Dental caries, although entirely preventable, remains a common oral disease. Tooth decay is the most chronic health problem among children age 6 to 19, but adults are also affected, with 90% of individuals older than 20 experiencing some form of caries.1,2 The management of oral health can become more difficult with age due to the increased prevalence of hypertension, diabetes, depression, and other health problems, as well as decreased manual dexterity. Changes in systemic health may require a medication regimen, in addition to modifications to lifestyle, diet, and recreational habits that can influence caries risk.3 The oral cavity is a balanced ecosystem that undergoes stress as teeth are continuously exposed to acidic challenges from foods and the acid produced by acidogenic bacteria.3,4 Acids dissolve calcium and phosphate ions from the enamel in the process of demineralization, which leads to dental caries.5 Oral health is sustained when there is a balance between protective factors and pathological factors. This balance is achieved when the net mineral loss (demineralization) and net mineral gain (remineralization) remain in equilibrium.6,7 Protective factors consist of exposure to fluoride, the presence of phosphate and calcium ions in saliva, and adequate salivary flow, while pathological factors include the presence of acidogenic bacteria, frequent ingestion of fermentable carbohydrates, and hyposalivation.6
Caries is a dynamic disease that results from an imbalance of the remineralization-demineralization scale, due to altered pH levels in the oral cavity.7–9 As the pH in the oral cavity falls below 5.5, the protective factors are overcome by the pathological factors.3,4 This decrease in pH results in a favorable environment for acidogenic and acid-tolerating cariogenic bacteria.3
The oral cavity is home to acidogenic bacteria, as well other types of bacteria. These pathogens are managed typically through the presence of saliva, which provides a buffering effect to neutralize the acid.4 Such controlled changes in the oral environment do not necessarily combat the oral microbes directly but, instead, alter the equilibrium and create an inhospitable environment for pathogenic bacteria.3,10 Acidogenic bacteria thrive in a low pH environment.11,12
When food is digested, acidogenic bacteria ferment the carbohydrates to produce lactic acid, which decreases the pH in the mouth and results in demineralization of dental enamel (Figure 1).3,10 Streptococcus mutans and Lactobacillus are both acidogenic bacteria that contribute to dental caries.4 S. mutans is the major microbiological cause of decay because it can metabolize carbohydrates at a low pH and adhere to hard dental surfaces.10 Lactobacillus is not as able to colonize into biofilm, making it less virulent than S. mutans.10,13
When patients consume a high cariogenic diet, fermentable carbohydrates become readily available to acidogenic bacteria.11 Individuals with hyposalivation (the inability to produce adequate amounts of saliva) also are at increased risk of caries because they lack the protection afforded by saliva.11,14
Xerostomia is the feeling of dry mouth caused by hyposalivation.10 The main causes of xerostomia include cancer therapy; autoimmune systemic diseases, such as Sjögren’s syndrome, lupus, and scleroderma; diseases affecting glandular tissues, including diabetes, Crohn’s disease, and human immunodeficiency virus/acquired immunodeficiency syndrome; and medication usage.4,10 More than 400 medications can cause hyposalivation as a side effect. Because older adults tend to be prescribed more medications as they age, this population may be at increased risk for hyposalivation and dental caries.10
Healthy salivary flow provides cleansing and buffering, which dilute and neutralize acidogenic bacteria.10 Saliva forms a protective layer on the tooth in the form of an enamel pellicle, replenishes the demineralized tooth surface with calcium and phosphate ions, provides antimicrobial benefits, and buffers acids.5 Continuous salivary flow clears unattached microorganisms and limits pathogenic bacteria from attaching to the tooth surface.10 Also, when the salivary flow is high, the acid becomes more diluted. Higher volumes of saliva lead to more frequent swallowing, reducing the length of acid exposure.15 Saliva also provides additional antimicrobial proteins such as lysozyme, lactoperoxidase, lactoferrin, and antimicrobial peptides.10
Saliva is essential to remineralizing demineralized tooth surfaces.10 The formation of the enamel pellicle prevents the loss of minerals from the tooth surface.5,16 It acts as a protective layer to slow the diffusion of acid against the tooth surface, while serving as a reservoir for the minerals calcium and phosphate—both of which are necessary for remineralization.3 Salivary proteins bind to the calcium ions, keeping saliva saturated with calcium phosphate. The availability of calcium and phosphate ions is an important component in promoting remineralization and protecting teeth against demineralization.16 Remineralization of the enamel occurs when calcium and phosphate ions from saliva, along with fluoride ions, enter the region of the demineralized lesion and form a new layer of fluorapatite.17 In order for the enamel to remineralize, a significant amount of calcium and phosphate ions are needed.4,18
