Dental caries is a chronic, non-communicable, endogenous infection caused by the dysbiosis of the resident commensal oral microbiome on tooth surfaces. The carious lesion, by contrast, is the result of demineralization of enamel—and later of dentine—by acids produced by dysbiotic plaque microbiota as they metabolize dietary carbohydrates. However, the initial process of enamel demineralization is usually followed by remineralization, and cavitation occurs when the former process overtakes the latter. Once the surface layer of enamel has been lost, the infection invariably progresses to dentine, with the pulp becoming firstly inflamed and then necrotic.
Caries is defined as localized destruction of the tissues of the tooth by bacterial fermentation of dietary carbohydrates.
Dental caries (with periodontal disease) is one of the most common human diseases and affects the vast majority of individuals. Although caries was not uncommon in the developing world, the recent affluence in these regions has resulted in a remarkable upsurge in caries due to the ready and cheap availability of fermentable carbohydrates. By contrast, caries prevalence is falling overall in the developed world due to the increasing awareness of cariogenic food sources and the general improvement in oral hygiene and the dental care delivery systems. Caries of enamel surfaces is particularly common up to the age of 20, after which it tends to stabilize. However, in later life, root surface caries becomes increasingly prevalent, due to gingival recession, exposing the vulnerable cementum to cariogenic bacteria.
Dental caries can be classified with respect to the site of the lesion (Fig. 32.1):
■ pit or fissure caries (seen in molars, premolars and the lingual surface of maxillary incisors)
■ smooth-surface caries (seen mainly on approximal tooth surfaces just below the contact point)
■ root surface caries (seen on cementum or dentine when the root is exposed to the oral environment)
■ recurrent caries (associated with an existing restoration).
The primary lesion of caries is a well-demarcated, chalky-white lesion (Fig. 32.2) in which the surface continuity of enamel has not been breached. This 'white-spot' lesion can heal or remineralize, and this stage of the disease is therefore reversible. However, as the lesion develops, the surface becomes roughened and cavitation occurs. If the lesion is not treated, the cavitation spreads into dentine and eventually may destroy the dental pulp, finally leading to the development of a periapical abscess and purulent infection (see Chapter 34).
Diagnosis is usually by a combination of:
1. Direct observation.
2. Probing. Some do not advocate probing as this may create an incipient breach of the enamel and spread the infection from one tooth surface to another.
3. Radiographs. Early white-spot lesions may easily be missed because they cannot be detected by the eye or by radiography. Similarly, it is possible for large carious lesions to develop in pits and fissures with very little clinical evidence of disease.
4. Experimental methods. Methods of potential practical value include laser fluorescence for diagnosis of buccal and lingual caries, and electrical impedance (resistance) to detect occlusal caries.
5. Microbiological tests may be helpful in the assessment of caries (see over).
Fig. 32.1 Nomenclature of dental caries. D, Dentine; E, enamel; P pulp. *Also termed occlusal caries.
Fig. 32.2 polarized light microscopic appearance of early enamel caries (ground section). The cone-shaped body of demineralization is evident.
The major factors involved in the aetiology of caries (Fig. 32.3) are:
■ host factors (tooth, saliva)
■ diet (mainly the intake of fermentable carbohydrates)
■ plaque biofilm microorganisms (i.e., supragingival plaque).
The structure of enamel, and of dentine in root caries, is important: some areas of the same tooth are much more susceptible to carious attack than others, possibly because of differences in mineral content (especially fluoride).
Fig. 32.3 Interplay of major aetiological factors in dental caries (all four factors must act simultaneously for caries to occur).
Flow rate and composition of saliva
The mechanical washing action of saliva is a very effective mechanism in the removal of food debris and unattached oral microorganisms. It has a high buffering capacity, which tends to neutralize acids produced by plaque biofilm bacteria on tooth surfaces, and it is supersaturated with calcium and phosphorus ions, which are important in the remineralization of white-spot lesions. Saliva also acts as a delivery vehicle for fluoride.
There is a direct relationship between dental caries and the intake of carbohydrates. The most cariogenic sugar is sucrose, and the evidence for its central role in the initiation of dental caries includes:
■ increases in the caries prevalence of isolated populations with the introduction of sucrose-rich diets
■ clinical association studies
■ short-term experiments in human volunteers using sucrose rinses
■ experimental animal studies.
