Streptococcus mutans

For example, Streptococcus mutans, which is involved in the pathogenesis of dental caries, synthesizes a homopolymer of glucose that anchors the bacterium to the tooth surface and contributes to the matrix of dental plaque.

From: Medical Microbiology (Eighteenth Edition) , 2012

Dental Caries

Norman Tinanoff , in Pediatric Dentistry (Sixth Edition), 2019

Microbiologic Factors

MS are most associated with the dental caries process and key to the understanding of caries in preschool children. MS contribute to caries formation with their increased ability to adhere to tooth surfaces, produce copious amounts of acid, and survive and continue metabolism at low pH conditions. Preschool children with high colonization levels of MS have greater caries prevalence, as well as a much greater risk for new lesions than those children with low levels of MS. 43,44 Additionally, colonization with MS at an early age is an important factor for early caries initiation. 45

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Dental Caries

M. Matsumoto-Nakano , in Reference Module in Biomedical Sciences, 2014

Microbiology

Streptococcus mutans is a gram-positive facultative anaerobic bacterium that belongs to a group of mutans streptococci consisting of S. sobrinus and several other species (Figure 4). The colony morphology of S. mutans is rough when grown on plates with mitis salivarius agar, a selective medium for mutans streptococci, whereas that of S. sobrinus is smooth (Figure 5). Streptococcus mutans is classified into serotypes c, e, f, and k, with serotype c being the most common type in the oral cavity with a prevalence of approximately 70–80%, followed by serotype e (approximately 20%). In contrast, the distribution frequencies of serotypes f and k in the oral cavity are quite low, with a prevalence of less than 5%. Streptococcus mutans is considered to be an important pathogen of dental caries, especially in regard to disease onset. As compared with S. mutans, the number of individuals who harbor S. sobrinus is lower. Streptococcus sobrinus is classified into serotypes d and g, with the prevalence of serotype d being higher and that of serotype g, quite low. The bacterium is reported to be isolated only from caries-active sites, while S. mutans has been isolated from both active and noncaries sites. Furthermore, S. sobrinus is known to be associated with the onset of caries on smooth surfaces and is more active in caries development as compared to S. mutans. However, there are a limited number of reports regarding S. sobrinus, because most researchers have investigated S. mutans.

Figure 4. Scanning electron microscopic image of Streptococcus mutans.

Figure 5. Colony morphology of Streptococcus mutans on mitis salivarius agar plate.

It has been reported that dental caries in children occurs more frequently in those who possess a high number of S. mutans organisms. A 3-year cohort study was carried out with 252 preschool children for early identification of caries-active individuals (Roeters et al., 1995). At the baseline examinations, mutans streptococci organisms were detected in 43% of the children, while the detection frequency of lactobacilli was low (11.5%) in caries-active sites. Among individual subjects, the numbers of colony-forming units of mutans streptococci and lactobacilli in dental plaque and saliva samples varied throughout the study period. Mutans streptococci are believed to be the major pathogens of dental caries, because they are frequently isolated from cavitated carious lesions, possess properties to induce caries formation in animals fed a sucrose-rich diet, show highly acidogenic and aciduric properties, and possess cell surface proteins associated with firm adherence of bacterial cells to tooth surfaces.

Recently, probiotic bacteria such as Lactobaccilli spp. have been proposed to have a strong relationship with early childhood caries. The bacteria most frequently used in food products are lactobacilli and bifidobacteria. Probiotic bacteria maintain an appropriate pH in the intestinal tract, and inhibit growth of potential pathogens by producing lactic acid and bacteriocins (Otles et al., 2003). Probiotic organisms are considered to be nonpathogenic and nontoxic on the basis of long years of safe usage with no harmful adverse effects. However, some species of Lactobacilli spp. are thought to be associated with development of dental caries (Van Houte, 1994).

