In consideration of the above, four essential components are to be included as part of the medical model if the management of caries is to be successful: (1) control of bacterial infection; (2) reduction of risk levels; (3) remineralisation of teeth; and (4) long-term follow-up. Although these components may be discussed separately in scientific literature, their connection and relationship in a medical model has not been thoroughly considered.
3.1. Control of Bacterial Infection
Caries results from acid production by acidogenic bacteria that forms and thrives in plaque biofilm in the presence of fermentable sugar. The relationship between caries and the bacteria responsible for the disease has been studied in the past. Recently, the role of bacteria and the aetiology of caries has been explained by the ecological plaque hypothesis, which encompasses ideas from the previous specific and non-specific plaque hypothesis as the cause of caries. The ecological plaque hypothesis is understood where specific pathogens which are commonly referred to as the ‘cariogenic bacteria’ are normally present in all tooth sites, even sound tooth tissue surfaces, and caries disease occurs as a result of an imbalance and environmental change in the biofilm that shifts the ecology into favouring the growth and metabolism of these ‘specific’ pathogens, most notably,
Streptococcus mutans and lactobacilli. These pathogens are able to endure and create acids which lead to the formation of cavities, or so we call it, ‘caries’ [
15].
In response to caries as an infectious disease, chemotherapeutic medications targeting bacterial biofilms would reasonably be expected to control the disease [
16]. A number of antimicrobials have been marketed and their effectiveness varies substantially. Chlorhexidine (CHX) is an antimicrobial suggested for anti-caries use, but research conclusions have been inconsistent. A 2015 Cochrane review on CHX treatments concluded that the evidence for CHX varnishes or gels to prevent caries or reduce
S. mutans count is weak [
17], while the same antimicrobials appear to inhibit caries of up to 46% according to a meta-analysis published in 1996 [
18]. Another report suggested that data might be ‘promising’ for CHX varnishes and gels, but not CHX rinses [
19]. Fluoride itself is also an antimicrobial, but its role in hard tissue remineralisation appears to be far more pronounced and clinically relevant than its antimicrobial effects at lower concentrations [
20]. Xylitol, a sugar substitute, is a known antimicrobial and has been shown to interrupt
S. mutans metabolism and reduce plaque acid formation [
21]. Other topical antimicrobials such as vancomycin have been suggested for removing specific cariogenic bacteria, but the idea has been met with resistance in the view that the superfluous use of antibiotics in the oral environment gives rise to possible bacterial resistance in the host [
16].
Indeed, controlling a biofilm disease would not simply be successful by dealing with only one or two ‘pathogenic’ species at a time, or using a one-drug-kills-all approach that wipes out the entire biofilm altogether considering that salivary pellicle and bacterial plaque forms all the time and is ubiquitous in the oral cavity. Furthermore, even when chemotherapeutic methods have been shown to reduce microbial counts, this might not directly translate into caries reduction [
16]. In spite of this, chemotherapeutic medications such as topical chlorhexidine may be used to some success to target the microbial aetiology of caries in individuals with high cariogenic bacteria counts.
3.2. Reduction of Risk Levels
An individualised caries preventive plan may be formulated for patients who have undergone proper caries risk assessment [
22]. The sequence first involves an identification of caries risk factors by the clinician, followed by calculation according to the significance of each risk factor towards future caries incidence. The third step is used to produce a preventive plan that may be unique and appropriate to the patient’s clinical conditions and sociodemographic background in order to tackle the caries disease in the most effective and practical manner.
Numerous risk factors have been reported throughout scientific literature that contribute to varying extents with the initiation and propagation of the caries process [
22]. Examples of caries risk factors explored involve clinical (past caries experience, time since tooth eruption, tooth site and morphology, denture or appliance usage), plaque or oral hygiene level, biochemical (saliva quality and quantity due to radiation or drug therapy, salivary proteins), microbiological profile, socioeconomic (education or family background, social level, income) and lifestyle parameters (diet, nursing and oral hygiene habits, history of drug abuse). The significance of each type of risk factor (in terms of odds ratio or relative risk) and accuracy of caries risk level prediction using single or a combination of risk factors (in terms of sensitivity and specificity) have been tested in many populations [
22]. Existence or co-existence of multiple factors in the same individual informs about his or her heightened caries risk and necessitates additional risk reduction measures.