Sucrose is highly soluble and diffuses easily into dental plaque biofilm, acting as a substrate for the production of extracellular polysaccharides and acids. Cariogenic streptococci produce water-insoluble glucan from sucrose, which, in addition to facilitating initial adhesion of the organisms to the tooth surface, serves as a nutritional source and a matrix for further plaque development. The relationship between sucrose and dental caries is complex and cannot be simply explained by the total amount of sugar consumed. The frequency of sugar intake rather than the total amount of sugar consumed appears to be of decisive importance. Also relevant are the stickiness and concentration of the sucrose consumed, both factors influencing the period for which sugar is retained in close contact with the enamel surface.
Carbohydrates other than sucrose (e.g., glucose and fructose) are also cariogenic, but less so than sucrose. Polyol carbohydrates, 'sugar alcohols' (e.g., xylitol), with low cariogenicity have been produced and are sought after as sugar substitutes in products such as chewing gum and baby foods.
Microorganisms in the form of dental plaque biofilm are a prerequisite for the development of dental caries. The different types of plaque and the factors involved in their development are described in Chapter 31.
Specific and non-specific plaque hypothesis
Although mutans streptococci have been recognized as the major group of organisms involved in caries, there is some controversy as to whether one or more specific groups of bacteria are principally involved in caries—the specific plaque hypothesis—or whether the disease is caused by a heterogeneous mixture of non-specific bacteria—the non-specific plaque hypothesis.
There is conflicting opinion for and against the specific plaque hypothesis:
■ mutans streptococci are involved in the initiation of almost all carious lesions in enamel
■ mutans streptococci are important, but not essential
■ the association of mutans streptococci and caries is weak and no greater than for other bacteria.
Given the extreme variation in the composition of supragingival plaque biofilm from the same site in the same mouth at different times, it is unlikely that the initiation and progression of all carious lesions are associated with specific organisms such as Streptococcus mutans. Further, other plaque biofilm bacteria also possess some of the biochemical characteristics thought to be important in cariogenicity. Therefore, it seems likely that combinations of bacteria other than mutans streptococci and lactobacilli may be able to initiate carious lesions, and the plaque flora may be non-specific in nature. The current evidence implies that some bacteria (mutans streptococci, Lactobacillus spp. and Actinomyces spp.) may be more important than others in the initial as well as subsequent events leading to both enamel and root surface caries.
The role of mutans streptococci
There is a vast literature on the role of the mutans streptococci in caries. 'Streptococcus mutans' is a loosely applied group name for a collection of seven different species (Streptococcus mutans, Streptococcus sobrinus, Streptococcus criceti, Streptococcus ferus, Streptococcus ratti, Streptococcus macacae and Streptococcus downei) and eight serotypes (a-h). Streptococcus mutans serotypes c, e and f and Streptococcus sobrinus serotypes d and g are the species most commonly found in humans, with serotype c strains being the most prevalent, followed by d and e. The others are rarely encountered. The evidence for the aetiological role of mutans streptococci in dental caries includes the following:
■ correlations of mutans streptococci counts in saliva and plaque with the prevalence and incidence of caries
■ mutans streptococci can often be isolated from the tooth surface immediately before the development of caries
■ positive correlation between the progression of carious lesions and 'Streptococcus mutans' counts
■ production of extracellular polysaccharides from sucrose (which help to reinforce the plaque biofilm and attach the biomass on to the tooth surface, thus permitting a sustained and concentrated assault of the specific enamel, dentinal or cemental surface)
■ most effective streptococcus in caries studies in animals (rodents and non-human primates)
■ ability to initiate and maintain microbial growth and to continue acid production at low pH values
■ rapid metabolism of sugars to lactic and other organic acids
■ ability to attain the critical pH for enamel demineralization more rapidly than other common plaque biofilm organisms
■ ability to produce intracellular polysaccharides (IPSs) as glycogen, which may act as a food store for use when dietary carbohydrates are low
■ immunization of animals with specific Streptococcus mutans serotypes significantly reduces the incidence of caries.
