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Caries Disease--New Understandings

Dental caries is the result of a chronic infectious disease that affects nearly half of the adult population of the world.1,2 This makes dental caries the most common infectious disease in the world. Bacteria in the mouth grow and flourish on ingested carbohydrates and residual food, creating acid as a byproduct of their metabolism. That acid removes calcium from the enamel of the teeth, leaving behind defects in the surface called caries. Removal of the bacterial “home” in the form of plaque, and strengthening of the enamel using fluoride, have been shown to be highly effective methods of fighting this global health problem.

Background  

Dental plaque is a naturally developed biofilm that builds up on the surfaces of teeth. (Figure 1) It is a general term for the diverse microbial community embedded in a matrix of polymers of bacterial and salivary origin. The process of attachment, growth, removal, and reattachment of dental plaque to the tooth surface is a continuous and dynamic one, even after professional or home intervention. If left uninterrupted and allowed to develop on teeth, the potential for demineralization and caries can increase. In individuals with a high-carbohydrate diet or with compromised salivary flow, the levels of potentially cariogenic bacteria can increase, compromising enamel health.3,4 For years, dental professionals have primarily focused on the removal of dental plaque for caries prevention.

The caries process has been well-described in the dental literature. Plaque accumulates on the surfaces of teeth. Certain bacteria within the plaque are acidogenic when they metabolize fermentable carbohydrates. The acids dissolve the calcium phosphate of the tooth enamel resulting in demineralization that, if not addressed, can result in caries. (Figure 2)

Research has shown there are two factors that determine caries progression: 1) pathological factors and 2) protective factors. Pathological factors include acidogenic bacteria (mutans streptococci and lactobacilli), salivary dysfunction, and ingestion of refined carbohydrates. Protective factors include salivary calcium, phosphate and proteins, salivary flow, fluoride in saliva, and antibacterial components. Caries progression (demineralization) or reversal (remineralization) is determined by the balance between these two types of factors. (Figure 3)

Treatment Paradigms  

There has been a shift in the paradigm for treating dental caries. We now know that caries is a reversible multifactorial process. In 2001, the National Institutes of Health sponsored a conference where a “shift toward improved diagnosis of noncavitated, incipient lesions, a treatment for prevention, and arrest of such lesions” was described.5 There are numerous ways in which a dental practice can achieve successful intervention in the caries process. Steinberg6 identified a “medical model” consisting of four steps: bacterial control, reduction of risk levels for at-risk patients, reversal of active sites by remineralization, and follow-up and maintenance. All these steps use a variety of evidence-based methods to prevent dental caries. Considering the pathological factors (acidogenic bacteria; salivary dysfunction; and dietary carbohydrates), encouraging the use of protective factors (regular dental visits; use of antimicrobial agents such as chlorhexidine; oral hygiene with contemporary dentifrices and powered brushes; and dietary practices) can affect caries incidence. Since these are individual behaviors, patient counseling and intervention by dental professionals is critically important to achieving balance in the demineralization-remineralization cycle.

Assessing the Risk of Caries Development  

Risk assessment is another critical aspect involving the paradigm shift in treating dental caries. The Caries Management by Risk Assessment model (Figure 4) evaluates the probability of caries incidence in a certain time period.7,8 The assessment should evaluate all factors involved with the disease including current caries, diet, fluoride exposure, presence of cariogenic bacteria, salivary status, general medical history, and sociodemographic influences. Caries risk assessment is receiving considerable attention, and new technologies are being developed to aid practitioners in assessing risk.9 Chairside molecular probes to assess a patient’s cariogenic bacteria, a caries vaccine, and improved early detection methods are on the horizon. A preventive and restorative management plan and frequency of recall visits should all depend on the patient’s caries risk.10

Recent scientific advances in the understanding of the caries process and prevention focus on protective factors including salivary calcium, phosphate, and proteins, salivary flow, fluoride concentration in saliva, and antibacterial components that can assist in the remineralization process. Saliva is essential for the protection of the tooth against dental caries and provides many natural protective factors. Salivary flow rate, buffering capacity, antimicrobial activity, microorganism aggregation and clearance from the oral cavity, immune surveillance, and calcium phosphate binding proteins all interact to inhibit or reverse demineralization. Topical fluoride therapy has been well established for inhibition of demineralization and enhancing remineralization.11-13 It has been found that prolonged and slightly elevated low concentrations of fluoride in the saliva and plaque fluid are beneficial. The intake of fluoride is typically derived from beverages, drinking water, foods, and fluoride-containing dental products such as toothpastes and rinses.

An ideal time to educate patients about caries and prevention is during the clinical examination visit. Selection and technique of toothbrushing, choice of dentifrice, and careful flossing can be emphasized by all members of the dental care team. Powered toothbrushes are generally recommended for home care since they achieve consistently significant improvements in plaque burden.14 While the mechanism of action is not well understood, baking soda containing dentifrices appear to be more effective at removal of dental plaque than dentifrices without baking soda.15 In fact, baking soda toothpastes were even more effective in plaque removal and control than antibiotic-containing pastes in a series of clinical trials.16

Chewing gum containing xylitol has also been shown to be variably effective for cariogenic bacteria reduction and in caries prevention.17 In fact, studies evaluating the effect of maternal use of chewing gums containing combinations of xylitol, sorbitol, chlorhexidine, and fluoride on caries prevalence in the mother’s children are showing promising results, underscoring the theory of caries disease being primarily an infectious disease that may be transmitted from parent to child.

