Cariogenicity of mutans streptococci

Cariogenicity of mutans streptococci
Mutans streptococci are acidogenic as well as aciduric and can adhere to tooth surfaces (Gibbons et al, 1986). Mutans streptococci can produce extracellular and intracellular polysaccharides from sucrose. Intracellular polysaccharides in particular can be degraded during periods of low nutrient supply, indicating that these polysaccharides increase the virulence of some MS species (S mutans and S sobrinus). 
Because the microbial ecology of the mouth is highly complex, strains of the same species could vary considerably in virulence (Bowden and Edwardsson, 1994). In other words, MS fulfill all the requirements of caries-inducing bacteria. 
Colonization of the teeth by mutans streptococci is highly localized; some tooth surfaces are colonized but not others. The amount of mutans streptococci in saliva is related to the number of colonized surfaces (Lindquist et al, 1989). This is the basis for saliva tests for MS. A high count in saliva (more than 1 million colony-forming units [CFUs] per 1 mL of saliva) indicates that most teeth are colonized by these bacteria, ie, that many tooth surfaces are subject to increased caries risk. However, a salivary MS count does not provide information about the origin of the bacteria, ie, the specific tooth surfaces which are colonized. 
The most common types of mutans streptococci, Streptococcus mutans (serotypes c, e, and f) and Streptococcus sobrinus (serotypes d and g), are present worldwide. Their prevalence differs among populations. Test values also differ, depending on the method of detection (Axelsson et al, 1987b; Bratthall et al, 1986; Beighton et al, 1989; Buischi et al, 1989; for reviews, see Bratthall, 1991; Carlsson, 1988). About 10% to 30% of a population may have little or no MS, 0 to 100,000 CFUs/mL of saliva. The percentage of individuals with very high levels of MS (> 1 million
CFUs/mL of saliva) in a population may vary considerably, depending on age, caries prevalence, dietary habits, and so on.
Several cross-sectional studies in human populations with relatively high caries prevalence have shown a correlation between very high salivary MS levels and very high caries prevalence (Axelsson et al, 1999b; Buischi et al, 1989; Klock and Krasse, 1977; Salonen et al, 1990; Zickert et al, 1982). This is exemplified in Fig 22, from a study of 12-year-old Brazilian children (Buischi et al, 1989). However, in populations with relatively low caries prevalence and high standards of oral hygiene, the threshold value of more than 1 million CFUs of MS/mL of saliva no longer seems to apply, as exemplified in Fig 23, from a study of 13- to 14-year-old schoolchildren in Karlstad, Sweden (Kristoffersson et al, 1986). In this population, the critical difference was between MS-negative and MS-positive subjects. 
As also shown in Fig 23, it was impossible to find any correlation between intake of sticky sugar products (estimated point scale) and caries prevalence, highlighting the multifactorial nature of dental caries: The lower the prevalence and incidence of caries in a population, the more difficult it is to demonstrate a significant correlation for one single etiologic or modifying factor.
Transmission. Because MS require a hard, nondesquamating surface for colonization (Berkowitz et al, 1975; Carlsson et al, 1975; Catalanotto et al, 1975; Stiles et al, 1976), infants do not harbor MS until some time after tooth eruption: The major source of the infection is thought to be maternal. Evidence for this comes from several studies showing that isolates of MS harbored by mothers and their children exhibit similar or identical bacteriocin profiles (Berkowitz and Jordan, 1975; Berkowitz and Jones, 1985; Davey and Rogers, 1984) and identical plasmid or chromosomal DNA patterns (Caufield et al, 1985, 1986, 1988; Caufield and Walker, 1989; Hagan et al, 1989; Kulkarni et al, 1989).
