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Intervention in Early Childhood Caries

Understanding the latest schools of thought on early childhood caries allows clinicians to devise effective treatment plans.

In the past five decades, the understanding of early childhood caries (ECC) has continued to evolve and expand. Risk factors such as previous caries, cariogenic bacteria, visible plaque, diet, enamel defects, socioeconomic status and lack of fluoride are associated ECC’S prevalence. The purpose of this article is to discuss ECC in the context of its epidemiology, risk factors, impact on children, and intervention strategies that individualize the treatment of patients most at risk for ECC.

Early childhood caries was first described in 1962 by Fass; referred to as “milk bottle mouth,” ECC was thought to be caused by putting a child to bed with a bottle of milk.1 Prior to an NIH sponsored “Early Childhood Caries Conference” in 1998,2 dental caries in preschool children was variously called “Baby Bottle Syndrome,” “Nursing Bottle Caries” and “Baby Bottle Tooth Decay.” Each name was associated with a form of rampant caries that was assumed to be caused by inappropriate use of baby bottles. During the 1998 conference, a better understanding of ECC emerged, including the awareness that ECC was multi-factorial, related to the eruption pattern of teeth, influenced by the frequency of sugar consumption in an environment of an ongoing local infection with a known bacteria and enamel hypoplasia.2

DEFINITION, EPIDEMIOLOGY AND IMPACT

Early childhood caries has been defined since 1999 as the presence of one or more decayed teeth, missing teeth (due to caries), or filled surfaces in any primary tooth of a child up to age 6. ECC continues to be the most common chronic disease in children, occurring five to eight times more frequently than asthma.3 Severe ECC is defined as any sign of smooth-surface caries in children younger than 3 years of age. Additionally, in children ages 3 through 5, one or more decayed missing filled (dmf) smooth surfaces in primary maxillary anterior teeth, or a dmf score of ≥4 (age 3), ≥5 (age 4), or ≥6 (age 5) surfaces also constitutes S-ECC.3

A better understanding of the prevalence of this disease in the United States can be derived from national reports and studies.4-5 These data clearly indicate that: ECC is highly prevalent in U.S. preschool children of low socioeconomic status; the prevalence of dental caries in children younger than 5 has increased; children with history of caries, regardless of income status, have a high number of teeth affected; and dental caries in preschool children is largely untreated.

The consequences of ECC are estimated to be substantial, including a negative impact on the quality of life, increased direct costs, and a relationship with other associated health problems. An immediate and apparent consequence of untreated dental caries is pain. A study of Head Start children in Maryland reported that 16.6% of children with caries complained of a toothache and 8.9% cried because of the pain associated with a toothache.6 Children experiencing dental pain are less able to engage in regular activities, including eating, sleeping, playing and school activities.7 It is difficult to estimate the total financial burden caused by ECC. To the best of our knowledge it appears that no representative data on medical or dental services specifically associated with ECC have been collected. However, some estimates of the cost of care are possible. According to the Agency for Healthcare Research and Quality (AHRQ) sponsored U.S. Medical Expenditures Panel Survey (MEPS), the average dental expense in 2004 for children younger than 6 was $186 per child.8 The total cost associated with this care can be estimated to be slightly more than $1 billion dollars annually. Treating ECC often requires extensive restorative treatment or the extraction of primary teeth. In addition to the expense of dental restorations, general anesthesia or sedation may be required if child patients lack the ability to cope with dental procedures. General anesthesia to facilitate dental treatment may add anywhere between $1,500 to $6,000 to the cost of dental care.9 Early childhood caries also may contribute to other health problems, such as weight loss, although the evidence for this is inconsistent.10

RISK FACTORS

ECC is a complex disease with several associated risk factors including: previous caries, bacteria, visible plaque, diet, enamel defects, socioeconomic status and a lack of fluoride exposure (Table 1). The above factors should be included when assessing risk for ECC.