Note: not all strains of mutans streptococci possess all of the aforementioned properties; thus some strains are more cari- ogenic than others. Caries may therefore be an infectious disease in a minority, with a highly pathogenic strain being transmitted from one individual to another. Despite this apparently strong relationship between Streptococcus mutans and caries, a number of longitudinal studies in children have failed to find such a strong correlation.
The role of lactobacilli
Lactobacilli were previously believed to be the causative agents of dental caries. They were considered to be candidate organisms for caries because of:
■ their high numbers in most carious lesions affecting enamel (many studies have now shown its high prevalence in root surface caries too)
■ the positive correlation between their numbers in plaque biofilm and saliva and caries activity
■ their ability to grow in low-pH environments (below pH 5) and to produce lactic acid
■ their ability to synthesize both extracellular and IPSs from sucrose
■ the ability of some strains to produce caries in gnotobiotic (germ-free) rats
■ the fact that their numbers in dental plaque biofilms derived from healthy sites are usually low.
On the negative side, however, lactobacilli are rarely isolated from plaque biofilm prior to the development of caries, and they are often absent from incipient lesions.
Although the role of lactobacilli in the carious process is not well defined, it is believed that:
■ they are involved more in the progression of the deep enamel lesion (rather than the initiation)
■ they are the pioneer organisms in the advancing front of the carious process, especially in dentine.
The role of Actinomyces spp.
Actinomyces spp. are associated with the development of root surface caries (root lesions differ from enamel caries in that the calcified tissues are softened without obvious cavitation).
The evidence for the involvement of Actinomyces viscosus in root surface caries is based on:
■ association studies in vivo
■ in vitro experimental work with pure cultures
■ experimental work in gnotobiotic rodents.
Despite the fact that Actinomyces spp. (especially Actinomyces viscosus) predominate in the majority of plaque biofilm samples from root surface lesions, some studies have reported both mutans streptococci and Lactobacillus spp. in these lesions. Furthermore, the sites from which these organisms were isolated appeared to have a higher risk of developing root surface caries than other sites. The role of Actinomyces spp. in caries is therefore not clear.
The role of Veillonella
Veillonella is a Gram-negative anaerobic coccus that is present in significant numbers in most supragingival plaque biofilm samples. As Veillonella spp. require lactate for growth, but are unable to metabolize normal dietary carbohydrates, they use lactate produced by other microorganisms and convert it into a range of weaker and probably less cariogenic organic acids (e.g., propionic acid). Hence this organism may have a beneficial effect on dental caries. This protective effect has been demonstrated in vitro and in animal experiments, but not in humans.
Big data and caries microbiology
Recent data from next-generation sequencing (NGS) studies have shed new light on the microbiota associated with dental caries. These indicate that many other non-cultivable bacteria are associated with this complex process. The list of caries- associated bacteria, apart from the traditional organisms such as Streptococcus mutans, Lactobacillus and Actinomyces species include species of the following genera: Atopobium, Dialister, Eubacterium, Olsenella and Scardovir to name a few. The role of these organisms in caries process is yet to be defined.
Plaque biofilm metabolism and dental caries
The metabolism of plaque biofilm is a complex subject and the following is a very simplified account.
The main source of nutrition for oral bacteria is saliva. Although the carbohydrate content of saliva is generally low, increased levels (up to 1000-fold) are seen after a meal. To make use of these transient increases in food levels, oral bacteria have developed a number of regulatory mechanisms, which act at three levels:
1. transport of sugar into the organisms
2. the glycolytic pathway
3. conversion of pyruvate into metabolic end products.
The bacterial metabolism of carbohydrate is critical in the aetiology of caries as the acidic end products are responsible for enamel demineralization. The process begins when dietary sucrose is broken down by bacterial extracellular enzymes such as glucosyl and fructosyl transferases, with the release of glucose and fructose, respectively. These monosaccharides are then converted into polysaccharides that are either water- soluble or water-insoluble: glucans and fructans, respectively. Glucans are mostly used as a major bacterial food source; the insoluble fructans contribute to the plaque biofilm matrix while facilitating the adhesion and aggregation of the resident bacteria and serving as a ready, extracellular food source. Some of the sucrose is transported directly into bacteria as the disaccharide or disaccharide phosphate, which is metabolized intracellularly by invertase or sucrose phosphate hydrolase into glucose and fructose. During glycolysis, glucose is degraded immediately by bacteria via the Embden-Meyerhof pathway, with the production of two pyruvate molecules from each molecule of glucose. The pyruvate can be degraded further:
■ Under low sugar conditions, pyruvate is converted into ethanol, acetate and formate (mainly by mutans streptococci).
