The most common question I get in my private practice is “why?” “Why does my child have so many cavities?” “Why does my child keep getting cavities?” “Why is this happening?” Parents go on to explain that they brush their child’s teeth on a regular basis, even floss! Parents tell me that they feed their child a healthy diet, and so on. Yet each time they come for a check-up there are more cavities. They are frustrated and they are disappointed.
It is a common question with a complex answer. In the preschool population dental decay is on the rise.1 According to the most recent data from the Center for Disease Control and Prevention we see an alarming trend. Prevalence of dental decay in the United States in children aged 2 – 5 years has increased by 15.2%.2 Similarly, the statistics show an increase in untreated dental decay in the same age group. Since early caries experience is a predictor of future caries experience,3-7 we have on our hands the beginning of a potential epidemic of dental caries.
If we look back to our lectures from dental school, when we were taught about the Keyes diagram. We were taught that three things combine to result in decay: the tooth, cariogenic bacteria, and fermentable carbohydrates. This is the model in it’s simplest of forms. We know that caries is indeed a multifactorial disease and that cavities are the result of that disease. We know that caries and the formation of cavities are affected by both controllable and uncontrollable factors. These factors then create a balance, or an imbalance as described by Dr. John Featherstone.8 If the exposure to pathogenic factors is greater than that of protective factors we have demineralization, which then leads to decay. If the protective factors out weigh the pathogenic factors then we have a healthy environment and the potential for remineralization.
The answer lies within and around the Keyes diagram, and the effects of the pathogenic factors and protective factors.9 In order to answer why a particular child presents with cavities, we must examine and then address those factors. Thus we have the treatment model of “caries management by risk assessment”. By definition, a risk assessment is an estimation of whether or not an event will occur in the future. A dental risk assessment is accomplished by an oral examination, a thorough history, a series of specific guided questions, and clinical and laboratory tests. Together, the answers and results allow us to place patients into risk categories. In the case of managing dental decay we can then have our clinical decisions guided with the precise knowledge of that patients risk factors. Caries management by risk assessment, then, is a series of clinical protocols that are based upon that patient’s individual situation. With this methodology, the cause of the disease or the imbalance can be identified. As a result, treatment can be specifically tailored to that patient by correcting or “balancing” those risk factors.10
Preventative measures specific to each patient can be implemented11 (Fig. 1).12
The outermost circle of the diagram in Figure 1 represents some of the risk factors or indicators that threaten the balance. They are all predictors of future dental decay.
Patients presenting with any of these factors can be categorized as high-risk patients.
Caries risk indicators are those circumstances that show the probability of developing dental decay. They are determined through patient / parent interview, clinical examination and bacterial testing. A brief explanation of some key caries risk indicators follows:
Active dental caries in the mother or primary caregiver: Studies have shown that the most common source of transmission of cariogenic bacteria is from the caregiver, most often the mother, to the child.13 Children whose mothers have a high bacterial culture for S. mutans or lactobacilli are much more likely to infect their children. Active dental caries in a caregiver is also a reflection of the attitude the mother or caregiver has towards dental health in general.
Socioeconomic status: It has long since been known that advantaged population enjoy better health.14 According to Macek and Wagner et al in 2004, a Maryland study of schoolchildren showed that 8% of 2 – 5 year olds represented 75% of decay in that age group and that these were the disadvantaged children.15
Dental IQ: This refers to the knowledge that the parent or caregiver has about the health and care of their child’s teeth. It has been shown that a low dental IQ was associated with higher incidence of early childhood caries.16 Dental IQ will determine the age at which dental care is first sought, home care, the reason that dental care is sought i.e. as prevention or as an emergency. It will also determine how the recommendations of the dental professional are or are not followed through.
Medical history: A thorough medical history is necessary to determine any developmental problems or medical conditions. Many types of conditions limit the patient’s ability to maintain proper oral hygiene. Often times oral hygiene is at the bottom of the list of necessities that must be provided for developmentally delayed or medically compromised patients. Medications are significant as well as they are often sweetened with sweeteners that are a ready source for bacteria to metabolize. As well, many medications leave patients with a side effect of a dry mouth, therefore the antibacterial properties of saliva are not available.
Dental Home: The dental home is modeled after the American Academy of Pediatrics “medical home.”17 Studies have shown that patients who have a “dental home” have more accessible complete and preventive care rather than those who only seek emergency care.