Previously, root caries was considered to be caused by Actinomyces naeslundii or Actinomyces viscosus from supragingival microflora. On the other hand, S. mutans and Lactobacilli spp. have been reported to be detected in samples obtained from root caries lesions in several studies. Therefore, there is no consensus on the microbial etiology of root caries at this time. The severity of these lesions is considered to be correlated with the numbers of pathogenic bacteria and the properties of the root. Root caries is classified into active lesions covered with microorganisms and inactive lesions covered with a small number of bacteria and a calcified mass (Schüpbach et al., 1992).

Oral microbial communities colonizing the teeth, dental plaque, are some of the most complex microbial floras in humans and consist of more than 700 bacterial species. As initially proposed by Costerton et al. (1999), the behavior displayed by oral microbial organisms grown in liquid culture (planktonic cells) is very different from the same organisms grown on a solid surface or within a community such as dental plaque. This is of significant medical interest, since it is well documented that there is an increased resistance of oral bacteria within dental plaque to antimicrobial agents relative to their planktonic susceptibility. Confirmation of these differences has been provided by investigations revealing that oral bacteria grown within biofilms show patterns of gene expression and protein synthesis distinct from comparable planktonic cells (Black et al., 2004).

Because of the multispecies nature of dental plaque, the oral microbial community is one of the best biofilm models for studying interspecies interactions. Based on current knowledge, it is reasonable to assume that interactions among oral microbial residents influence the properties of the whole community. As for dental caries, it is now recognized that this disease results not solely due to the presence of S. mutans or any single organism in dental plaque, but is rather caused by interactions of multiple acid-producing organisms such as S. mutans with other biofilm residents (Kleinberg, 2002). Such a microbial ecology-based theory serves as a new paradigm to understand the relationships between dental plaque and host in both health and disease conditions and offers new strategies for disease treatment and prevention.

Since 1940, considerable numbers of caries-related studies have centered on the 'Stephan curve.' There is little doubt that Stephan's observation (1944) contributed considerably to our understanding of the pathogenesis of dental caries. Unfortunately, too many researchers have focused on this concept and have not proceeded beyond consideration of the acid production phase. It is clear that resting pH in the low-caries group in Stephan's curve is higher (more alkaline) than that in the caries-active group. Furthermore, it is apparent that the pH of plaque in caries-free subjects returns to neutral or becomes alkaline much more rapidly than that in caries-active subjects (Geddes, 1975). Alkali generation and disposal of acid play an essential role in plaque physiology. Many oral microorganisms, in contrast to mutans streptococci or lactobacilli, display poor acid tolerance; nevertheless, they are found in relatively large numbers in dental plaque (Marquis et al., 1987). Clearly, these microorganisms have evolved a mechanism for overcoming the inimical influences of acid in their environment (Quivey et al., 2000).

Mutans streptococci organisms catabolize sugars by glycolysis to pyruvate and convert pyruvate to lactate mediated by lactate dehydrogenase only under anaerobic conditions, when sugars are in excess, while formate, acetate, and ethanol are the major products of metabolism under sugar-limiting conditions (Abbe et al., 1991). As a result of sugar metabolism, mutans streptococci can generate a low-pH environment and are also able to tolerate low pH stress. Mutans streptococcal survival in an acidic environment depends on the ability of the cell to maintain intracellular pH homeostasis via a mechanism of proton extrusion mediated by a membrane-associated proton-translocating adenosine triphosphate (ATP) synthase (H+/ATPase). In addition, mutans streptococci undergo specific alterations in physiology in order to survive under acidic conditions. One of these is involved in the synthesis of stress response proteins, such as BrpA. The brpA gene encodes the predicted surface-associated protein BrpA, which has a high level of similarity to LytR of Bacillus subtilis and CpsX of Streptococcus agalactiae (Wen and Burne, 2002). BrpA is expressed under acidic conditions, which induces self-aggregation of the bacteria. Also, a lack of BrpA significantly affects regulation of acid and oxidative stress tolerance and biofilm formation inS. mutans, which are key acid tolerance attributes of the bacterium.

