Overview
Early Childhood Caries: An Overview With Reference to Our Experience in California
Pamela DenBesten, DDS, and Robert Berkowitz, DDS
Pamela DenBesten, DDS, is chair of the Division of Pediatric Dentistry
at the University of California at San Francisco.
Robert Berkowitz, DDS, is the chief of Division of Pediatric Dentistry at the University of Rochester, Rochester, N.Y.
Copyright 2003 Journal of the California Dental Association.
 |
Dental caries in young children frequently appears first on the maxillary primary incisors, where the liquids ingested by the infant sucking on a bottle or breast remain pooled away from salivary flow. This so-called early childhood caries can rapidly progress to result in rampant destruction of the primary dentition. ECC can affect children from all socioeconomic classes but is most often found in children of new immigrants or those with lower socioeconomic status. The treatment of ECC is costly, and treatment relapses are frequent. Prevention and treatment of ECC focus on inhibition of the growth of oral bacteria. Strategies include reducing the frequency of exposure to bacterial substrates, as well as controlling the growth of oral bacteria. Topical antibacterials such as 10 percent povidone iodine show promise for future use in the inhibition of ECC in young children.
|
Caries in children frequently manifests in a pattern of progression related to the feeding requirements of young children who suck from a bottle or breast. Early initiation of caries in infants and toddlers has been termed early childhood caries. In young children, caries can begin as soon the teeth erupt and can rapidly progress to extensive decay of all primary teeth (Figure 1). The pattern of decay in early childhood caries is related to salivary flow patterns within an infant’s mouth. The mandibular incisors are protected by the tongue and bathed in saliva and thus show decay only with extremely severe caries challenge. Milk or other liquids sucked from a bottle pool in areas of the mouth that are less exposed to salivary flow, particularly the facial surfaces of the maxillary primary incisors, where early childhood caries is first detected. As caries becomes more severe, the decay appears on the occlusal surfaces of the maxillary primary molars and then spreads throughout the mouth, which can result in an overwhelming infection with destruction of primary teeth throughout the mouth.
Cariogenicity
Studies of the cariogenicity (caries-causing potential) of infant foods show that milk has minimal cariogenicity relative to that of infant formulas and fruit juices.1-3 However, by the time the mandibular and maxillary primary incisors erupt, bottle or breast feeding is supplemented by a variety of solid foods. These foods include starches and other sucrose-containing foods with cariogenic potential, which provide an improved substrate to promote the proliferation of cariogenic bacteria. In addition, adding a sweetener in bottles fed to infants is a major risk factor for early caries.4,5
Young infants may feed from a bottle or breast six or more times per day. As the infant grows older, the number of feedings does not dramatically change, but the variety and amount of food that a child ingests increases. The frequency of feeding of infants and toddlers makes them particularly susceptible to caries. If the frequent feedings are accompanied by prolonged exposure of the teeth to liquids, as occurs when liquid is ingested from a bottle, susceptibility increases even more.4-8 The relative frequency with which young children feed is likely to affect the so-called "caries balance" between factors that promote demineralization and those that promote remineralization.9 The frequent and prolonged introduction of cariogenic food substrates (as occurs in bottle feeding with sweetened liquids), with the subsequent lowering of plaque pH and tooth demineralization, can push the balance toward tooth demineralization. By far the most caries-promoting food substrate is sucrose;2,3,10 but other carbohydrates -- including glucose, fructose, and cooked starch -- also contribute.
Prevalence and Distribution
This childhood dental disease is a public health problem that affects babies, toddlers, and preschool children worldwide. The epidemiology of early childhood caries shows that disadvantaged children -- regardless of race, ethnicity, or culture -- are most vulnerable.11,12 Early caries in infants and toddlers also results in a higher risk for continued tooth decay as the children grow older.
High-risk North American populations include children of new immigrants and children from lower socioeconomic populations. In California, the relative size of the new immigrant population is high compared with other states. Early childhood caries is particularly prevalent in this population.13 Mexican-Americans, who were shown in the NHANES III data to be a vulnerable population for caries in children,14,15 make up a large percentage of the immigrant population in California. In 1993, Serwint and co-workers found that 20 percent of the 110 Mexican-American children (18 to 36 months of age) who were patients of a hospital-based pediatric practice in Los Angeles, had early childhood caries.16 More recently, Ramos and coworkers found that in a predominantly Mexican-American population in San Francisco, 43 percent of the children younger than 5 had caries in their primary teeth.17
Native American children are at high risk for caries, with prevalence rates of early childhood caries reported from 40 percent to 72 percent.18,19 In 1996, George and coworkers examined 4-year-old Apache children to determine how caries levels and patterns were different from 15 years before. Neither the caries prevalence (95 percent) nor the prevalence of caries patterns differed between the 1978-79 and 1993 cohorts. However, the level of treatment received in 1993 was greater than that in 1978-79. Studies such as this one suggest that our current effort at caries prevention, which are largely confined to caries treatment for high-risk populations, has had minimal effect in reducing the prevalence of this disease.
