visually confused with mutants. The recovery of mutans on MSKB was approximately 13% less than on MSB. The selectivity and recovery of MSB and MSKB were evaluated over 1–5 months of storage at 4°C. Streptococcus mutans anginosus grew on MSB after 1 month, but not on MSKB. Streptococcus mutans milleri type 2 grew on both media after 4 months.     

Low-cariogenicity of trehalose as a substrate

Objectives: The effects of trehalose on cariogenesis by mutans streptococci were investigated.

Methods: Inhibited effect of trehalose on water-insoluble glucan (WIG) synthesis from sucrose by glucosyltransferase (GTase) of mutans streptococci was assayed. The acid fermentability of trehalose by mutans streptococci was determined by the measurements of pH, and amounts of lactic acid production. Plaque pH was determined by the measurements of collected plaque from volunteers after sugar mouth-rinse. Rat experimental caries was investigated by feeding a sucrose and/or trehalose diet.

Results: Trehalose was not utilized as a substrate for GTase. In addition, trehalose inhibited synthesis of WIG by GTase in the presence of sucrose. Trehalose showed weaker and slower acid fermentation than sucrose by mutans streptococci. The levels of lactic acid production from trehalose by Streptococcus mutans and Streptococcus sobrinus were 24.2 and 59.8% of those from sucrose, respectively. The minimum plaque pH after sucrose mouth-rinse was lower than those after trehalose mouth-rinse in all subjects. Plaque pH after trehalose mouth-rinse never reached critical pH. The substitution of trehalose for sucrose in the rat diet significantly reduced caries scores. Furthermore, rats fed diets containing sucrose and trehalose had significantly lower caries scores than those fed a sucrose diet.

Conclusions: These results suggested that trehalose might be not only lowly cariogenic but also anti-cariogenic, and is promising as a sugar substitute.     

Effects of mouthrinses with triclosan, zinc ions, copolymer, and sodium lauryl sulphate combined with fluoride on acid formation by dental plaque in vivo

Bacteriological tests demonstrated a slight synergistic effect of triclosan and sodium lauryl sulphate (SLS) on the growth of Streptococcus mutans NCTC 10449 and Streptococcus sanguis ATCC 10556 in vitro. A single mouthrinse with SLS (17.4 mM) or SLS plus triclosan (3.5 mM) significantly decreased the number of salivary mutans streptococci in a group of 12 subjects up to 90 min after rinsing. The effect on plaque pH of a mouthrinse with either 12.0 mM NaF, NaF plus 10.0 mM zinc acetate, NaF plus 17.4 mM SLS, or NaF plus SLS plus 3.5 mM triclosan with or without the addition of zinc ions or 0.65% w/v of a polyvinylmethyl ether/maleic acid copolymer was investigated. The plaque pH responses to a 10% w/v sucrose mouthrinse were measured in 2-day-old plaque with microtouch pH electrodes in six groups of 10 subjects 90 min after a single mouthrinse with test solution. There was no significant difference in plaque pH between the various mouthrinses. In conclusion, triclosan enhanced the growth-inhibitory activity of SLS against oral streptococci in vitro but not against salivary mutans streptococci in vivo. Neither triclosan incorporated into a mouthrinse containing SLS plus fluoride, nor the addition of zinc ions or copolymer affected acid formation by dental plaque in vivo.     

The effect of a single application of 40% chlorhexidine varnish on the numbers of salivary mutans streptococci and acidogenicity of dental plaque

The relationship between the numbers of salivary mutans streptococci and the acid production in dental plaque after a single application of the 40% chlorhexidine varnish EC40 has been studied. Thirteen healthy subjects were treated with EC40 varnish. Saliva samples were taken before and up to 12 weeks after treatment to count mutans streptococci and lactobacilli. At the same time points plaque samples were taken before and after sucrose challenge and analyzed for protein and organic acid. Suppression of salivary mutans streptococci was observed together with a reduced production of lactic acid in sucrose-challenged dental plaque in 9 subjects while inhibition of acid production without significant suppression of mutans streptococci was observed in the other 4 participants. The duration of the effects differed among the individuals but never exceeded 6 weeks. We conclude that a prolonged suppression of mutans streptococci and acid production was not achieved by a single treatment with EC40 varnish in all subjects. Moreover, reduced acidogenicity of dental plaque after chlorhexidine treatment was not necessarily predicted by suppression of mutans streptococci in saliva.     

Bacteriological evaluation of mutans streptococci using modified mitis-salivarius-bacitracin (MSB) agar medium in primary dentition period

Mutans streptococci considered causative agents of dental caries are indigenous to the oral cavity. Modified mitis-salivarius-bacitracin (MSB) agar medium was supplied by BML. This media has characters to grow mutans streptococci very well and to inhibit of non-mutans streptococci. However, little is known about studies using this medium. In this study, we assessed the utility of modified MSB medium and discuss the relation between mutans streptococci and dental caries in primary dentition period. Modified MSB medium was found to be a suitable medium to isolate and quantify mutans streptococci since it could permit selective growth of mutans streptococci. Moreover, this medium inhibited to non-mutans streptococci (S. anginosus and S. intermedius), completely. The detection rate of Streptococcus mutans and Streptococcus sobrinus increased in proportion to the severity of dental caries in the nursery children. From these results, modified MSB agar medium is useful in the judgment to detect the mutans streptococci.     