■ In sugar excess, pyruvate is converted into lactate molecules.
Different species produce acids at different rates and vary in their ability to survive under such conditions. The mutans group streptococci, being the most acidogenic and aciduric (acid tolerant), are the worst offenders and reduce the pH of plaque biofilm to low levels, creating hostile conditions for other neighbouring biofilm bacteria. The resultant overall fall in pH to levels below 5.5 initiates the process of enamel demineralization. This characteristic fall in plaque biofilm pH, followed by a slow return to the original value in about an hour, produces a curve that is termed the 'Stephan curve'.
Ecological plaque hypothesis
A key feature of a number of caries studies is the absence of mutans streptococci at caries sites, suggesting that bacteria other than the latter can contribute to the disease process. Conversely, in some studies where mutans streptococci were found in high numbers, there was apparently no demineralization of the underlying enamel. This may be due to the presence of lactateconsuming species such as Veillonella, or to the production of alkali at low pH by organisms such as Streptococcus salivarius and Streptococcus sanguinis. These and other related findings have led to the development of the 'ecological plaque hypothesis' of caries (Fig. 32.4). According to this proposal, cariogenic flora found in natural plaque biofilm are weakly competitive and comprise only a minority of the total community. With a conventional diet, levels of such potential cariogenic bacteria are clinically insignificant, and the processes of remineralization and demineralization are in equilibrium. If, however, the frequency of intake of fermentable carbohydrates increases, then the plaque biofilm pH level falls and remains low for prolonged periods, promoting the growth of acid-tolerant (aciduric) bacteria while gradually eliminating the communal bacteria that are acid labile. Prolonged low pH conditions also initiate demineralization. This process would turn the balance in the plaque biofilm community in favour of mutans streptococci and lactobacilli. The hypothesis also explains, to some extent, the dynamic relationship between the bacteria and the host, so that alterations in major host factors such as salivary flow on plaque biofilm development can be taken into account.
Fig. 32.4 Ecological plaque hypothesis. MS, mutans streptococci; S. oralis, Streptococcus oralis; S. sanguinis, Streptococcus sanguinis.
Fig. 32.5 Dip slide test to detect mutans streptococci in saliva: a high density of white colonies indicates a higher caries risk.
Management of dental caries
The conventional approach to the treatment of dental caries was to remove and replace diseased tissue with an inert restoration. This approach made no attempt to cure the disease, and the patient often returned some months later requiring further fillings due to new or recurrent caries. By contrast, the modern philosophy in caries management highlights:
■ early detection
■ the importance of accurate diagnosis
■ minimal cavity preparation techniques
■ active prevention.
The result of such measures should be less, rather than more, demand for restorative treatment by individual patients.
In patients with a low incidence of caries, a case history and clinical and radiographic examination are probably adequate for treatment planning. However, for patients with rampant or recurrent caries, or where expensive crown and bridge work is planned, additional investigations are necessary. These include:
■ assessment of dietary habits
■ determination of salivary flow rate and buffering capacity
■ microbiological analysis (discussed below).
Microbiological tests in caries assessment
Saliva samples can be used to establish the numbers of Streptococcus mutans and Lactobacillus spp. in the oral cavity as follows:
1. A paraffin wax-stimulated sample of mixed saliva is collected.
2. In the laboratory, the saliva is appropriately diluted and cultured on selective media (mitis salivarius bacitracin agar for Streptococcus mutans; Rogosa SL agar for Lactobacillus spp.).
3. The number of typical colonies (colony-forming units (CFUs)) is then quantified and extrapolated to obtain the count per millilitre of saliva:
• high caries activity: >106/ml Streptococcus mutans and/ or >100 000/ml Lactobacillus spp.
• low caries activity: <100 000/ml Streptococcus mutans and <10 000/ml Lactobacillus spp.