Dietary habits: Any fermentable carbohydrate is food for the cariogenic bacteria. Metabolization of the carbohydrates lead to acid production, which in turn leads to a demineralization process of enamel. Some carbohydrates are easier for bacteria to metabolize than others and so provide a more readily available source for acid production. In addition to the type of carbohydrate, it is important to take into account the duration of exposure. For example, sticky foods, or those that dissolve slowly like suckers or hard candies provide a source for the bacteria for a prolonged period of time.
These types of food sources are particularly harmful to teeth. Not only are the types of foods important to recognize, but also the frequency of consumption and timing of consumption. For example, children that use “sippy” cups are exposing their teeth to whatever liquids are in that cup frequently throughout the day.18,19 The pH of the mouth often does not have time to recover to a “safe zone” -that where demineralization does not occur before it is exposed to another sip of the liquid.
Dental conditions: Visible cavitations, decay that has occurred in the past two years, white spot lesions, plaque score, gingivitis, saliva flow, and dental appliances are all assessed and documented. A carious lesion is the end stage of the carious process. Cavitations not only indicate an active disease process but are also a strong predictor of caries in the permanent dentition.20,21 White spot lesions – decalcified areas, are an indicator of a high risk.22 It is important to remember that at young ages in the primary dentition caries progresses very rapidly. The risk of developing an active carious lesion, once a white spot lesion is discovered, is extremely high.
A visual examination after disclosing will reveal the plaque score of a patient. Plaque provides a biofilm and matrix for bacteria in the oral cavity. Gingivitis, as determined by visual clinical examination is a determinant of a high-risk patient.
Saliva acts in several different ways to balance the pathological factors of the caries process. First, saliva acts to wash away food debris by its bathing action. Second, saliva provides calcium and pho
sphate that act to remineralize areas that have been attacked by acids produced by cariogenic bacteria. Third, saliva provides proteins and lipids that form a protective pellicle. Fourth, saliva acts to transport fluoride.23 Several different products are available to measure saliva flow. A saliva flow between 1 and 4 mL/minute is considered normal.24 Patients presenting with inadequate saliva flow are at higher risk to develop tooth decay. Patients presenting with orthodontic, or habit breaking appliances are at an increased risk for caries due mainly to difficulties in proper oral hygiene.25
Bacterial Testing is essential to accurately determine a patient’s caries risk. An excellent product available is SALIVA CHECK-MUTANS by GC America. It is a simple fast test, which will give a qualitative result of S mutans levels. A positive or negative result can be established within 15 minutes. A positive result is indicative of a level of S mutans equal to or more than 500,000 colony forming units per ml. The test can be used as a predictor for risk of future caries. However, even when a patient presents with active dental caries and an obvious S mutans infection it is imperative to complete a bacterial culture in order to determine the initial baseline bacterial level. Featherstone points out that although we believe excavating a caries lesion and placing a restoration eliminates the bacteria and thereby stops caries progression, we are mistaken. The excavation and restoration will serve to eliminate the bacteria only at the site of the restoration, however bacterial levels in the remainder of the mouth remain unchanged, and so the caries process continues.26 The caries process is not eliminated by restoration of the carious lesion.27,28 It is imperative to address bacterial load in the oral cavity if one hopes to make a change in the caries process.29
Risk assessment forms like the one produced by 3M ESPE (Fig. 2) give us an easy to follow guide. The forms consist of a convenient checklist. Highlighted here is the form for ages 0 – 5 years. A modified form is used for patients aged six years and older.
The form is divided into five sections for parent interview and clinical examination. An additional section allows for recording of bacterial levels (Fig. 2).
Just as the caries process is a multi factorial one affected by biological, environmental and behavioural factors, the prevention of the caries process is also multi factorial. Although we search for that “magic bullet”, it has not yet been uncovered. We have instead a variety of tools at our disposal to stop the caries process before it ends in cavitation. The innermost circle surrounding the Keyes diagram (Fig. 1) represents the protective factors that we have at our disposal. This illustrates some of the “tools” in our “toolbox” that we have available to prevent dental decay.
Preventive tools These can include but are not exclusive to, the following therapeutic interventions and therapies: fluoride, chlorhexidine, xylitol, and sealants.
Fluoride varnish and toothpaste allow for remineralization, inhibition of bacterial colonization and act to strengthen enamel. Studies show that individuals brushing with a fluoride dentifrice show a statistically significant decrease in demineralization than those brushing without a fluoride dentifrice.30
Fluoride varnish is a lacquer containing 5% sodium fluoride in a colophony/resin base.