Bacterial transmission is the initial step in the pathogenesis of dental caries induced by S. mutans. The results of various subtyping methods, including bacteriocin activity profiles (Berkowitz and Jordan, 1975; Davey and Rogers, 1984), a chromosomal deoxyribonucleic acid fingerprint technique (Caufield and Walker, 1989), arbitrarily primed polymerase chain reaction (Li and Caufield, 1998), ribotyping (Köhler et al., 2003), and multilocus sequence typing (Lapirattanakul et al., 2008), have confirmed the notion of vertical transmission of S. mutans from mothers to their children (Figure 6). Since a nonshedding surface is necessary for colonization, acquisition of the bacterium is considered to occur after eruption of primary teeth (Jordan, 1976), with a window of infectivity between 19 and 31 months of age suggested to be the critical period (Caufield et al., 1993). However, some studies of children from lower socioeconomic populations with high risk factors for dental caries showed the possibility of earlier acquisition of S. mutans (Florio et al., 2004; Mohan et al., 1998). Moreover, since saliva is indicated to be the major vehicle of transmission, a high level of salivary S. mutans in the mother may result in early acquisition and establishment of the bacterium in her children (Alaluusua and Renkonen, 1983; Köhler et al., 1983). Such early establishment has also been shown to increase the risk of dental caries (Köhler et al., 1988). In contrast to early acquisition, some observations have suggested late transmission of S. mutans in children who were free from S. mutans for 5 years. Such acquisition is believed to be due to the new environment provided at the time of eruption of the permanent first molars (Straetemans et al., 1998; van Loveren et al., 2000). Since mothers are an important source of S. mutans infection in their children, many studies with a focus on enhancing maternal oral health have provided important implications for caries prevention (Tenovuo et al., 1992).

Figure 6. Representative images of electrophoresis after arbitrarily primed polymerase chain reaction. M, molecular marker; no. 1–10, samples.

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Elucidating Human Migrations by Means of their Pathogens

Aude Gilabert , Thierry Wirth , in Genetics and Evolution of Infectious Disease, 2011

Streptococcus mutans

Streptococcus mutans belongs to the mutans streptococci group and is associated with human caries. This bacterium has a ubiquitous distribution and seems to be indigenous to humans. The transmission of S. mutans is mainly vertical (Lapirattanakul et al., 2008), the colonization is stable and probably lifelong, which makes the bacterium a good candidate to infer human evolutionary history although its population structure and phylogeny has been poorly investigated (Caufield et al., 2007). A recent study presented results in agreement with this idea albeit it emphasizes the importance of the choice of markers (Caufield et al., 2007; Caufield, 2009). Indeed, the authors investigated the population structure of S. mutans from five continents using several genetic markers to reconstruct molecular phylogenies. They observed a certain number of incongruences between the different trees, possibly due to horizontal gene transfers. One phylogeny was based on a 600 bp hypervariable region (HVR) of a plasmid because this noncoding region presented high polymorphism. However, the HVR phylogenies showed evolutionary incongruence with ethnic or geographic human hosts. The second phylogeny was based on the intergenic spacer region (IGSR) between the 16S and 23S rRNA genes, which showed only few polymorphisms (nine informative sites over 388 bp). Using a polyphasic approach, which combines genetic traits (here the serotype and mutacin types) and DNA sequences, Caufield et al. (2007) reconstructed a phylogeny in which geographical substructures were visible but apart from the Asian group, the other groups (African1, African2, and Caucasian) were supported by low bootstrap values (Caufield, 2009). In addition, the phylogenetic position of the Caucasians was intriguing. An important shortcoming in Caufield's studies (Caufield et al., 2007; Caufield, 2009) is that they were restricted to S. mutans strains that harbored a plasmid, dismissing 95% of the natural occurring strains that do not harbor this genetic element (Do et al., 2010). Nakano et al. (2007) developed a MLST scheme to address S. mutans population structure and observed no genetic structure in strains lacking the plasmid. However, this study only contained strains from Japan and Finland and does not reflect the true diversity. Therefore, before using S. mutans as an inferential tool, complementary studies with extended datasets based on MLST are required and both plasmid-positive and plasmid-negative strains should be investigated.