Simplified detection kits for estimation of both lactobacilli and Streptococcus mutans in saliva are available. The results correlate well with laboratory plate counts, and the tests can be performed in the dental clinic without special facilities (Fig. 32.5).
The presence of high salivary levels of Streptococcus mutans or lactobacilli does not necessarily mean that the patient has an increased risk of developing dental caries, as it is a disease of multifactorial aetiology. Other factors, such as diet, buffering capacity, fluoride content of enamel and degree of oral hygiene, should also be considered. Further, the presence of large numbers of cariogenic organisms in saliva does not imply that all teeth are caries prone, as the salivary organisms may have originated from a few foci with high caries activity. There fore these tests at best give a generalized approximation of the caries risk. It should be noted that the microbiological tests used in caries assessment differ from conventional tests used in medical microbiology, where the presence of a pathogen indicates a positive diagnosis (e.g., syphilis). The main uses of microbiology tests in caries assessment are:
■ to identify patients who have unusually high numbers of potential pathogens, so that these data can be taken into account when integrating all the factors that may contribute to the carious process in an individual patient
■ to monitor the efficacy of caries prevention techniques, such as dietary and oral hygiene advice and the use of antimicrobial agents such as chlorhexidine.
Microbiology of root surface caries
Approximately 60% of individuals in the West aged 60 or older now have root caries. This has arisen mainly because of the reduction in enamel caries and the consequential retention of teeth later into life, accompanied by gingival recession. The soft cemental surfaces thus exposed are highly susceptible to microbial colonization by virtue of their irregular and rough surfaces.
Early studies showed a high prevalence of Actinomyces naeslundii, Actinomyces odontolyticus and Rothia dentocariosa from human root surface caries. However, more recent data suggest a stronger association between lactobacilli, mutans streptococci and root caries. Indeed, the presence of lactobacilli is considered to be predictive of subsequent development of such lesions. The latter organisms, together with pleomorphic Gram-positive rods, are also frequent in the deeper dentinal parts of the lesion. Recent molecular analyses of deep dentinal surfaces of root caries lesions, to some extent, confirm previous findings and indicate Streptococcus mutans, lactobacilli and R. dentocariosa to be the predominant species. However, these organisms were associated with a vast number (>40) of new taxa!
The current information available therefore suggests:
■ a polymicrobial aetiology for caries initiation and progression on root surfaces
■ bacterial succession during the progression of the lesion with deeper lesions having flora different from those of the superficial lesions.
Prevention of dental caries
The major approaches to prevention of caries are:
1. sugar substitutes: stopping or reducing between-meal consumption of carbohydrates, or substituting non-cariogenic artificial sweeteners (e.g., sorbitol, xylitol or LYCASIN)
2. fluorides: making the tooth structure less soluble to acid attack by using fluorides
3. sealants: to protect susceptible areas of the tooth (e.g., pits and fissures) that cannot easily be kept plaque free by routine oral hygiene measures
4. reducing cariogenic flora: so that even in the presence of sucrose, acid production will be minimal (e.g., oral hygiene aids, antimicrobial agents and possibly immunization)
5. probiotics replacement of cariogenic bacteria by organisms with low or no cariogenic potential.
The rationale for these procedures is outlined below.
Artificial sweeteners or sugar substitutes cannot be absorbed and metabolized to produce acids by the vast majority of plaque biofilm bacteria. Two types of sugar substitute are available:
■ nutritive sweeteners with a calorific value, for example, the sugar alcohols, sorbitol and xylitol, and LYCASIN (prepared from cornstarch syrup)
■ non-nutritive sweeteners, for example, saccharin and aspartame.
Fluoride can be delivered to the tooth tissue in many ways. When administered systemically during childhood, it is incorporated during amelogenesis. The best delivery vehicle is the domestic water supply (at a concentration of 1 ppm); failing this, tablets, topical applications of fluoridated gel or fluoridated toothpaste may be used.
Fluoride ions exert their anticariogenic effect by:
1. substitution of the hydroxyl groups in hydroxyapatite and formation of fluoroapatite, which is less soluble in acid during amelogenesis
2. promotion of remineralization of early carious lesions in enamel and dentine
3. modulation of plaque metabolism by:
• interference with bacterial membrane permeability
• reduced glycolysis
• inactivation of key metabolic enzymes by acidifying the cell interior
• inhibition of the synthesis of IPSs, especially glycogen.