Fluoride varnish is easy to apply, allows for better patient compliance and a much greater efficacy. Several recent studies show that fluoride varnish is efficacious in reducing decay in primary teeth of high-risk children.31,32 The action of fluoride varnish is to increase the concentration of fluoride in the outer surface of teeth, and so during early stages of demineralization fluoride uptake is enhanced. As soon as saliva contacts the varnish, it hardens on the tooth. This allows the fluoride to be in contact with tooth enamel for an extended period of time. When compared to other high-dose topical fluorides such as gels, the contact is typically only 10 to 15 minutes. Another advantage is that the amount of fluoride deposited on demineralized versus sound tooth surfaces is considerably greater thereby making the benefits for high-risk patients even more attractive.33-36 Fluoride varnishes contain 22,600 ppm fluoride. There are several varnishes available on the market today, for example Vanish from 3M ESPE, Profluorid from VOCO, Enamel Pro with ACP from Premier. Profluorid (VOCO) is available in “kid-friendly” flavours and is very well liked by the children in my practice. Enamel Pro (Premier) contains amorphous calcium phosphate which is proven to be effective on sub-surface lesions.
One fluoride varnish that has been very well accepted in my private practice is Vanish 5% Sodium Fluoride White Varnish (3M ESPE). It is an innovative varnish, which delivers calcium and phosphate in the form of tri-calcium phosphate. Tri-calcium phosphate (TCP) is a stable crystal structure similar to hydroxyapatite. It is optimized to release calcium and phosphate at the tooth surface.37 TCP is only slightly more soluble than hydroxyapatite at a pH of seven. This means that TCP is likely to remain on the tooth surface at a neutral pH and is available to combine with fluoride to create calcium fluoride to enhance the remineralization process (Fig. 3).
Application is simple. Teeth need only be “toothbrush clean”. A prophylaxis is not required prior to varnish application. A thin layer should be applied to all treatment surfaces. Patient should be instructed not to eat or drink for at least 15 minutes after fluoride treatment and not to brush their teeth until the next morning (Fig. 4).
Anti-microbials: An example of an anti-microbial is chlorhexidine gluconate. This inhibits S. mutans in plaque. Chlorhexidine gluconate is a bisguanide antiseptic (Fig. 5). The mechanism of action is to damage the cell wall of a microorganism. It is effective against a wide array of microorganisms, including gram -ve, gram +ve, anaerobes and yeast. It is adherent over prolonged periods of time. A decrease in cariogenic bacteria leads to a decrease in acid production and therefore a decreased pH drop.
Chlorhexidine has been the subject of many studies. A meta-analysis of clinical studies determined an average caries inhibiting effect of 46%.38 It is supplied in one of its many forms as an oral rinse – in the form of 0.12% chlorhexidine gluconate. Available are Peridex from 3M ESPE and Periogard from Colgate. Clinical protocol for prevention is for use twice daily for one week per month. For ease of compliance, patients are instructed to use the rinse beginning the first of every month for the full week and to repeat once a week monthly.
Xylitol: Xylitol has a two-fold action. It is a sugar substitute and an anti-bacterial. Xylitol is a natural sugar alcohol, which acts as a replacement for fermentable carbohydrates, increases saliva production, and selects for a bacterial flora without S. mutans. It has been studied extensively. The Turku studies were an extensive trial, which resulted in a dramatic decrease in decay in those patients using xylitol.39 Xylitol is provided in several forms, but the most common use in prevention is in the form of a chewing gum or a mint. Chewing gums containing xylitol should have a minimum of 1 gram of xylitol per piece. They have the added advantage of a cleansing action when chewed. Examples include Epc chewing gum, Spry from Xclear. An excellent alternative for children too young to have mastered chewing gum, are the TheraMints from 3M ESPE.
TheraMints (3M ESPE) are 100% xylitol sweetened mints (Fig. 6). Recommended dosage is a minimum of 4 grams per day. An additional benefit of xylitol is to prolong the effect of chlorhexidine.40
Sealants: Sealants physically obstruct the pits and fissures of the occlusal surfaces of the most caries susceptible teeth. Colonization and penetration of fermentable carbohydrates is then
prevented. Sealants are highly effective in preventing decay in pits and fissures.41
Placement of sealants should not be dismissed as an insignificant procedure. In order to be successfully retained, a dry field must be maintained. Sealant materials can be of a glass ionomer material or a composite material. Glass ionomer sealants such as Riva Protect (SDI) have added benefits of high fluoride release and ability to recharge their fluoride content from available fluoride in saliva and dentifrice, as well as fluoride varnish application. Additionally glass ionomers do not require a completely dry field and so are ideal for partially erupted molars and patients in whom it is difficult to maintain moisture control. Excellent composite sealant materials on the market today include Grandio Seal from VOCO, which is a highly filled nano fissure sealant with an impressive 70.2% w/w fill and is an excellent chice for primary teeth and children who brux. Also available is ClinPro sealant from 3M ESPE.