Remineralization can be accomplished in several ways, including targeting the pathogenic factor (eg, acidogenic bacteria) and modifying the key environmental factors, such as diet, salivary flow, and mineral ion availability.12 Comprehensive caries prevention strategies are moving away from the separate treatment of hard tissue and microbiological causes. In order to achieve this, antimicrobial modalities may be implemented, in addition to other remineralization strategies.19
Chlorhexidine is effective in reducing the number of S. mutans and other acidogenic and cariogenic bacteria in the mouth, but the number of pathogenic bacteria often returns to pretreatment levels within months of discontinuing chlorhexidine use.4 Also, reducing the number of S. mutans does not always reduce caries risk because there are many other contributing factors, such as xerostomia, diet, and poor oral self-care. Chlorhexidine varnish may exert a longer effect on acidogenic bacteria, but this product is not currently available in the United States. For some patients, chlorhexidine mouthrinse is an effective adjunct to other anticaries treatments.4
The amount of acid produced by bacteria in the oral cavity can be greatly reduced by replacing sugar with sweeteners such as xylitol, reducing consumption of acidic foods, and drinking more water.4 Xylitol is a natural sweetener that is safe and noncariogenic because it is unable to be fermented by bacteria.20
Strategies that provide symptomatic relief, as well as therapies to stimulate salivary flow should be recommended for patients with xerostomia. Artificial saliva products, oral lubricants, and xylitol gum may provide relief from symptoms.4,10 Secretagogues, including pilocarpine and cevimeline, encourage salivary flow through salivary gland tissue and may be helpful for individuals with hyposalivation. To encourage remineralization, calcium phosphate-based systems—including amorphous calcium phosphate (ACP), casein phosphopeptide-ACP (Recaldent®), calcium sodium phosphosilicate (NovaMin®), and tricalcium phosphate—can be implemented to incorporate the ions into the enamel matrix. These systems can be effective when a patient’s saliva does not contain enough calcium and phosphate to provide adequate levels of the ions for fluorapatite to form on the demineralized area.4,18,21
Fluoride is the only compound acknowledged by the US Food and Drug Administration (FDA) for the prevention of caries.22 With adequate levels of calcium and phosphate ions, fluoride ions promote the formation of fluorapatite in enamel.23,24 The fluorapatite created through the remineralization process is more resistant to subsequent acidic attack.25 Topical application is the most common delivery method, and the 2014 American Dental Association guidelines recommend applying topical fluoride, consuming fluoridated water, and using over-the-counter fluoride toothpastes for all individuals, regardless of their caries risk.22,26
Research is currently underway to find new ways to boost fluoride’s role in remineralization. For example, investigators are working on a toothpaste that is based on interactions between calcium ions and profluoride compounds. The theory is that after approximately 30 seconds of brushing with this compound-based toothpaste, ionic fluoride is released and reacts with the calcium ions to form the calcium fluoride reservoirs necessary for remineralization.22,27 Another study is investigating a new generation of fluoride mouthrinses containing soluble calcium salts to help retain fluoride in the oral cavity that can be released over time, encouraging remineralization.27 The FDA has approved the use of silver diamine fluoride in the US for preventing and arresting early caries lesions, and research shows it is highly effective.28,29 While silver diamine fluoride can cause tooth discoloration, adding the use of potassium iodide during the fluoride application can prevent this problem.29
The delicate balance of the oral ecosystem is constantly challenged by internal and external factors. Even in a healthy oral cavity, demineralization occurs due to tooth enamel’s porous structure and its susceptibility in a low pH environment.3,5,30 Clinicians with a deep understanding of the demineralization process and available approaches to encourage remineralization will be best prepared to treat lesions before the cavitation of tooth structure progresses.31 Accurately assessing an individual’s caries risk and implementing preventive measures comprise a conservative approach to caries prevention.
- Rethman MP, Beltran-Aguilar ED, Billings RJ, et al. Non-fluoride agents for caries prevention. J Am Dent Assoc. 2011;142:1065–1071.
- Dye BA, Tan S, Smith V, et al. Trends in oral health status, United States, 1988-1994 and 1999-2004. Vital Health Stat 11. 2007;248:1–92.
- Yanase RT, Le HH. Caries management by risk assessment care paths for prosthodontic patients: oral microbial control and management. Dent Clin North Am. 2014;58:227–245.
- Su N, Marek CL, Ching V, et al. Caries prevention for patients with dry mouth. J Can Dent Assoc. 2011;77:85.