Etiology
The fact that caries is a transmissible disease involving the cariogenic bacteria mutans streptococci has been well-established.20-25 The major reservoir from which babies acquire mutans streptococci is their mothers or primary caregivers, though cariogenic bacteria can be transmitted from other caregivers or children in close contact.26 Suppression or alteration of maternal reservoirs of mutans streptococci has shown that infection of a baby can be prevented or delayed.27,28 However, a single treatment of mothers with an oral antibacterial may not be sufficient to prevent mutans streptococci transmission and subsequent caries in children.29 Likewise, antibacterial treatment of children may not be sufficient to reduce infection if maternal levels remain high.
Current Treatment With Reference to Northern California
The current standard of care for treatment of severe early childhood caries usually necessitates general anesthesia with all of its potential complications, because the level of cooperative behavior of babies and preschool children is less than ideal. The cost of treating a child with ECC exceeds $2,000.30 More recent data show that costs have escalated. For example, the estimated cost for facilities and general anesthesia, excluding dental services, for the treatment of a child with ECC at the University of California in San Francisco is between $3,700 and $4,700. Costs may be even higher when the child has a medical condition requiring that treatment be completed in the main operating rooms.
The need for treatment of children for rampant and progressing caries in California may be increasing. Early childhood caries places a huge financial burden on third-party carriers (insurance companies and state government medical welfare agencies) as well as parents least able to afford it. Studies have shown that restorative dentistry alone has little to no long-term impact on oral populations of mutans streptococci.31 Not surprisingly, clinical outcomes for treatment of early childhood caries are poor. Studies by Berkowitz and coworkers have shown that 53 percent (13 of 24) of children treated for early childhood caries under general anesthesia relapsed within four to six months with new smooth-surface carious lesions.32 Almeida and co-workers retrospectively evaluated 42 children treated for ECC under general anesthesia at the Franciscan Children’s Hospital and Rehabilitation Center in Boston. By the end of 12 months, 19 of 42 (45 percent) of these children had relapsed with new carious lesions.33
Prevention and Treatment
The rapidity with which early childhood caries can progress suggests that means other than the traditional approach of remineralizing incipient carious lesions through the use of topical fluoride administered either in the drinking water or in toothpastes are required. Improved clinical outcomes for treatment of early childhood caries are likely to be realized through treatments that address the infectious characteristics of this disease and place emphasis on controlling the disease dental caries as opposed to surgical treatment as an end in itself. Suppression of oral bacterial reservoirs in children should include inhibition of the transmission of mutans streptococci to children, reducing exposure of children to fermentable carbohydrates, in particular sucrose, and developing safe and effective antibacterial approaches to reducing the number of acidogenic (acid-producing) oral bacteria in children.
A variety of topical antimicrobial agents has been tested to suppress oral populations of mutans streptococci. These agents, in part, include antibiotics (vancomycin and kanamycin), stannous fluoride, the bisguanidines (alexidine and chlorhexidine), iodine, and combinations of these agents. Selection of an agent to suppress oral mutans streptococci and lactobacilli reservoirs must consider a number of factors; safety is of particular concern in babies and preschool children. Utilization of stannous fluoride is contraindicated in children younger than 4 because of the potential risk of fluorosis (Clinical Guidelines, American Academy of Pediatric Dentistry, 2000). The bisguanidines are not recommended for use in young children because of lack of information regarding safety, alcohol content, staining of teeth, and the potential for disruption of taste. The antibiotics -- vancomycin34 and kanamycin35 -- have very short-term suppressive effects on oral populations of mutans streptococci and have not been shown to be effective in reducing caries. One promising approach is the use of topical iodine formulations, which are approved for pediatric use and have prolonged suppressive effects on oral reservoirs of mutans streptococci. They may also suppress lactobacilli. A recent study (unpublished) in which ECC children were treated with 10 percent povidone iodine while undergoing their restorative procedures showed that mutans streptococci and lactobacilli were markedly reduced for up to three months. Details of that study will be published elsewhere. Another modality that can be used to inhibit transmission from mother to child is the use of xylitol gum or mints by the mothers during the first two years of the child’s life. Studies have show that caries in infants can be inhibited significantly in this way.36