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History, Science and Methods

Z. Hossain , in Encyclopedia of Food Safety, 2014

Disease of the Oral Health

Streptococcus mutans or other cariogenic streptococci, such as Streptococcus sanguinis could be potentially the causative agent of an oral infection if present in salivary substances from an infected individual mixed with food or drinks. High salivary S. mutans count (>105 colony forming units) is likely to pass the infectious bacteria to an unaffected person, especially children. Dental caries or tooth decay is strongly associated with S. mutans, which is normally present in dental plaque of humans. It is defined as demineralization and destruction of hard tissue of the teeth, enamel, dentin, and cementum. Occurrence of a dental caries largely depends on the time of the tooth surface exposure to acidic by-products fermented by the bacteria. A lesion presenting as a chalky white spot on the tooth, also known as microcavity, is the early sign of demineralization of the tooth enamel. A dull-brown lesion represents an active caries, which eventually leads to cavities or holes on the teeth and swelling on the gums. Common clinical symptoms of the disease are pain and discomfort when chewing food, difficulty in facial movement, sensitivity of tooth, jaw pain, discoloration on tooth surface, inflammation on the face, and mild fever. Dental caries can also manifest with bad breath and foul tastes. Such pyogenic oral infectious processes can be acute or chronic. During an acute carious state, the dental caries spreads laterally causing a rapid early deterioration of the pulp tissues. The pain is intense, and the dentin is light yellowish in color. There is only limited lateral spread in case of a chronic caries, and the involvement of the tooth pulp is a much slow process. Therefore, the cavity is shallow with no pulp tissue implication. Oral pain is generally not involved in this type of caries (Figure 8). Other plaque-derived forms of infection include inflammation of the gum tissue (gingivitis), gingival recession (retraction of gum tissue), bleeding gums, and more severe periodontal diseases as a result of loss of gum tissue and underlying bone. Prolonged untreated dental caries may confer a risk of bacteremia, which in turn triggers the likelihood of an opportunistic heart valve endocarditis. Also, highly virulent S. mutans strains have been proposed to be implicated in the aggravation of ulcerative colitis. Such possibilities should not be ruled out without an accurate pathological explanation.

Figure 8. Acute dental caries illustrating destruction of tooth tissue while forming deep cavity on the tooth.

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Infections Caused by Viridans Streptococci

Bertha Ayi , in xPharm: The Comprehensive Pharmacology Reference, 2007

Pathophysiology

Streptococcus mutans has a high association with dental caries. It has been shown, however, that colonization of teeth does not take place in the absence of dietary sucrose. The organism utilizes sucrose to produce polysaccharides, such as dextran, a complex extracellular polysaccharide, and glycoproteins. These polysaccharides enable the organism to bind tightly to dental enamel and to other organisms. This leads to formation of large masses of organisms that produce high concentrations of acid from dietary sugars. These acids cause demineralization and dissolution of enamel, leading to dental caries. These expose the pulp of the teeth leading to pulpitis, pulpal necrosis, periapical abscess, and acute alveolar abscess.

The S. intermedius group are frequently agents in periapical dental abscess and other endodontic infections. These frequently lead to bacteremia. They are also associated with acute pansinusitis with subsequent intracranial spread, orbital empyemas, and fulminant fasciitis of the head and neck. The reasons for the pyogenic nature of this group are not fully understood.