Previous Caries: Children who are younger than 6 who have a history of caries (thus diagnosed as ECC) are considered at high risk for future caries. Previous dental caries is a significant predictor of future caries.11 Additionally, those children without cavitated lesions but with “white spot” lesions also are to be considered at risk.12

Bacteria: The bacteria most often associated with ECC are mutans streptococci (MS). MS metabolize sugars to produce copious amounts of acid, lowering the pH of oral plaque. Low pH for an extended period results in a higher rate of enamel demineralization, increasing the risk for caries. In other words, a longer period of MS colonization is associated with the likelihood of caries formation. Colonization often begins with a transmission to a child from a primary caregiver, usually the mother.13 Mutans streptococci colonization is more likely to occur in a child frequently exposed to sugar or a caregiver’s saliva. Low socioeconomic status, high levels of MS in a caregiver, and frequent snacking increase the chance of MS colonization in children.11 MS transmission may also occur as a result of encounters with other family members or other children in daycare centers or schools.13

Visible Plaque: Visible plaque on primary teeth is another risk factor associated with ECC. A direct correlation was found between MS levels or colonies, and plaque scores in young children. The more MS colonized, the higher the plaque score calculated risk.14

Diet: Nutritional status is also associated with ECC. High frequency sugar intake is common in lower socioeconomic status groups, (allowing acidogenic bacteria such as MS to derive energy. This results in a lowering of pH levels within the oral cavity, thereby increasing the risk for caries activity.15 The frequency of meals and snacking and types of foods consumed may also be factors in developing ECC. “At will” feeding practices, including prolonged use of a baby bottle with sweetened fluids or milk, and continuous consumption of sugars make the development of ECC more likely. Foods high in sugar content that also have a sticky consistency facilitate an environment conducive for bacterial growth and increase risk for developing ECC. Sugar intake before a nap or at bedtime further increases the risk of caries since saliva flow and its associated buffering effect are reduced during sleep.16

Enamel Defects: Individuals with defective enamel also have been associated with a higher risk of caries in primary teeth because they are less able to withstand acid attack. Combined with other risk factors, especially nutritional concerns, enamel hypoplasia is considered a reliable predictor in assessment of ECC risk.17

Socioeconomic Status: A significant predictor of ECC incidence continues to be low socioeconomic status (SES). Infants and preschoolers of low SES have a higher incidence of ECC.11 Race, social class, education and low income are all factors that increase risk. Additionally, decreased access to care, diminished neighborhood support and increased family demands may further increase the risk of ECC in poor families. Finlayson and colleagues showed that an increase in stress, often associated with the problems of low SES, is a complicating factor of ECC.18 Finally, the presence of convenience stores as opposed to full supermarkets in low SES neighborhoods and the associated availability of low nutrient dense cariogenic foods found in convenience stores increases the chance of ECC.19

MANAGEMENT OF EARLY CHILDHOOD CARIES


Caries management protocols and treatment recommendations to prevent and control ECC are shown in Table 2. These protocols and recommendations are based on the results of clinical trials, systematic reviews, and expert panel recommendations.

Altering a child’s risk for ECC by reducing the levels of MS in their primary caregivers has been shown to be a successful interventional approach. Kohler, Bratthall and Krasse20 described the use of frequent prophylaxis, topical fluoride treatment, restorative care and chlorhexidine gel treatment to reduce MS in mothers as well as their children, and subsequently lower caries scores in those children whose mothers were in the intervention group.20-21 Various combinations of treatments, including antimicrobial agents, fluoride, xylitol chewing gum and restorative care reduce MS among mothers and their children, however, few have shown an effect on caries incidence in the children.22

The principal approaches to prevent or reduce ECC in high-risk children include altering dietary patterns and fluoride protocols. Diet counseling helps parents change their childrens’ dietary behaviors to favor low or non-cariogenic snacks and limit sweet foods to mealtimes. Such dietary recommendations must be realistic and based on the dietary behaviors of the family.

There is evidence that diet counseling can be effective for families that have a high caries risk. Two studies show that dietary counseling and reinforcement resulted in reduced caries incidence.23-24 Although the data are limited, results are promising enough to suggest that diet counseling should be recommended for families who are at high caries risk.