Several studies have suggested that the extent of MS colonization and, to some degree, subsequent carious activity experienced by a child may be correlated with the mother’s salivary level of MS: Mothers with high levels of MS tend to have children with high levels and vice versa (Caufield et al, 1988; Kohler et al, 1984; Kohler and Bratthall, 1978; van Houte et al, 1981). While correlations between caries or MS levels in mothers and those in their children may be explained in part by common genetic or environmental factors, others have suggested that a child’s degree of
colonization or disease may be dictated by the mother’s levels of MS at the time of transmission. In a landmark study, Kohler and coworkers (1983, 1984) selected mothers with initially high levels of MS in saliva and determined the effects of various preventive and treatment regimens aimed at reducing MS below a predetermined threshold level. Children of these mothers were monitored for initial acquisition of MS and, subsequently, for carious activity over a 3-year period. A statistically significant difference was observed between control and experimental
groups in terms of when a child acquired MS, the levels of MS harbored by the mother and child, and the child’s caries outcome. Figure 24, from the longitudinal study by Kohler et al (1988), illustrates that the earlier the colonization by MS, the higher the caries prevalence at 4 years of age.
In a recent study by Caufield et al (1993), oral bacterial levels of 46 mother-child pairs were monitored from the birth of the child to 5 years of age to study the acquisition of MS by the children. In 38 children, initial acquisition occurred at the median age of 26 months, during a discrete period that was designated as the “window of infectivity.” In the remaining eight children (17%), MS was undetectable throughout the study (median age 56 months). 
No significant differences were found in salivary levels of MS or lactobacilli of mothers of children with and without MS. Comparisons between a caries-active cohort colonized by MS (9 of 38) and children without detectable MS revealed similar histories in terms of antibiotic usage, gestational age, and birth weight. Interestingly, half the children who were MS negative between the ages of 1 and 2 years were minded by caregivers other than the mother, while all the children who were caries active during this age interval were cared for by their mothers; the difference was statistically significant. This study by Caufield et al (1993) was the first to present evidence that MS is acquired during a defined period in the ontogeny of a child. 
Support for the notion of a discrete window of infectivity comes from other sources, including animal models. By studying mother-child and father-child pairs, Alaluusua et al (1991) found a strong correlation between teenagers and mothers with high numbers of decayed, missing, or filled surfaces and high salivary MS levels, but no such correlation in father-child pairs.
The above studies in humans confirm the earlier animal studies by Fitzgerald and Keyes (1960) that dental caries is an infectious disease, transmissible by MS. Several experimental and clinical studies have also confirmed that MS can be isolated from dental plaque covering active carious lesions in enamel (Axelsson et al, 1987; Kristoffersson et al, 1985) and at the root (van Houte et al, 1990) as well as secondary carious lesions (Gonzales et al, 1995) and the margins of restorations (Wallman and Krasse, 1992; for reviews, see Bowden and Edwardsson, 1994; Loesche, 1986a). 
Caries incidence. Many longitudinal human clinical studies have shown correlations between high salivary MS counts and high caries incidence. In preschool-aged children (primary dentition), correlations between salivary MS counts and caries incidence have been shown by Alaluusua et al, 1990; Kohler et al, 1988; Roeters et al, 1995; Thibodeau and O’Sullivan, 1996; and Twetman et al, 1996. In the permanent dentition, Klock and Krasse (1978, 1979) showed that 9 to 12 year olds with high salivary MS levels developed significantly more new carious surfaces than did
children with low levels of MS during a 2-year period. However, when a test group of children with more than 1 million CFUs of MS/mL of saliva received high-quality plaque control by frequent professional mechanical toothcleaning, they developed fewer new carious surfaces than did the control groups with high and low salivary MS levels (0.9 new carious surfaces versus 2.2 and 4.3 new carious surfaces, respectively). In Molndal, Sweden, Zickert et al (1982b) also attained a significant correlation between the prevalence of MS in saliva and the incidence of new carious 
lesions. During a 3-year period, children with high levels of salivary MS (> 106 CFUs/mL) developed about three times as many new carious lesions as did control groups with lower levels of MS. Subjects in test groups on a treatment program including chlorhexidine developed significantly fewer cavities. 
In US adolescents, Kingman et al (1988a) also showed that subjects with high salivary MS levels developed more new carious surfaces than did subjects with lower MS levels.
In particular, controlled intraindividual longitudinal studies monitoring the microflora at the tooth surface level have clarified the cariogenic potential of MS (Axelsson et al, 1987b; Kristoffersson et al, 1985; MacPherson et al, 1990). An advantage of such studies is that several other external and internal modifying factors such as diet, fluoride, and saliva are equal for test and control sites. These studies have clearly shown that, in the same mouth, a tooth surface colonized by MS is at greater risk for caries than is a similar surface without MS.