ClinPro sealant (3M ESPE) is a unique sealant in that it has a colour change feature (Fig. 7). ClinPro sealant goes on pink in its application and once cured becomes tooth coloured. This allows for ease of application. It is a low viscosity that flows easily into pits and fissure. Sealants are recommended for all permanent molars. In high-risk patients they are also recommended for primary molars. Re-evaluation is critical for success and retention.
Thus, a simple question has a complex answer. The method of treating patients through risk assessment and prevention is the future of dentistry. Evidence-based preventive interventions including use of fluorides, anti-microbials, xylitol and sealants must be vigorously expanded. Through these methods and with these tools we have the hope to change the trends of tooth decay in the pre-school population. As dentists we are masters at adapting to an ever-changing world in which we practice. Materials and techniques change on a continual basis, but our attitude towards our method remains stubbornly the same as it did hundreds of years ago. We must emerge from the dark ages of dentistry. We must no longer look at dentistry in a surgical manner. Gone are the days where all we had to rely on was a drill or extraction forceps. If we wait until cavitation, the end stage of the disease has been reached and we have failed our patients. The time has come where we must eradicate the disease of caries by prevention. Let us all move forward to a brighter future. OH
Dr. Cohn maintains a private practice at Kid’s Dental and at Western Surgery Centre, in Winnipeg. She is a clinical instructor, part-time, in the department of Preventive Sciences at the University of Manitoba. Dr. Cohn lectures internationally on children’s dentistry for the general practitioner. She can be reached at firstname.lastname@example.org
Oral Health welcomes this original article.
1. Dye BA et al, Trends in oral health status: United States, 1988-1994 and 1999-2004, Vital Health Stat 11. 2007 Apr;(248):1-92.
3. Li and Wang, J Dent Res 81:561, 2002.
4. Zero D, FontanaM, Lennon AM, Clinical applications and outcomes of using indicators of risk in caries management. J Dent Educ 2001; 65 (10): 1126-32.
5. National Institutes of Health. Diagnosis and management of dental caries throughout life. BethesdaMd.: National Institutes of Health 2001 Reich E, Lussi A, Newbrun E, Caries risk assessment, Int Dent Journal 1999;49(1):15-26.
6. Steiner M, Helfenstein U, Marthaler T M. Dental predictors of high caries increments in children. J Dent Res, 1992; 71:1926.
7. Demers M, Brodeur JM, Simard PL etal, Caries predictor suitable for mass screenings in children: a literature review. Community Dent Health 1990; 7:11.
8. Featherstone J, Caries Prevention and Reversal based on the Caries Balance, Pediatric Dentistry, 28:2 128 – 132, 2006.
9. Keyes PH. Research in dental caries. J Am Dent Assoc 1968;76:1357-1373.
10. Young D, Featherstone JDB, Roth JR. Curing the silent epidemic: caries management in the 21st century and beyond. CDA Journal, Vol 35 No. 10, Oct 2007,
11. Tinanoff N, Kanellis MJ, Vargas CM Current understanding of the epidemiology, mechanisms, and prevention of dental caries in preschool children, Pediatr Dent 2002; 24: 5443-551.
12. Ten Cate, JM The Need for Antibacterial Approaches to Improve Caries Control Adv Dent Res 21:8 – 12, August 2009.
13. Lapirattanakul J, Nakano K, Nomura R, Hamada S, Nakagawa I, Ooshima T, Demonstration of mother to child transmission of Streptococcus mutans using multilocus sequence typing. Caries Res, 2008;(42(6):466-74, Epub 2008 Nov 7.
14. Adler NE, Ostrove JM, Socioeconomic status and health: what we know and what we don’t. Ann N Y Acad Sci 1999; 896:3 – 15.
15. Macek MD, Wagner ML, et al, Survey of oral health status if Maryland schoolchildren 2000 – 2001. Pediatr Dent 26 (4): 329 – 36, 2004.
16. Schroth R, Brothwell D, Moffatt, Caregiver knowledge and attitudes of preschool oral health and early childhood caries, International Journal of Circumpolar Health 66:2 2007.
17. American Academy of Pediatrics, Recommendations for preventive pediatric health care. Pediatrics 105:645, 2000.
18. Berkowitz RJ, Causes treatment and prevention of early childhood caries: A microbiologic perspective Can Dent Assoc 2003;59(5):304-7.
