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Demineralization and Remineralization

Introduction

While the underlying pathophysiologic process in caries disease is infection, the outward manifestation of the disease is a defect in enamel. This defect is an end result of a process of gradual dissolution of the calcium and phosphate of the tooth by acid leading to softening of the enamel. The oral cavity is a balanced ecosystem where teeth are continuously exposed to acidic challenges from foods and the acid produced by fermenting bacteria. Acid dissolves calcium and phosphate ions from the enamel in the process of demineralization, allowing defects to form in the enamel. Homeostasis 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. 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 acidic foods, and decreased saliva.1

Caries is a dynamic disease that results from an imbalance between demineralization and remineralization due to altered pH levels in the oral cavity. As the pH in the oral cavity falls below 5.5, the protective factors are overwhelmed by the pathological factors. This decrease in pH results in a favorable environment for acidogenic and acid-tolerant cariogenic bacteria. (See Figure 1 and Figure 2.)

Acidogenic Bacteria

The oral cavity is home to a wide variety of aerobic and anaerobic bacteria, many of which produce acid as a result of their metabolism. Saliva provides a buffering effect to neutralize the acid. Such controlled changes in the oral environment do not necessarily combat the oral microbes directly but instead reduce the impact of these bacteria.

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.  Streptococcus mutans and Lactobacillus are both acidogenic bacteria that contribute to dental caries. S. mutans is the major microbiological cause of decay because it can metabolize carbohydrates at a low pH and adhere to hard dental surfaces and plaque. Lactobacillus is not as able to colonize into biofilm, making it less virulent than S. mutans. S. mutans and other pathogens may be passed from mother to child.2

Pathogenic Factors

When patients consume a diet high in acid or simple sugars, fermentable carbohydrates become readily available to acidogenic bacteria. 3 Individuals with poor saliva production (xerostomia) also are at increased risk of caries because they lack the buffering effect of saliva. Xerostomia is often seen in cancer therapy, autoimmune systemic diseases such as Sjögren's syndrome, lupus, and scleroderma, systemic diseases including diabetes, Crohn's disease, and HIV/AIDS, and the use of certain medications such as antihistamines, antidepressants, and some antihypertensives. With decreased flow of saliva, the acid produced by fermenting bacteria is allowed to remain in contact with the enamel, leaching the calcium and phosphate ions and softening the enamel.

Protective Factors

Healthy salivary flow provides cleansing and buffering, effectively diluting and neutralizing the acids produced by bacteria. 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 a hostile environment for bacteria, and buffers acids. Continuous salivary flow clears unattached microorganisms and limits pathogenic bacteria from attaching to the tooth surface. Higher volumes of saliva lead to more frequent swallowing, reducing the length of time of acid exposure. Saliva also provides additional antimicrobial proteins such as lysozyme, lactoperoxidase, lactoferrin, and antimicrobial peptides.

Saliva is essential to remineralizing demineralized tooth surfaces. The formation of the enamel pellicle retards the loss of minerals from the tooth surface and acts as a protective layer against the tooth surface while also serving as a reservoir for calcium and phosphate. The availability of calcium and phosphate ions is an important component in promoting remineralization and protecting teeth against demineralization. Remineralization of the enamel occurs when calcium and phosphate ions from saliva are reintegrated with the hydroxyapatite of the enamel.

Promoting Remineralization

Remineralization can be accomplished in several ways, including targeting the pathogenic factor (acidogenic bacteria) and modifying key environmental factors, such as diet, salivary flow, and mineral ion availability. Comprehensive caries prevention strategies involve not only removal of damaged enamel but also treatment of infection and restoration of healthy saliva.1 In order to achieve this, antimicrobial treatments may be required in addition to other remineralization strategies.

Fluoride controls the rate at which caries develop. When fluoride ions are present in plaque fluid along with dissolved hydroxyapatite, and the pH is higher than 4.5, a fluorapatite-like remineralized veneer is formed over the remaining surface of the enamel. This veneer is much more acid-resistant than the original hydroxyapatite, and is formed more quickly than ordinary remineralized enamel would be. 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. 4-7

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. 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 mouth rinse is an effective adjunct to other anticaries treatments.8

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. Xylitol is a natural sweetener that is safe and noncariogenic because it is unable to be fermented by bacteria.

Strategies that provide symptomatic relief of xerostomia, as well as therapies to stimulate salivary flow, should be recommended for patients with reduced saliva flow. Artificial saliva products, oral lubricants, and xylitol gum may provide relief from symptoms. Secretagogues, including pilocarpine and cevimeline, stimulate salivary flow and may be helpful for individuals with dry mouth. To encourage remineralization, calcium phosphate-based systems such as 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.9 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 calcium hydroxyapatite to form in the demineralized enamel.

New Directions

From a public health standpoint, much work has been done in developing outreach programs for delivery of fluoride toothpastes, dentifrices, and varnishes to preschool and school-age children, the elderly, and institutionalized populations.10 Mobile dental clinics have been able to reach inner city impoverished populations and rural communities with poor access to care.11 Through these efforts, dental hygienists have been able to identify early caries disease and treat evidence of demineralization.