During a 30-month period, S mutans on all the approximal surfaces was studied in a selected group of 13 year olds with more than 1 million CFUs of MS/mL of saliva. From a population of 720 13 year olds, subjects with more than 1 million CFUs/mL were selected (n = 187). Every 6 months, S mutans was sampled from saliva, the dorsum of the tongue, and every approximal tooth surface. Interproximal samples were obtained with a sterile wooden toothpick, as described by Kristoffersson and Bratthall (1982) (Fig 25). The contaminated sides of the toothpick were then pressed directly against selective (mitis-salivarius-bacitracin) agar plates (Fig 26). After incubation, the number of colonies formed (CFUs) was evaluated for every approximal surface.
In 17 subjects who consistently had a minimum of one surface highly colonized with MS and a minimum of one MS-negative or lightly colonized surface, about 60% of the highly colonized surfaces developed carious lesions (Fig 27, left), but only 3% of the MS negative or sparsely colonized surfaces did (Fig 27, right) (Axelsson et al, 1987b).
A prior study showed the surfaces most heavily colonized with MS to be the approximal surfaces of the molars and the second premolars (Fig 28) (Kristoffersson et al, 1984). In fact, a previously mentioned study of more than 600 14 year olds (Axelsson, 1989, 1991) showed that the same surfaces also had the highest PFRI scores. These observations explain why, in toothbrushing populations, these approximal surfaces have the highest prevalence of decayed, missing, or filled surfaces (Fig 29). For optimal caries prevention in such populations, plaque control
and topical application of fluorides should target these key-risk surfaces.
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Articles for theme “caries”:
Role of Specific Cariogenic MicrofloraIntroductionMicroorganisms implicated in the etiology of dental caries must be acidogenic as well as aciduric. To initiate carious lesions in enamel, the microorganisms must also be able to colonize the tooth surface and survive in competition with less harmful species, forming biofilms¾the so-called dental plaque. As early as 1960, Fitzgerald and Keyes showed that certain microorganisms isolated from human dental plaque, when inoculated in germ-free rodents on a high-sucrose diet, resulted in the spread of rampant caries.
Strategies for prevention and control of caries based on plaque ecology hypothesis According to the plaque ecology hypothesis, low pH (less than 5) will promote overgrowth of aciduric microorganisms, such as the cariogenic mutans streptococci and lactobacilli, at the expense of less acid-tolerant plaque microorganisms, such as S oralis, which are associated with healthy tooth surfaces.  Therefore the treatment strategy would be to increase plaque pH and thereby promote reestablishment of the harmless normal microflora of the tooth surfaces.
Effect of plaque ecologyOwing to differences in local environmental conditions, the microflora of mucosal surfaces differs in composition from that of dental plaque. Similarly, the plaque microflora varies in composition at distinct anatomic sites on the tooth ¾ for example, in fissures, on approximal surfaces, and in the gingival crevice. The resident microflora of a site acts as part of the host defenses by preventing colonization by exogenous (and often pathogenic) microorganisms.
Colonization of microenvironmentsThe oral cavity consists of several major and minor compartments, each constituting a separate microenvironment not easily affected by major events in the oral cavity. Examples of major compartments are the tongue, the oral mucosa, and the tonsils. The different approximal tooth surfaces, occlusal fissures, and gingival sulci are regarded as minor compartments. A specific area that supports a bacterial flora is termed a habitat. The flora of a habitat develops through a series of stages, collectively called colonization.
Role of the Oral EnvironmentIntroductionIn certain aspects, the oral cavity may be regarded as a single microbial ecosystem. A major regulatory factor is the flow rate of saliva, which decreases to almost 0.0 mL/min during sleep, is approximately 0.4 mL/min at rest, and increases to 2.0 mL/min after stimulation. Although saliva is not a good medium for supporting the growth of many bacteria, 1.0 mL of whole saliva may contain more than 200 million microorganisms, representing more than 300 different species.