19. Marshal TA, Chairside diet assessment of caries risk. JADA 2009;140(6):670-4.
20. Peretz B, Ram D, et al, Preschool caries as an indicator of future caries: a longitudinal study. Pediatr Dent, 265 (2) : 114-8, 2003
21. Tagliaferro EP, Pereira AC, et al, Assessment of dental caries predictors in a seven year longitudinal study. J Public Health Dent 66(3):129-33, 2003.
22. Tagliaferro EP, Ambrosano GM, Meneghim Mde C, Pereira AC, Risk indicators and risk predictors of dental caries in schoolchildren. J Appl Oral Sci, 2008 Nov – Dec; 16(6): 408-13.
23. Mandel ID, The role of saliva in maintaining oral homeostasis, J Am Dent Assoc 1989; 119: 298 – 304.
24. Featherstone J, Caries Prevention and Reversal based on the Caries Balance, Pediatric Dentistry, 28:2 128 – 132, 2006
25. Al-Khateeb S, Forsberg CM, de Josselin de Jong E, Angmar-Mansson B, A longitudinal laser fluorescence study of white spot lesions in orthodontic patients. Am J Othod Dentifacial Orthop, 1998 Ju; 113(6):595- 602.
26. Featherstone JBD. The science and practice of caries prevention. J Am Dent Assoc Vol 131, No 7, 887 – 899.
27. Raadal M Espeil I, Mejare I, The caries lesion and its management in children and adolescents. In: Koch G, Poulson S, eds. Pediatric Dentistry: A Clinical Approach. Cpoenhagen: Munksgaard; 2001.
28. Raadal M. Management of early carious lesions in primary teeth In: Hugoson A etal, eds. Consensus conference on caries in the primary dentition and its clinical management. Jonkoping, Sweden: The Institutuon for Post Graduate Dental Eduction; 2002.
29. Jenson L, Budenz A, Featherstone J, Ramos-Gomez F, Spolsky V, Young D, Clinical Protocols for Caries Management by Risk Assessment, CDA Journal, Vol 35, No. 10, October 2007.
30. Duggal MS, Toumba KJ, Amaechi BT, Kowash MB, Higham SM (2001). Enamel demineralization in situ with various frequencies of carbohydrate consumption with and without fluoride toothpaste. J Dent Res 80:1721-1724.
31. Weintraub JA et al, Fluoride varnish efficacy in preventing early childhood caries, J Dent Res. 2006 Feb;85(2):172-6.
32. Lawrence HP, Binquis D, Douglas J et al. A 2-Year Community Trial of Fluoride Varnish for the Prevention of Early Childhood Caries in Aboriginal Children, Canadian Ass
ociation of Public Health Dentistry Conference, St John’s, Newfoundand, August 25-26, 2006
33. Skold-Larsson K, Modeer T, Twetman S. Fluoride concentration in plaque in adolescents after topical application of different fluoride varnishes. Clin Oral Invest 2000; 4(1): 31-4.
34. ten Cate JM, Featherstone JDB. Mechanistic aspects of the interactions between fluoride and dental enamel. CRC Crit Rev Oral Biol Med 1991; 2: 283-296.
35. Marinho VCC, Higgins JPT, Sheiham A, Logan S. Combinations of topical fluoride (toothpastes, mouthrinses, gels, varnishes) versus single topical fluoride for preventing dental caries in children and adolescents. Cochrane Database of Systematic Reviews 2004, Issue 1. Art. No.: CD002781. DOI:10.1002/14651858.CD002781.pub2
36. ADA. Report of the Council on Scientific Affairs. Evidence-based Clinical Recommendations: Professionally Applied Topical Fluoride, May 2006.
37. Karlinsey RL, Mackey AC, Walker ER, Frederick KE. Preparation, characterization and in vitro efficacy of an acid-modified beta-TCP material for dental hard-tissue remineralization. Acta Biomaterialia 2010;6:969-978.
38. van Rijkom HM, Truin GJ, van ‘t Hof MA (1996). A meta-analysis of clinical studies on the cariesinhibiting effect of chlorhexidine treatment. J Dent Res 75:790-795.
39. Scheinin A eta al Final report of the effects of sucrose fructose and xylitol diets on caries incidence in man. Acta Odontol Scand 1976; 34 (4) 179 – 216.
40. Hildebrandt et al, Maintaining Mutans Streptococci Suppression with Xylitol Chewing Gum.,Journal of American Dental Association, Vol. 131, No. 7, July 2000.
41. A Longitudinal Evaluation of Fissure Sealants Applied in Dental Practices, A.I. Ismail and P. Gagnon J DENT RES,1995.