Caries risks, however, are not static, but change throughout the life of an individual. Factors significantly increasing a child’s probability of having caries may play a lesser role in caries progression to the same individual as an adult. Elderly persons, on the other hand, are distinctly influenced by risk factors such as xerostomia and gingival recession by increased exposure of root surfaces [
19]. It could be safely inferred that even risk management strategies differ across the age group, which further accentuates the importance of individualised risk assessment and tailored management plans.
The caries preventive plan incorporates risk reduction strategies from multiple perspectives in order to be effective. It involves the input of professional advice and treatment, as well as patient input by behavioural or lifestyle modifications. From the point-of-view of practicality and efficacy, caries risk reduction is an integration of four approaches: (1) dietary analysis and advice to reduce sugar intake; (2) plaque control by reinforcing oral hygiene; (3) use of chewing gum to increase salivary protection; (4) dental sealants to prevent fissure caries; and (5) use of fluoride. The use of fluoride pertains to the remineralisation of dental hard tissues, which is a major component of the medical model in caries management, and is elaborated in detail in the next section.
Frequent sugar intake is a major cause of dental decay and is additionally responsible for other health threats, most notably, diabetes mellitus. The presence of simple sugars in the oral cavity perpetuates the caries process, favouring certain acidogenic bacteria and the formation of cariogenic plaque. The frequency to which an individual is exposed to fermentable sugars, including sucrose or its monosaccharides, greatly accelerates the formation of caries [
23]. Reducing the frequency of intake of cariogenic carbohydrates lowers an individual’s caries risk. Recommending lower daily sugar consumption by means of a dietary consultation and advice to consume less cariogenic alternatives is most often the suggested method to cut down on fermentable carbohydrates and discontinue the caries process.
Plaque control by the individual is intended for disrupting the cariogenic biofilm that is favourable for cariogenesis. Oral hygiene instruction by a dental professional, such as a dentist or dental hygienist, is essential in reinforcing the use of a correct technique for plaque removal by the individual on a daily basis. The effectiveness of plaque control lies not only within the removal of plaque, but also with the concurrent use of fluoridated dentifrice. Proper plaque control is a prerequisite for teeth without decay or periodontal disease.
While destructive factors such as sugar and cariogenic biofilms are taken care of, protective factors should be enhanced to further minimise caries risk as far as possible. This includes increasing salivary protection, use of fluorides for remineralisation of dental hard tissues and fissure sealants.
Saliva stimulation utilises saliva as a natural protection against caries by its flushing activity; reservoir of calcium, phosphate and fluoride ions; and buffering potential against a drop in pH [
21]. It also contains proteins with antimicrobial and anticaries activity [
24]. Reduction in salivary content, regardless of cause, has been shown to increase the risk and rate of cariogenesis. Use of chewing gums, pastille or lozenges that are sugar free or with sugar substitutes (such as xylitol or sorbitol) stimulates salivary flow and is protective against caries and may be recommended for individuals [
25,
26].
Finally, dental sealants remain a valuable armamentarium in the fight against dental caries. Systematic reviews have shown that pit and fissure sealants are effective in reducing caries incidence with similar outcomes between resin and glass ionomer varieties [
27,
28]. Glass ionomer sealants might possibly have an additional cariostatic benefit by local fluoride release. Sealants reduce caries risk by mechanically blocking the accumulation and formation of cariogenic plaque from uncleansable deep pits and fissures and alter the microenvironment within the fissure into a cariostatic one. A recent guideline has reflected the strength of the recommendation of fissure sealant placement in tooth surfaces at risk of caries [
29].