Sealants prevent caries in pits and fissures by eliminating stagnation areas and blocking potential routes of infection. Early lesions that are well sealed can be effectively arrested by this technique, whereas more extensive lesions may extend into pulp, as the trapped cariogenic bacteria are able to use the carious dentinal matrix as a source of nutrition.
Control of cariogenic plaque biofilm flora
Control may be achieved by mechanical cleansing, antimicrobial therapy, immunization and replacement therapy.
Mechanical cleansing techniques
Conventional tooth-brushing with a fluoridated toothpaste is not very successful in reducing the caries incidence as it is entirely dependent on the motivation and skill of the patient. Further, it is unlikely that mechanical cleansing even with flossing, interdental brushes and wood sticks will affect pit and fissure caries.
Chlorhexidine as a 0.2% mouthwash is by far the most effective antimicrobial for plaque control:
1. Chlorhexidine disrupts the cell membrane and the cell wall permeability of many Gram-positive and Gram-negative bacteria.
2. It is able to bind tenaciously to oral surfaces and is slowly released into the saliva.
3. It interferes with the adherence of plaque-forming bacteria, thus reducing the rate of plaque accumulation.
4. Compared with other bacteria involved in plaque biofilm formation, mutans streptococci are exquisitely sensitive to chlorhexidine and are therefore preferentially destroyed.
Unfortunately, because of the problems of tooth staining and unpleasant taste, chlorhexidine is normally only used for short-term therapy.
Active immunization against dental caries
Using either cell wall-associated antigens (antigen I/II) or glucosyl transferases (extracellular enzymes) from mutans streptococci is effective in reducing experimental dental caries in rats and monkeys. The vaccine may produce its protective effect by:
■ inhibition of the microbial colonization of enamel by secretory immunoglobulin A (IgA)
■ interference with bacterial metabolism
■ enhancement of phagocytic activity in the gingival crevice area due to the opsonization of mutans streptococci with IgA or IgG antibodies.
However, convincing proof that any of these mechanisms prevents the development of dental caries in vivo is lacking. Vaccination trials on humans have been unsuccessful because of fears of possible side effects, which would be unacceptable as caries is not a life-threatening disease. (The antibodies that develop after immunization with most antigens of Streptococcus mutans tend to cross-react with heart tissue, and the possibility that heart damage could result has made human vaccine trials very difficult.) Furthermore, the incidence of dental caries is falling in the West and the disease can be adequately controlled using other techniques.
A caries vaccine could, however, be useful for developing countries with limited dental services and increasing prevalence of caries, and also for prevention of disease in high-risk groups, for instance, children with mental or physical disabilities.
Experimental studies indicate that when the natural levels of oral mutans streptococci are suppressed by chlorhexidine, topical application of monoclonal antibodies against antigen I/II of mutans streptococci prevents recolonization by the organisms. Transgenic plants could be used to produce dimeric antibodies with specificity to antigen I/II of streptococci that are stable in the mouth and persist for longer periods than the monomeric antibody. These new developments have heightened the hopes of an alternative caries-preventive strategy for the future.
Experimental studies indicate that genetically engineered, low-virulence mutants of mutans streptococci that are deficient in glucosyl transferase or deficient in lactate dehydrogenase activity can be 'seeded' into the oral environment. These organisms can replace their more virulent counterparts and prevent their re-emergence. The term probiotic therapy or probiotics is now used for approaches where the offending pathogen is replaced artificially by innocuous commensals that are allowed to obtain a permanent foothold in the locale (e.g., oral cavity, intestines, vagina). It is feasible that replacement therapy of this nature may be exploited to control cariogenic flora in the future. However, assurances of the safety of these replacement strains are needed by both the public and the authorities before these methods are realized.
• Caries is defined as localized destruction of the tissues of the tooth by bacterial fermentation of dietary carbohydrates.
• Dental caries is a multifactorial, plaque biofilm-related chronic, non-communicable infection of the enamel, cementum or dentine.