Systemic and topical fluoride treatments have also been shown to be effective for infants and toddlers at risk. Water is the predominant source of systemic fluoride for most children living in communities where the fluoride concentration in water supplies is between 0.7 and 1.2 ppm F. Fluoride supplements were introduced in the late 1950s to provide anti-caries benefits to populations that resided in areas where optimally fluoridated water was not available.25

Topical fluoride, as a fluoridated toothpaste or professional application, also is of benefit to prevent ECC. To prevent fluorosis, parents should supervise their child’s brushing, making sure that only a “peasized” amount of toothpaste (approximately 1/4 gm) is used for children younger than 6. A recent recommendation suggests that children younger than 2 at caries risk may brush with a “smear” of fluoridated toothpaste.26 Care must be taken to insure that fluoride is not ingested by the child.

Fluoride varnish is ideal for preschool children due to its single dose packaging, making it easy and safe to use. Application of varnish is simple and doesn’t require a completely dry surface. Varnish dries on contact with saliva, making it a safe product to use on preschoolers. Products that are now available include single-use containers of 0.25, 0.4, or 0.6 ml of NaF varnish, corresponding to 12.5, 20 or 30 mg fluoride, respectively. The caries-preventive effect of fluoride varnish is generally equal to that of other topical fluorides;27 and their efficacy to reduce caries in primary teeth has been demonstrated in numerous studies.25 The ADA has recommended that fluoride varnish be administered twice a year for preschool children at moderate caries risk, and four times a year for children at high caries risk.28

Screening infants at age 1 allows for the early identification of those who are most at risk for ECC and would benefit from early preventive interventions and anticipatory guidance. Such examinations can be done by dental or medical personnel who have been trained to identify ECC risk factors and signs of enamel demineralization. Follow-up examinations at three months coincide both with the periodicity schedule for physicians’ “well baby” visits and the ADA protocol for topical fluoride treatments for high risk infants and toddlers.28

INTERVENTION STRATEGIES

Historically, the restorative approach to treating dental caries was based on the understanding that caries was a progressive disease that eventually destroyed the tooth unless there was surgical and restorative intervention. It is now known that surgical intervention of dental caries alone does not stop the disease process. Additionally, many lesions do not progress and can be stabilized; what’s more, tooth restorations have a finite longevity.29 Therefore, modern management of dental caries in infants and toddlers should be more conservative and include early detection of noncavitated lesions, identification of an individual’s risk for caries progression, and active surveillance (i.e., a carefully monitored preventive program to halt caries progression and arrest early lesions). If cavitations are detected, interim therapeutic restorations should be considered, including the placement of temporary glass ionomer restorations when traditional cavity preparation and placement are not feasible.29

Early childhood caries (ECC) is a complex disease associated with multiple risk factors that continues to be a significant health problem today. By carefully assessing factors associated with ECC for both a child and caregiver, a dental or medical professional can develop a personalized and individualized treatment plan specifically aimed at reducing a child’s ECC risk. Dental hygienists are an important part of the professional team and are in a unique position to provide early intervention strategies.