Injury to cardiac endothelium is a prerequisite for bacterial endocarditis. This injury may be in areas of trauma, turbulence and metabolic changes. Structural, congenital and degenerative heart diseases create regions that cause turbulent blood flow. Injury of endothelium leads to the deposition of platelet and fibrin, known as the nonbacterial thrombotic endocarditis. Bacteria adhere to this tissue and are covered with fibrin. The vegetation enlarges by bacterial multiplication and additional platelet-fibrin deposition Bayer and Scheld (2000). After entrapment in areas of vascular injury, some adherence factors increase the propensity of some viridans streptococci to cause endocarditis. Strains that produce dextran, a complex extracellular polysaccharide, have an increased ability to adhere to heart valves and tend to produce larger vegetations compared to the nondextran producing strains. FimA, a surface protein of S. parasanguis, is recognized as an adherence factor that mediates attachment of viridans streptococci to platelet-fibrin matrices. Fibronectin, which is secreted by endothelial cells, platelets and fibroblasts in response to vascular injury, seems to play an important role in endocarditis. Endocarditis-producing strains bind better to fibronectin by way of lipoteichoic acid (adhesin). This causes further propagation of the vegetation by stimulating the production of tissue factor from the underlying vascular tissue. Endocarditis-producing strains of viridans streptococci stimulate platelet aggregation and the release reaction both in vivo and in vitro. This mechanism leads to a further increase in the size of the vegetation.

Mechanisms involved in the rare cases of septic shock in neutropenic patients are thought to be similar to those mediated by gram-negative organisms.

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Mucosal Vaccines for Dental Diseases

Martin A. Taubman , Daniel J. Smith , in Mucosal Immunology (Fourth Edition), 2015

Characteristics of Antigen Elicitation of Antibody

Mutans streptococci can elicit antibodies both in saliva (mucosal; predominantly IgA) and in serum (predominantly IgG). Salivary SIgA antibody to antigens of S. mutans and S. sobrinus has been detected between the ages of 1 and 5   years, when this antibody could influence colonization. Salivary SIgA antibody to S. mutans Gtf was detected in only 6% of two- to 48-month-old children, although most adults demonstrate IgA antibody to S. mutans Gtf (Smith and Taubman, 1992). The absence or low level of salivary antibody to specific mutans streptococcal antigens (including antigen I/II) prior to colonization may increase the risk of permanent infection (Smith and Taubman, 1992).

Others have concluded that low caries experience was positively correlated with elevated serum IgG antibody to a surface protein of S. mutans in young people and have suggested that serum immunity, manifested in the oral cavity via the GCF, could alter cariogenic mutans streptococcal colonization and disease (Challacombe et al., 1984). With advancing age, however, serum antibody levels ultimately appear to reflect the cumulative antigenic challenge provided by infections that lead to disease (Kent et al., 1991). The presence of gingival crevicular IgG antibody (Smith et al., 1994d) or salivary SIgA (Gregory et al., 1985) antibody to S. mutans has been associated with short-term modifications of indigenous (Smith and Taubman, 1987) or implanted (Camling et al., 1991) mutans streptococcal colonization of teeth.

Nogueira et al. (2005) provided suggestive evidence that salivary IgA antibody reactive to certain virulence antigens could delay S. mutans colonization in very young children at high risk for infection. Five to 13-month-old children were paired with respect to age, number of teeth, IgA concentration, and racial background, but differed in the presence or absence of S. mutans. Antibody reactivity to Gtf and antigen I/II was detected in most of the children regardless of the infection status. However, salivary IgA antibody reactive to GbpB was observed in only 38% of infected children, in contrast to 76% of the uninfected children. Furthermore, densitometrically determined GbpB IgA antibody levels were generally much higher in the uninfected group versus GbpB-antibody-positive S. mutans-infected children. Thus, children under heavy challenge with mutans streptococcal antigens appear to mount secretory IgA responses, which are reactive to important S. mutans-virulence components, in the first year of life. These potentially protective responses theoretically could have been provoked through antigenic stimulation by similar epitopes on earlier colonizing oral streptococci.