One of the latest research efforts involves the use of casein phosphopeptide-amorphous calcium phosphate (CPP-ACP).18 Products containing CPP-ACP have been shown to increase resistance to acid and increase remineralization. Casein phosphopeptide-amorphous calcium phosphate is derived from the milk protein casein. A tooth-protective effect occurs due to a casein protein called casein phosphopeptide (CPP), which carries calcium and phosphate ions in the form of amorphous calcium phosphate (ACP). Calcium phosphate is normally insoluble at neutral pH; however the CPP keeps the calcium and phosphate in an amorphous non-crystalline state. When CPP-ACP is added to the oral cavity, parts of the CPP component bind directly to the enamel, biofilm, and soft tissue, delivering calcium where and when it is needed. Its incorporation into the salivary pellicle also seems to significantly reduce the adherence of certain plaque bacteria. The free calcium and phosphate ions then move out of the CPP, enter the enamel rods, and reform apatite crystals, resulting in remineralization. CPP-ACP combined with chewing gum, pastes, mousses, glass ionomers, temporary cements, and rinses have all been examined, showing an increase in enamel remineralization.

Conclusion  

Dental caries is now being seen more as a medical rather than a surgical illness. Like any chronic medical disease, prevention is very effective in reducing complications and improving dental-related quality of life for our patients.19 As a result, the dental hygienist acting as a prevention specialist can now determine dental caries risk factors and introduce remineralization strategies into the dental hygiene diagnosis and treatment plan to prevent this all-too-common infectious disease.

References  

1. Baelum V. Dentistry and population approaches for preventing dental diseases. J Dent Dec 2011;39 Suppl 2:S9-19.

2. Bagramian RA, Garcia-Godoy F, Volpe AR. The global increase in dental caries. A pending public health crisis. Am J Dent 2009;22(1):3-8.

3. 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 2013;73(4):304-310.

4. 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 J Public Health 2013;103(3):494-500.

5. Health NIo. Diagnosis and management of dental caries throughout life. NIH consensus statement. 2001;18(1):1.

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

7. Cheng J, Chaffee BW, Cheng NF, Gansky SA, Featherstone JD. Understanding treatment effect mechanisms of the CAMBRA randomized trial in reducing caries increment. J Dent Res. Jan 2015;94(1):44-51.

8. American Academy of Pediatric Dentistry CoCA. Guideline on Caries-risk Assessment and Management for Infants, Children, and Adolescents. Clinical Guidelines. Vol 352013:123-130.

9. Amaechi BT, Ramalingam K. Evaluation of fluorescence imaging with reflectance enhancement technology for early caries detection. Am J Dent. Apr 2014;27(2):111-116.

10. Domejean S, White JM, Featherstone JD. Validation of the CDA CAMBRA caries risk assessment--a six-year retrospective study. J Calif Dent Assoc. Oct 2011;39(10):709-715.

11. Dean H, Arnold F, Jay P, Knutson J. Studies on mass control of dental caries through fluoridation of the public water supply. Public Health Rep. 1950;65(43):1403-1408.

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

13. Burt B, Tomar S. Changing the face of America: water fluoridation and oral health. In: Ward J, Warren C, eds. Silent Victories: The History and Practice of Public Health in Twentieth-century America: Oxford University Press; 2007:307-322.

14. Ghassemi A, Vorwerk L, Hooper W, Patel V, Sharma N, Qaqish J. Comparative plaque removal efficacy of a new children's powered toothbrush and a manual toothbrush. The Journal of clinical dentistry. 2013;24(1):1-4.

15. Thong S, Hooper W, Xu Y, Ghassemi A, Winston A. Enhancement of plaque removal by baking soda toothpastes from less accessible areas in the dentition. The Journal of clinical dentistry. 2011;22(5):171-178.

16. Putt MS, Milleman KR, Ghassemi A, et al. Enhancement of plaque removal efficacy by tooth brushing with baking soda dentifrices: results of five clinical studies. The Journal of clinical dentistry. 2008;19(4):111-119.

17. Affairs AAoPDCoC. Policy on the Use of Xylitol in Caries Prevention. Reference Manual. 2010;35:45-47.

18. Agarwal R, Singh C, Yeluri R, Chaudhry K. Prevention of Dental Caries-Measures beyond Fluoride. Oral Hyg Health. 2014;2(122):2332-0702.1000122.

19. Chou R, Cantor A, Zakher B, Mitchell JP, Pappas M. Prevention of Dental Caries in Children Younger Than 5 Years Old: Systematic Review to Update the US Preventive Services Task Force Recommendation. 2014.

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