- Featherstone JD. The science and practice of caries prevention. J Am Dent Assoc. 2000;131:887–899.
- Featherstone JD, White JM, Hoover CI, et al. A randomized clinical trial of anticaries therapies targeted according to risk assessment (caries management by risk assessment). Caries Res. 2012;46:118–129.
- Silverstone LM. Remineralization phenomena. Caries Res. 1977;11:59–84.
- Centers for Disease Control and Prevention. Hygiene-Related Diseases. Available at: cdc.gov/healthywater/hygiene/disease/dental_caries.html. Accessed April 21, 2015.
- Burne RA, Marquis RE. Alkali production by oral bacteria and protection against dental caries. FEMS Microbiol Lett. 2000;193:1–6.
- Ligtenberg AJM, Almståhl A. Xerostomia and the oral microflora. In: Carpenter G, ed. Dry Mouth: A Clinical Guide on Causes, Effects, and Treatments. Berlin: Springer-Verlag Berlin Heidelberg; 2015:81–101.
- Marsh PD. Dental diseases—are these examples of ecological catastrophes? Int J Dent Hyg. 2006;4(Suppl 1):3–10.
- Marsh PD. Are dental diseases examples of ecological atastrophes? Microbiology. 2003;149:279–294.
- Takahashi N, Nyvad B. The role of bacteria in the caries process: ecological perspectives. J Dent Res. 2011;90:294–303.
- Guggenheimer J, Moore PA. Xerostomia: etiology, recognition and treatment. J Am Dent Assoc. 2003;134:61–69.
- Rudney JD, Ji Z, Larson CJ. The prediction of saliva swallowing frequency in humans from estimates of salivary flow rate and the volume of saliva swallowed. Arch Oral Biol. 1995;40:507–512.
- Martins , Castro GF, Siqueira MF, Xiao Y, Yamaguti PM, Siqueira WL. Effect of dialyzed saliva on human enamel demineralization. Caries Res. 2013;47:56–62.
- ten Cate JM, Featherstone JD. Mechanistic aspects of the interactions between fluoride and dental enamel. Crit Rev Oral Biol Med. 1991;2:283–296.
- Reynolds EC. Calcium phosphate-based remineralization systems: scientific evidence? Aust Dent J. 2008;53:268–273.
- ten cate JM. Novel anticaries and remineralizing agents: prospects for the future. J Dent Res. 2012;91:813–815.
- Fontana M, Gonzalez-Cabezas C. Are we ready for definitive clinical guidelines on xylitol/polyol use? Adv Dent Res. 2012;24:123–128.
- Cochrane NJ, Cai F, Huq NL, Burrow MF, Reynolds EC. New approaches to enhanced remineralization of tooth enamel. J Dent Res. 2010;89:1187–1197.
- Carey CM. Focus on fluorides: update on the use of fluoride for the prevention of dental caries. J Evid Based Dent Pract. 2014;14 (Suppl):95–102.
- ten Cate JM. Current concepts on the theories of the mechanism of action of fluoride. Acta Odontol Scand. 1999;57:325–329.
- Lynch RJ, Navada R, Walia R. Low-levels of fluoride in plaque and saliva and their effects on the demineralization and remineralization of enamel; role of fluoride toothpastes. Int Dent J. 2004;54(Suppl):304–309.
- Featherstone JD. Prevention and reversal of dental caries: role of low level fluoride. Community Dent Oral Epidemiol. 1999;27:31–40.
- Maguire A. ADA clinical recommendations on topical fluoride for caries prevention. Evid Based Dent. 2014;15:38–39.
- Vogel GL. Oral fluoride reservoirs and the prevention of dental caries. In: Buzalaf MAR, ed. Fluoride and the Oral Environment. Basel, Switzerland: Karger Monogr Oral Sci; 2011:146–157.
- Targino AG1, Flores MA, dos Santos Junior VE, et al. An innovative approach to treating dental decay in children. A new anti-caries agent. J Mater Sci Mater Med. 2014;25:2041–2047.
- Chu CH, Lo EC. Promoting caries arrest in children with silver diamine fluoride: a review. Oral Health Prev Dent. 2008;6:315–321.
- Hegde MN, Devadiga D, Jemsily PA. Comparative evaluation of effect of acidic beverage on enamel surface pre-treated with various remineralizing agents: an in vitro study. J Conserv Dent. 2012;15:351–356.
- Hemagaran G, Neelakantan P. Remineralization of the tooth structure—the future of dentistry. International Journal of PharmTech Research. 2014;6:487–493.
From Dimensions of Dental Hygiene. May 2015;13(3):38,40–42.