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Passive Immunization

Harold Marcotte , Lennart Hammarström , in Mucosal Immunology (Fourth Edition), 2015

Streptococcus mutans

Streptococcus mutans is a normal resident of the human oral cavity recognized as one of the major etiologic agents of caries. Passive immunization against caries was developed using oral administration of antibody preparation against whole cells of Str. mutans or associated virulence factors involved in bacteria adherence (Table 1). Oral administration of hyperimmune bovine milk or chicken antibodies against Str. mutans and glucosyltransferases resulted in a reduction in Str. mutans in dental plaque and caries formation in rats and reduced counts of Str. mutans in saliva or dental plaque in humans (Filler et al., 1991; Hamada et al., 1991; Hatta et al., 1997; Kruger et al., 2004; Loimaranta et al., 1999a; Michalek et al., 1987; Otake et al., 1991). These antibody preparations may protect against Str. mutans by different mechanisms, such as inhibiting the formation of extracellular polysaccharides (glucan and fructan) and preventing the adherence of Str. mutans to salivary coated hydroxyapatite and aggregation of Str. mutans (Loimaranta et al., 1998, 1999b).

Another approach is the use of mAbs against the cell surface antigen I/II (SAI/II) adhesion molecule of Str. mutans (Lehner et al., 1985; Ma et al., 1987, 1989, 1990). Human volunteers receiving a treatment consisting of oral chlorhexidine disinfection followed by repeated topical applications of anti-AgI/II mAb (Guy's 13) onto the teeth showed a lack of re-colonization by indigenous Str. mutans for up to 2   years (Ma et al., 1989, 1990). Because the functional mAb was only detected on the teeth for only up to 3 days after application, it was speculated that the ecological niche vacated by Str. mutans was filled by other bacteria (Ma et al., 1990). This mAb was subsequently re-engineered as a chimeric IgA/IgG Ab with a rabbit secretory component for expression in tobacco plants. The plant-derived SIgA/G (CaroRx Planet Biotechnology) was reported to be effective in passive immunization trials in humans (Ma et al., 1995, 1998) although another study reported only a trend in reducing colonization by Str. mutans (Weintraub et al., 2005). The product is currently undergoing phase II clinical trials in the United States.

An scFv was also derived from the mAb Guy's 13 and expressed in lactobacilli (Kruger et al., 2002). Administration of fresh lactobacilli expressing surface anchored scFv in drinking water reduced Str. mutans bacterial counts and caries development in rats (Kruger et al., 2002, 2005). Modified lactobacilli could prevent caries by different mechanisms such as blocking the SAI/II adhesion and aggregation of Str. mutans in combination with the production of inhibitory substances (e.g., bacteriocin) (Kruger et al., 2005). A VHH antibody fragment against the SAI/II adhesin (S36-VHH) also reduced the development of smooth surface caries in the desalivated rat caries model (Kruger et al., 2006).

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Dental Caries and Associated Risk Factors

JOHN P. BROWN , MICHAEL W.J. DODDS , in Prevention in Clinical Oral Health Care, 2008

Indicator Bacterial Load

Estimates of mutans streptococci in whole stimulated saliva are indicative of caries risk, and the counts are typically stable over time. The negative predictive value is superior to the positive, so the validity and reliability of these counts help to identify individuals who are less likely to develop future caries. Another major use is to assess dietary adherence when major reductions in sweet food and drink intake have been recommended. With patient adherence to the recommended diet, high levels of mutans streptococci will fall. For these reasons and to identify those with high levels of these indicator bacteria, persons whose oral screening and history indicate a moderate or high caries risk should be tested for mutans streptococci bacterial load in saliva. Commercial kits are available to test indicator organisms. These methods are described in Chapter 9.

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Cariology and Caries Management

V. Kim Kutsch , Tomás Seif , in Contemporary Esthetic Dentistry, 2012

Dental Plaque

The prevalence of mutans streptococci (Streptococcus mutans) and lactobacilli is associated with dental caries. S. mutans is involved in caries formation from its initiation. Lactobacilli are so-called "secondary organisms" that flourish in a caries environment and contribute to caries progression (Figure 1-8). Dental plaque may be more cariogenic locally whereas S. mutans and lactobacilli are concentrated. In everyday practice, it is difficult for the dentist to identify cariogenic plaque to make this knowledge useful in treating individual patients. Plaque can be sampled and S. mutans and lactobacilli quantified, but the procedure is quite complicated and requires the support of a microbiology laboratory.