REFERENCES

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  2. Tinanoff N. Proceeding Conference on Early Childhood Caries Conference. Community Dent Oral Epidemiol, 1998;26 (Suppl 1).
  3. Drury TF, Horowitz AM, Ismail AI, et al. Diagnosing and reporting early childhood caries for research purposes. J Public Health Dent. 1999;59(3):192-197.
  4. Tinanoff N, Kanellis M, Vargas C. Current understanding of epidemiology, mechanisms and prevention of dental caries in preschool children. Pediatr Dent. 2002;24:543-551.
  5. Dye BA, Tan S, Smith V, et al. Trends in oral health status: United States, 1988-1994 and 1999-2004. National Center for Health Statistics. Vital Health Stat. 2007;11:248.
  6. Vargas CM, Monajemy N, Khurana P, Tinanoff N. Oral health status of preschool children attending head start in Maryland, 2000. Pediatr Dent. 2002; 24:257-263.
  7.  Edelstein BA, Vargas CM, Candelaria D, et al. Characteristics of children visiting emergency rooms at dental schools. Pediatr Dent 2006;28:431-437.
  8. Manski, R. J. and Brown, E. Dental use, expenses, private dental coverage, and changes, 1996 and 2004. Rockville (MD): Agency for Healthcare Research and Quality; 2007. MEPS Chartbook No.17. http://www.meps.ahrq.gov/mepsweb/data_files/publications/cb17/cb17.pdf
  9. Griffin SO, Gooch BR, Beltran E, et al. Dental services, costs, and factors associated with hospitalization for Medicaid-eligible children, Louisiana 1996-7. J Pub Health Dent. 2000;60:21-27.
  10. Thomas CW, Primosch RE. Changes in incremental weight and well-being of children with rampant caries following complete dental rehabilitation Pediatr Dent. 2002; 24:109-113.
  11. Tinanoff N, Reisine S. Update on Early Childhood Caries since the Surgeon General’s Report. Acad Pediatr. 2009; 9:396-403.
  12. Ismail AI. Prevention of Early Childhood Caries. Community Dent Oral Epidemiol. 1998:26 (Supp 1): 49-61.
  13. Berkowitz RJ. Mutans Streptococci: Acquisition and transmission. Pediatr Dent. 2006;28(2):106-109.
  14. Lee CL, Tinanoff N, Minah G, Romberg E. Effect of mutans streptococci colonization on plaque formation and regrowth. J Pub Health Dent. 2008;22:86-9.
  15. Featherstone JDB. The Caries Balance. Dimensions of Dental Hygiene. 2004;2(2):14-16,18.
  16. Stegeman CA, Davis JR. Dental Hygienists Guide to Nutritional Care. 3rd ed. St. Louis, MO: WB Saunders: 2010.
  17. Hong L, Levy SM, Warren JJ, Broffitt B. Association between enamel hypoplasia and dental caries in primary second molars: A Cohort Study. Caries Res. 2009;43:345-353.
  18. Finlayson TL, Siefert K, Ismail AI, Sohn W. Psychosocial factors and early childhood caries among lowincome African-American children in Detroit. Community Dent Oral Epidemiol. 2007;35:435-38.
  19. Mobley C. Marshall TA, Milgrom P, Coldwell SE. The contribution of dietary factors to dental caries and disparities in caries. Acad Pediatr. 2009;9:420-424.
  20. Kohler B, Bratthall D, Krasse B. Preventive measures in mothers influence in the establishment of the bacterium Streptococcus mutans in their infants. Arch Oral Biol. 1983;28(3):225-31.
  21. Kohler B, Andreen I. Influence of caries-preventive measures in mothers on cariogenic bacteria and caries experience in their children. Arch Oral Biol. 1994;39(10):907-911.
  22. Douglass JM, Li Y, Tinanoff, N. Association of mutans streptococci between caregivers and their children. Pediatr Dent. 2008;30:375-387.
  23. Becks H. Rampant dental caries: Prevention and prognosis. A five-year clinical study. J Am Dent Assoc. 1944;31:1189-1200.
  24. Krasse B. Approaches to prevention. In: Stiles HM, Loesche WJ, O’Brein TC, Proceedings “Microbial Aspects of Dental Caries’, Sp Supp Microbiology Abstracts. 1976; 867-876.
  25. Tinanoff N. Use of Fluorides, in Early Childhood Oral Health, eds, Berg J and Slayton RA, Wiley-Blackwell 2009;pp 92-10.
  26. Maternal and Child Health Bureau Expert Panel. Topical fluoride recommendations for high-risk children: Development of decision support matrix. October 22–23, 2007, Altarum Institute, Washington, DC.
  27. Beltran ED, Burt BA. The pre- and posteruptive effects of fluoride in the caries decline. J Pub Health Dent. 1998;48:233-40.
  28. American Dental Association, Council on Scientific Affairs. Professionally applied topical fluoride. J Am Dent Assoc 2006;137:1151-1159.
  29. Council on Clinical Affairs, American Academy of Pediatric Dentistry. Guidelines on Caries Risk Assessment and Management. Pediatr Dent (in press, 2010).

From Dimensions of Dental Hygiene. May 2010; 8(5): 28-29, 31-32, 34.

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