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A MIXED-BACTERIA ECOLOGICAL APPROACH TO UNDERSTANDING THE ROLE OF THE ORAL BACTERIA IN DENTAL CARIES CAUSATION: AN ALTERNATIVE TO STREPTOCOCCUS MUTANS AND THE SPECIFIC-PLAQUE HYPOTHESIS

Department of Oral Biology and Pathology, State University of New York, Stony Brook, New York 11794-8702

View larger version (29K): [in a new window]   Figure 1. Relation between the Stephan pH challenge test and dental caries activity in maxillary and mandibular incisor plaque of subjects with different levels of caries activity. The challenge was a 10% (w/v) glucose solution administered as a rinse (25 mL) for two min, and the pH was measured with an antimony-rod touch-type pH electrode (adapted from Stephan, 1944, and reproduced from Kleinberg et al., 1982).

View larger version (32K): [in a new window]   Figure 2. The effect of the availability of glucose and urea substrate on the pH of dental plaque in situ. Availability can be prolonged as shown here by raising the concentration of the challenge substrate or extending the time that substrate is available to the plaque bacteria (from Kleinberg, 1970b).

View larger version (13K): [in a new window]   Figure 3. Vector format of the two types of acid-base pH curves that result from short and long periods of exposure to glucose or urea as seen in Fig. 2. A Type A response results when substrate is limited. A Type B response results when substrate is in excess (adapted from Kleinberg, 1977b).

View larger version (22K): [in a new window]   Figure 4. (a) Relation between time of eating and the pH of dental plaque in 18 different interproximal and facial/lingual dentition locations throughout the human mouth. Highest pH occurred in plaque in the mandibular interproximals of the lower incisors. Lowest pH occurred in the same sites of the upper incisors (see Kleinberg and Jenkins, 1964, for the specifics of the individual sites). Mean resting saliva pH was 6.7 (from Kleinberg, 1970b). (b) Range of pH of plaque on upper and lower approximal incisor surfaces in slower and faster salivary secreters. The dotted lines represent the mean resting salivary pH of the two groups (from Jenkins, 1979, based on data in Kleinberg and Jenkins, 1964).

View larger version (21K): [in a new window]   Figure 5. The effect on plaque pH levels of rinsing for 2 min, first with 100 mL of a 1% and then with 100 mL of a 20% (w/v) glucose solution. Each point is the mean pH of 2 plaque sites in each of five subjects. Each rinse was divided into two 50-mL portions, and rinsing with each was for 1 min (adapted from Kleinberg et al., 1981).

View larger version (31K): [in a new window]   Figure 6. Effects of various levels of salivary supernatant on the pH of salivary sediment incubation mixtures incubated with (a) 2.8, (b) 5.6, and (c) 28.0 mM glucose (0.05, 0.1, and 0.5% w/v, respectively). Shown in (d) are the effects in salivary sediment incubation mixtures of 33.3% (v/v) salivary supernatant from centrifuged whole saliva on the utilization of glucose at 2.8 and 28.0 mM glucose (adapted from Kleinberg et al., 1973).

View larger version (22K): [in a new window]   Figure 7. Examples of pH responses of related arginolytic and non-arginolytic bacteria (see Table) mixed in a 1:1 ratio and incubated with glucose at 4.2 mM and arginine at 3.3 mM. Total bacterial cell concentration was 8.3% (v/v). In all cases, the mixing of pure cultures of oral bacteria produced an intermediate result (from Wijeyeweera and Kleinberg, 1989b).

View larger version (25K): [in a new window]   Figure 8. In vitro pH response of pooled dental plaque to which (a)S. mutans GS-5 (serotype c), (b)S. sanguis II (i.e., oralis) isolated from saliva, (c)L. casei, or (d)A. viscosus had been added. Incubation mixtures were prepared as in Fig. 7. All four strains are generally considered to be cariogenic. Note that none has pH-raising capability (Table). In each case, the Stephan pH response was made more acidogenic with their addition (from Wijeyeweera and Kleinberg, 1989a).

View larger version (22K): [in a new window]   Figure 9. (a) Main metabolic processes associated with the pH vectors that characterize dental plaque acid-base metabolism. Vectors 1 and 4 produce base; Vectors 2 and 3 produce acid. Dashed line represents neutrality, and SCCA is the abbreviation for short-chain carboxylic acids. (b) Diagrams 1 and 2 characterize plaque with balanced acid-base metabolisms; 1 is for thicker and 2 is for thinner plaque (Imfeld, 1983). Diagram 3 characterizes plaque where alkali formation is more dominant, whereas in 4, acid formation dominates (modified from Kleinberg and Westbay, 1992).

View larger version (26K): [in a new window]   Figure 10. Catabolism of 2.8 mM glucose when a rapid glucose fermenter, L. fermentum, is added to salivary sediment in A and to dental plaque in C at a 1:1 ratio. Shown in B and D are the results when a slow glucose fermenter, H. parainfluenzae, is similarly provided (from Ryan and Kleinberg, 1995a).

View larger version (23K): [in a new window]   Figure 11. Relation between the pH of the supernatant of whole saliva (after 10,000 g centrifugation) and aggregation of its constituents. A high-pH plaque favors formation of a higher calcium phosphate and lower carbohydrate protein containing aggregate; a low-pH plaque favors the reverse. Indicated in the Fig. are pH ranges of different kinds of plaque. Possible variation in saliva pH is shown in Fig. 13 (from Kleinberg et al., 1977).

View larger version (26K): [in a new window]   Figure 12. Comparison of the solubilization rates of human tooth enamel slices and salivary precipitin samples prepared from seven different subjects (identified by initials) (from Kleinberg et al., 1994).

View larger version (18K): [in a new window]   Figure 13. Role of saliva in the various calcium phosphate reactions that occur at the tooth-plaque-saliva interface. Saliva provides calcium and phosphate (i) as ions and (ii) as part of a calcium phosphate carbohydrate protein complex (i.e., salivary precipitin). Both help provide a continuous supply of calcium and phosphate for plaque and tooth mineralization. At acidic pH (high H+ concentration), movement of calcium and phosphate from tooth and plaque to saliva is favored, whereas at alkaline pH, the reverse is favored. The calcium and phosphate ions produced in the plaque from plaque calcium phosphate during acid formation are in a position to suppress or retard tooth solubilization by mass action as well as to facilitate tooth remineralization (from Kleinberg et al., 1983).

View larger version (22K): [in a new window]   Figure 14. Relationship between pH and rate of solubilization of calcium phosphate at the tooth-plaque-saliva interface. Enamel calcium phosphate is mostly hydroxyapatite. Plaque calcium phosphate is x-ray amorphous or poorly crystalline brushite and apatite (Kaufman and Kleinberg, 1973). Since tooth and plaque in vivo are parts of an open system, rates of solubilization are expressed as Ca or P solubilized per unit time. Because plaque calcium phosphate is solubilized more easily than enamel hydroxyapatite, higher plaque fluid levels of calcium and phosphate ions are ensured. As shown, one can expect cariogenic plaque to range over the acidic part of the range shown, calculogenic plaque over the alkaline part, and normal plaque in between (see Fig. 11). Saliva pH covers a narrower range (from Kleinberg et al., 1983).