It is easier to count mutans streptococci and lactobacilli in saliva, and kits are commercially available for this purpose. These counts, however, do not give site-specific information and are poor predictors for high carious activities in general. Nevertheless, low counts and the absence of S. mutans are good predictors of low caries activity.

High numbers of S. mutans organisms and lactobacilli are probably the result of a high sugar intake and the resulting periods of lower pH levels in dental plaque. Inversely, the restriction of sugar intake reduces the number of S. mutans organisms and lactobacilli.

In one study of individuals complying with the Weight Watcher's diet, the number of mutans streptococci and lactobacilli was reduced by half. A comparable reduction was found in subjects who reduced their sugar intake frequency from 7.2 to 1.8 times a day. Interestingly, after a period of sugar restriction the pH response to glucose was reduced in buccal but not in interdental plaque. Apparently the reduced numbers of mutans streptococci and lactobacilli are insufficient to lower the acidogenicity of interdental plaque.

The oral flora colonizes on teeth continuously, but it takes up to several days before the dental plaque contains enough acidogenic bacteria to lower plaque pH to the level that causes demineralization. Theoretically, plaque removal every second day would be sufficient. If the dentition is professionally cleaned, an even lower frequency of cleaning has been demonstrated to prevent caries. However, we have only to consider the caries prevalence in the prefluoride era to realize that few people are capable of cleaning their teeth to a level adequate to prevent caries. Very few people even use dental floss.

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Management of dental caries

David Ricketts , ... Andrew Hall , in Advanced Operative Dentistry, 2011

Saliva microbiology

Salivary tests for mutans streptococci and lactobacilli have been used for many years and commercially available kits have been produced to measure the counts of both organisms within saliva. It is assumed that if the levels of these cariogenic organisms are high in the dental biofilm on the surface of the tooth or within active carious lesions, the levels will also be high in the saliva. Indeed, a number of studies have found associations with these two organisms in saliva and the caries experience of individuals. More recent evidence suggests that these salivary counts are not good in predicting future caries; however, they may be useful in assessing patients' compliance with dietary advice, for as the level and frequency of sugar in the diet reduces, the ensuing modification in the local oral environment is reflected in a reduced count of both species. This can serve as a tangible reward to a compliant patient and spur on their efforts in changing their dietary lifestyle.

Figure 1.15 illustrates one such kit (CRT Bacteria, Ivoclar Vivadent, Schaan, Liechtenstein). In this a sample of stimulated mixed saliva is collected and applied, at the chairside, to selective culture plates. Following incubation at 37°C for 48 hours, the numbers of colony forming units (CFUs) are estimated by comparing the cultures to a chart (Figure 1.16). Figures 1.17 and 1.18 illustrate this for a high caries risk patient and one of low risk.

The various caries risk factors described are subjectively drawn together for each patient, with the outcome influencing the patient's treatment plan. A more formal and objective way of assessing this is by using a computer-based caries risk model. The Cariogram is such a system which was developed in Malmö Dental School by Douglass Bratthall and co-workers. Information is gathered from the patient about caries risk, clinical and radiographic findings, and the results from various salivary tests. This information is given a score of 0–3 (or in some cases 0–2). These scores are then entered into the Cariogram program, from where information is weighted according to its impact on caries risk. The program evaluates the data and then presents it as a pie chart with a clear indication of future caries risk expressed as a 'Chance to avoid caries'. The various risk factors described above and those evaluated in the Cariogram and the corresponding scores given are detailed in Table 1.3. Table 1.3 also summarizes actions that can be taken to address each factor positively, with an aim to change the patient's caries risk. Figures 1.19 and 1.20 show what the Cariogram would look like for a low- and a high-risk patient, respectively.

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