3.3. Remineralisation
Remineralisation of enamel and dentine damaged by the caries process is an essential step in promoting the healing of these tissues and protecting them from future cariogenesis to maintain their integrity. A great diversity of products containing remineralisation agents have been marketed, which may contain different levels of fluoride, casein phosphopeptide-amorphous calcium phosphate (CPP-ACP), arginine, functional tricalcium phosphate etc. Amongst the group, the chemical most extensively and successfully used for this purpose is fluoride. Fluoride remineralisation is capable of arresting the disease and even reversing the early signs of caries by the formation of an ion reservoir in plaque or on the surface of enamel in various forms of calcium fluorides [
30]. Fluoride is released at different rates in various acidity levels, depending on the compound type and formulation [
31], which is then available for biomineralisation. Ensuring a low fluoride level in saliva at a slightly acidic range of pH 4.5 to 5.5 maintains the formation of a fluorapatite or fluorohydroxyapatite during the simultaneous dissolution of a more soluble hydroxyapatite, thus preventing a net loss of minerals from the tooth surface [
30] while increasing the acid resistance of enamel and propensity for further caries attack. These mechanisms moderate the caries process such that not only is net demineralisation prevented, but demineralised lesions may also have the potential to be remineralised and ‘healed’.
A plethora of fluoride agents have existed on the market for individual or home-use, as well as for professional application. Fluoride levels are normally measured by fluoride ion concentration in parts per million (ppm) in order to compare different forms of fluoride. The actual bioavailability of the fluoride ions determines the effect of the dentifrice in question. Currently, fluorides could be incorporated as remineralisation agents in the forms of sodium fluoride, stannous fluoride, sodium monofluorophosphate, acidulated phosphate fluoride and silver diamine fluoride. The type of fluoride compound determines its physical properties, including the solubility and stability in solution, which dictates how much of it that could be mixed into home or professional use agents.
At the individual level, fluoride agents can be applied at the individual level on a daily basis by the use of over-the-counter fluoride toothpastes at a 1000–1500 ppm fluoride concentration following the FDI policy statement revised in 2018 [
32]. Low-dose toothpastes (500 ppm or below) are also available, although guidelines for usage have varied. Taking into account the risk of fluorosis associated with fluoride dentifrice usage by young children, the most recent Cochrane review recommends dental practitioners to ‘[balance] against the risk of fluorosis’ when deciding to prescribe fluoride toothpastes [
33], while other reviews have suggested simply reducing the amount of toothpastes containing moderate or high fluoride concentrations for a maximum benefit [
34], or for young children to use such toothpastes (1000–1500 ppm) only when supervised, as stated in the FDI policy statement in 2018 [
35]. High fluoride toothpastes (up to 5000 ppm) could be prescribed by the dentist for high risk individuals. Fluoride mouth wash are available at even lower fluoride concentrations with 0.02% acidulated phosphate fluoride or neutral 0.05% sodium fluoride. At the other end of the spectrum, dental professionals may deliver topical fluorides at a higher range of concentrations, typically from 1.23% sodium fluoride gel or foam to commonly used 5% sodium fluoride varnish (22,600 ppm) and even 38% silver diamine fluoride solution (44,800 ppm). The form of delivery is up to the discretion and preference of the dentist after the caries risk level of the patient is taken into consideration. Evidently, there is no lack of fluoride products on the market or available for use by the dental professional for the remineralisation of teeth. Remineralisation methods are versatile and the value of topical fluoride application in preventing caries and remineralising early caries lesions should never be denied or underestimated as the literature has shown it to be effective, plus it is simple to apply, painless, and low cost, compared with any other surgical methods of caries intervention.
3.4. Long Term Follow-Up
Successful dental health maintenance relies on long term follow-up. The follow-up has two main aims: first, to re-evaluate the outcomes of the caries intervention and plan for new interventions, if necessary; and second, to screen for new early caries lesions so that the disease can still be managed in its reversible stage. Re-evaluating the outcomes may include several aspects, including reviewing the compliance of the patient on his or her oral hygiene and dietary adjustments and checking to see if early caries lesions are arrested. At this stage, a follow-up allows the dental professional to feedback to the patient what has been achieved since the past appointment and adjust the oral hygiene and dietary suggestions. Communication between the dentist and the patient may reveal challenges to caries control and can be dealt with during the follow-up session. When indicated, topical fluoride or sealants may be re-applied during this maintenance phase of treatment. In the long run, yearly follow-up or review appointments serve to detect new changes in risk factors or behaviours, as well as screening for new initial caries so that the dental professional and patient may act towards keeping caries activity to a minimum. All this effort recalls the primary objective of the medical model in caries management, which is to optimise dental health, prevent new disease and arrest ongoing disease process. It goes without saying that without an effective recall system, the effect of successful intervention could gradually wane off until the patient returns to or reaches a state of caries imbalance again.