On the pH-lowering potential of lactobacilli and mutans streptococci from dental plaque related to the prevalence of caries

Abstract The common method used today to identify persons at risk of dental caries is to estimate the numbers of cariogenic bacteria such as lactobacilli and mutans streptococci in saliva or plaque samples taken from the patient. However, the value of these bacterial counts for explaining and predicting individuals at risk of caries has not been powerful enough. Evaluating one virulence factor such as the acidogenicity of these bacteria might increase their explanatory values for caries. Sixty children aged 14–15 yrs participated in this study. Smooth surface caries and restorations were registered and total plaque samples collected. Counts of lactobacilli and mutans streptococci were estimated, and the pH-lowering potential of both bacteria was measured in an adapted glucose broth. The results showed a weak association between dental caries and lactobacilli, but in the subgroup with this bacterium the explanatory value increased to 14% and in the subgroup with a strong pH-lowering potential it was as high as 27%. For mutans streptococci the associations were weak in all groups.     

Effect of xylitol on mutans streptococci and lactic acid formation in saliva and plaque from adolescents and young adults with fixed orthodontic appliances

This study aimed to investigate two dose regimens of xylitol-containing tablets on the ecology of dental plaque and saliva during treatment with fixed orthodontic appliances. The study group comprised 56 healthy patients (mean age 15.8 yr) randomly assigned into the following groups: A, (n = 23) two xylitol tablets two times a day (1.7 g xylitol d(-1)) for 18 wk; B, (n = 23) two tablets four times per day (3.4 g xylitol d(-1)) for 18 wk; and C, (n = 10) no tablets. The levels of mutans streptococci (ms) were enumerated in plaque and saliva and the proportion of xylitol-sensitive (X(S)) strains in saliva was determined by autoradiography with [(14)C]-xylitol at baseline and at 6, 12, and 18 wk. The lactic acid formation rate was assessed enzymatically in sucrose-challenged plaque suspensions. A drop in salivary ms levels was found in Group A after 6 wk but not after 12 or 18 wk. The proportion of X(S) ms was decreased after 6 wk in groups A and B and remained so during the experimental period. The lactic acid formation rates decreased slightly ( approximately 10%) in the two xylitol groups compared with baseline. In conclusion, our results showed that although an alteration of ms strains was demonstrated following a regular daily low-dose intake of xylitol, the long-term total ms counts in plaque and saliva as well as plaque acidogenicity remained unchanged.     

Lactobacillus-mediated interference of mutans streptococci in caries-free vs. caries-active subjects

In order to assess whether naturally occurring oral lactobacilli have probiotic properties, lactobacilli were isolated from saliva and plaque from children and adolescents, with or without caries lesions. The interference capacities of these lactobacilli were investigated against a panel of 13 clinical isolates and reference strains of Streptococcus mutans and Streptococcus sobrinus, as well as against the subject's autologous mutans streptococci, using the agar-overlay technique. Lactobacillus-mediated inhibition differed significantly between the three subject groups (no caries, arrested caries, or active caries), demonstrating increased inhibition in subjects without present or previous caries experience compared to subjects with arrested caries or subjects presenting with frank lesions. Lactobacilli from subjects lacking S. mutans inhibited the growth of the test panel of mutans streptococci significantly better than lactobacilli from subjects who were colonized. Furthermore, subjects without caries experience harbored lactobacilli that more effectively repressed the growth of their autologous mutans streptococci. Twenty-three Lactobacillus spp. completely inhibited the growth of all mutans streptococci tested. Species with maximum interference capacity against mutans streptococci included Lactobacillus paracasei, Lactobacillus plantarum, and Lactobacillus rhamnosus. Naturally occurring oral lactobacilli significantly inhibited the growth of both test strains of mutans streptococci and the subject's autologous mutans streptococci in vitro, and this effect was more pronounced in caries-free subjects.     

Utilization and acid production of beta-galactosyllactose by oral streptococci and human dental plaque

Beta-galactosyllactose is a trisaccharide containing the beta-galactosidic linkage at the nonreducing end. The purpose of this study was to determine whether certain oral streptococci could utilize four kinds of beta-galactosyllactoses. Three of four beta-galactosyllactoses were unable to support growth of the oral streptococci and to be a substrate for producing acid from the cell suspensions and dental plaque. 4'-beta-Galactosyllactose supported growth of Streptococcus sanguis ATCC 35105, ATCC 49298, Streptococcus mitis ATCC 15914, Streptococcus oralis ATCC 35037, ATCC 10557 and Streptococcus milleri 10707 and produced acid from dental plaque. Although beta-galactosidase activities were observed in all the strains, 4'-beta-galactosyllactose could not be used as a carbon source for the growth of mutans streptococci. Enzymes metabolizing 4'-beta-galactosyllactose were induced when S. oralis ATCC 10557 was cultured in medium containing galactose. These results suggested that 4'-beta-galactosyllactose could be as cariogenic as lactose if it is consumed frequently and retained for a long period in the mouth.