• Key factors in the development of tooth caries are the host (susceptible tooth surface and saliva), plaque biofilm bacteria and diet (mainly fermentable carbohydrates).
• The initial caries lesion is the ‘white spot’ created by the demineralization of enamel; this is reversible and can be remineralized; cavitation represents irreversible disease.
• The specific plaque hypothesis postulates that mutans streptococci are important in caries initiation, whereas heterogeneous groups of bacteria are implicated in the nonspecific plaque hypothesis.
• Lactobacilli are implicated in the progression of caries, especially in the advancing front of the carious lesions (dentinal interface).
The properties of cariogenic flora that correlate with their pathogenicity are the ability to metabolize sugars to acids rapidly (acidogenicity), to survive and grow under low pH conditions (aciduricity) and to synthesize extracellular and intracellular polysaccharides.
Strategies to control or prevent caries include sugar substitutes, fluoridation (to increase enamel hardness mainly), fissure sealants and control of cariogenic flora (by antimicrobials, vaccination or passive immunization, or replacement therapy).
Microbiological tests should be undertaken to identify caries risk factors in patients with extensive (rampant) or recurrent caries, prior to delivering dental care (e.g., extensive crown and bridge treatment).
High salivary or plaque counts of mutans streptococci
(>106/ml) and lactobacilli (>10 000/ml) indicate high risk of disease.
Review questions (answers on p. 367)
Please indicate which answers are true, and which are false.
32.1 Which of the following statements on dental caries are true?
A. signs of fissure caries can be first detected in dentine
B. fissure caries is commonly seen in the lingual surface of the incisors
C. approximately 90% of people aged over 60 years in the West have root surface caries
D. smooth-surface caries is mainly seen on the adjacent tooth surfaces
E. recurrent caries is commonly associated with an existing restoration
32.2 The mutans group of streptococci are key cariogenic pathogens. Which of the following belongs to the mutans group?
A. Streptococcus mutans
B. Streptococcus pyogenes
C. Streptococcus sobrinus
D. Streptococcus ratti
E. Streptococcus pneumoniae
32.3 Which of the following statements supports the role of mutans streptococci as cariogenic?
A. positive correlation of the salivary mutans streptococci count and the prevalence of caries
B. their aciduric and acidogenic characteristics
C. their isolation from supragingival plaque biofilm samples
D. production of extracellular polysaccharides
E. their association with Veillonella species in root surface caries
32.4 With regard to microbiological evaluation of cariogenic activity, which of the following statements are true?
A. it can be accomplished by saliva culture on blood agar to isolate mutans streptococci
B. a salivary count of >100 000/ml lactobacilli indicates high caries activity
C. the procedure is more helpful to monitor the response to treatment than making the initial diagnosis
D. isolation of cariogenic organisms signifies that all teeth are at equal risk of developing caries
E. it is particularly useful for caries risk diagnosis in high-risk groups
32.5 With regard to prevention of dental caries, which of the following statements are true?
A. probiotic therapy with 'non-cariogenic' bacteria is the most promising approach
B. caries vaccine may be useful for disease prevention in high caries-risk groups
C. chlorhexidine mouthwash is by far the most effective approach for plaque reduction
D. water fluoridation, though effective, leads to other major systemic illnesses
E. remineralization of early lesions can be accomplished by fluoridated toothpaste
Bowden, G. H. W. (1990). Microbiology of root surface caries. Journal of Dental Research, 69, 1205-1210.
Kidd, E. A. M., & Fejerskov, O. (2003). Dental caries: The disease and its clinical management. Copenhagen: Blackwell Munksgaard.
Kilian, M., Chapple, I. L., Hannig, M., et al. (2016). The oral microbiome - an update for oral healthcare professionals. British Dental Journal, 221, 657-666.
Marsh, P. D., & Marin, M. V. (2009). Oral microbiology (5th ed.). London: Churchill Livingstone.
Russell, M. W., Chiders, N. K., Michalek, S. M., et al. (2004). A caries vaccine? The state of the science of immunization against dental caries. Caries Research, 38, 230-235.
Shen, S., Samaranayake, L. P., Yip, H. K., et al. (2002). Bacterial and yeast flora of root surface caries in elderly, ethnic Chinese. Oral Diseases, 8, 207-217.