Advocates of minimal intervention dentistry have investigated simply sealing early and incipient caries lesions with epoxy rather than removing damaged enamel. The effect is to protect the vulnerable softened enamel from oral acids and bacterial invasion. While sealed, the enamel remineralizes. Results have been positive, with very few failures in carefully selected patients. 12-15

Studies have evaluated the use of silver diamine fluoride for preventing and arresting early caries lesions, finding significantly higher levels of fluoride in biofilm without significant changes in caries rate relative to fluoride pastes.16 Another product, 45S5 bioglass paste, was studied in comparison with fluoride treatment and produced significantly greater improvements in microhardness of enamel.17 Topical application of antimicrobials helps control bacterial invasion of vulnerable tooth surfaces and may allow remineralization to occur.18,19

Conclusions

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. Clinicians with an understanding of the demineralization process and available approaches to encourage remineralization will be better prepared to treat lesions before the cavitation of tooth structure progresses. Accurately assessing an individual's caries risk and implementing preventive measures comprise a conservative approach to caries prevention.

References

1.            Steinberg S. A paradigm shift in the treatment of caries. General dentistry. 2001;50(4):333-338.

2.            Berkowitz R, Jordan H. Similarity of bacteriocins of< i> Streptococcus mutans</i> from mother and infant. Archives of oral biology. 1975;20(11):725-730.

3.            Armfield JM, Spencer AJ, Roberts-Thomson KF, Plastow K. Water fluoridation and the association of sugar-sweetened beverage consumption and dental caries in Australian children. American journal of public health. Mar 2013;103(3):494-500.

4.            Broffitt B, Levy SM, Warren J, Cavanaugh JE. Factors associated with surface-level caries incidence in children aged 9 to 13: the Iowa Fluoride Study. J Public Health Dent. Fall 2013;73(4):304-310.

5.            American Academy of Pediatric Dentistry. Liaison with Other Groups C. Guideline on fluoride therapy. Pediatric dentistry. Sep-Oct 2012;34(5):166-169.

6.            Marinho VC, Worthington HV, Walsh T, Clarkson JE. Fluoride varnishes for preventing dental caries in children and adolescents. Cochrane Database Syst Rev. 2013;7(7):CD002279.

7.            Weyant RJ, Tracy SL, Anselmo TT, et al. Topical fluoride for caries prevention: executive summary of the updated clinical recommendations and supporting systematic review. Journal of the American Dental Association. Nov 2013;144(11):1279-1291.

8.            James P, Parnell C, Whelton H. The caries-preventive effect of chlorhexidine varnish in children and adolescents: a systematic review. Caries Res. 2010;44(4):333-340.

9.            Li J, Xie X, Wang Y, et al. Long-term remineralizing effect of casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) on early caries lesions in vivo: a systematic review. J Dent. Jul 2014;42(7):769-777.

10.          Guay AH. Access to dental care: solving the problem for underserved populations. Journal of the American Dental Association. Nov 2004;135(11):1599-1605; quiz 1623.

11.          Ramos CM. The Mobile Care Health Project: Providing Dental Care in Rural Hawai'i Communities. Journal of Community Psychology. 2011;1(3).

12.          Hesse D, Bonifacio CC, Mendes FM, Braga MM, Imparato JC, Raggio DP. Sealing versus partial caries removal in primary molars: a randomized clinical trial. BMC Oral Health. 2014;14(1):58.

13.          Holmgren C, Gaucher C, Decerle N, Doméjean S. Minimal intervention dentistry II: part 3. Management of non-cavitated (initial) occlusal caries lesions–non-invasive approaches through remineralisation and therapeutic sealants. British dental journal. 2014;216(5):237-243.

14.          Wierichs RJ, Meyer-Lueckel H. Systematic review on noninvasive treatment of root caries lesions. J Dent Res. Feb 2015;94(2):261-271.

15.          Zero DT, Fontana M, Martinez-Mier EA, et al. The biology, prevention, diagnosis and treatment of dental caries: scientific advances in the United States. Journal of the American Dental Association. Sep 2009;140 Suppl 1:25S-34S.

16.          Shah SG, Bhaskar V, Chawla S, et al. Efficacy of silver diamine fluoride as a topical fluoride agent compared to fluoride varnish and acidulated phosphate fluoride gel: An in vivo study. Journal of Pediatric Dentistry. 2014;2(1):5.

17.          Bakry AS, Marghalani HY, Amin OA, Tagami J. The effect of a bioglass paste on enamel exposed to erosive challenge. J Dent. Nov 2014;42(11):1458-1463.

18.          Aguzzi C, Sandri G, Cerezo P, et al. A novel bioadhesive semisolid formulation containing chitosan and tetracycline/layered clay complexes for local delivery into periodontal pocket. Materials Technology. 2014.

19.          Pragati S, Ashok S, Kuldeep S. Recent advances in periodontal drug delivery systems. International Journal of Drug Delivery. 2011;1(1).

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