Iodine as an Oral Bactericidal Agent
Iodine is among the most potent of bactericidal agents. Its effect is not time-dependent; once bacterial contact is made, its action is immediately lethal. Iodine has excellent penetrability into dental plaques.37,38 These characteristics make it an excellent agent for oral use. Earlier studies by Gibbons and coworkers showed that a single two-minute application of a 2 percent iodine/potassium iodine ( I2-KI ) solution eliminated mutans streptococci from accessible human tooth sites for up to 13 weeks.39 In 1977, Caufield and Gibbons showed that a dental prophylaxis followed by three applications of a 2 percent I2-KI solution significantly reduced mutans streptococci levels in fissure and proximal-surface plaques and saliva. Reductions persisted for 20 to 24 weeks in proximal plaque and saliva; fissure plaques were significantly suppressed for four weeks but gradually returned to baseline levels in the absence of dietary restrictions.40
Recently, the influence of bimonthly topical application of 10 percent povidone iodine was assessed in a placebo-controlled double-blind clinical trial in preventing the development of white spot lesions on the maxillary primary incisors of Puerto Rican babies at high risk for developing early childhood caries.41 The study population consisted of 83 subjects (age 12 to 19 months, 40 female and 43 male). The healthy caries-free children were included in the study if they had four maxillary primary incisors with no visible defects, used a nursing bottle at naptime and/or bedtime that contained a cariogenic substrate, and had two consecutive mutans streptococci positive cultures from pooled maxillary primary incisor plaque. The subjects were randomized into two groups that were evaluated every two months during the study period. At each evaluation, the subjects had 10 percent povidone iodine (experimental group) or placebo (control group) applied to their dentition. The results of this study showed that the children who received topical treatment with 10 percent povidone iodine were significantly more likely to remain caries-free.
Collectively, the preceding information strongly suggests that topical iodine agents are efficacious for preventing dental caries in babies and young preschool children at high risk for this disease. Dr. Reed Snow, director of the Delta Dental special programs in California, has many times stated over the past several years that it is time for a paradigm shift in our understanding of caries etiology, prevention, and treatment. The use of safe and effective means to inhibit bacterial transmission subsequent infection should be at the cornerstone of this paradigm shift.
References
1. Bowen WH, Pearson SK, et al, Assessing the cariogenic potential of some infant formulas, milk and sugar solutions. J Am Dent Assoc 128(7):865-71, 1997.
2. Bowen WH, Pearson SK, Effect of milk on cariogenesis. Caries Res 27(6):461-6, 1993.
3. Mundorff SA, Featherstone JD, et al, Cariogenic potential of foods. I. Caries in the rat model. Caries Res 24(5):344-55, 1990.
4. Dini EL, Holt RD, and Bedi R, Caries and its association with infant feeding and oral health-related behaviours in 3-4-year-old Brazilian children. Community Dent Oral Epidemiol 28(4):241-8, 2000.
5. Mohan A, Morse DE, O’Sullivan DM, The relationship between bottle usage/content, age, and number of teeth with mutans streptococci colonization in 6-24-month-old children. Community Dent Oral Epidemiol 26(1):12-20, 1998.
6. Wendt LK and Birkhed D, Dietary habits related to caries development and immigrant status in infants and toddlers living in Sweden. Acta Odontol Scand 53(6):339-44, 1995.
7. Milgrom P, Riedy CA, et al, Dental caries and its relationship to bacterial infection, hypoplasia, diet, and oral hygiene in 6- to 36-month-old children. Community Dent Oral Epidemiol 28(4):295-306, 2000.
8. Maupome G, An introspective qualitative report on dietary patterns and elevated levels of dental decay in a deprived urban population in northern Mexico. ASDC J Dent Child 65(4):276-85, 230, 1998.
9. Featherstone JD, The science and practice of caries prevention. J Am Dent Assoc 131(7):887-99, 2000.
10. Wendt LK, Hallonsten AL, et al, Analysis of caries-related factors in infants and toddlers living in Sweden. Acta Odontol Scand 54(2):131-7, 1996.
11. Milnes AR, Description and epidemiology of nursing caries. J Public Health Dent 56(1):38-50, 1996.
12. Edelstein BL, Disparities in oral health and access to care: findings of national surveys. Ambul Pediatr 2(2):141-7, 2002.
13. Pollick HF, Rice AJ, and Echenberg D, Dental health of recent immigrant children in the Newcomer schools, San Francisco. Am J Public Health 77(6):731-2, 1987.
14. Kaste LM, Drury TF, et al, An evaluation of NHANES III estimates of early childhood caries. J Public Health Dent 59(3):198-200, 1999.
15. Ramos-Gomez FJ, Tomar SL, et al, Assessment of early childhood caries and dietary habits in a population of migrant Hispanic children in Stockton, California. ASDC J Dent Child 66(6):395-403, 366, 1999.
16. Serwint JR, Mungo R, et al, Child-rearing practices and nursing caries. Pediatrics 92(2):233-7, 1993.
17. Ramos-Gomez FJ, Weintraub JA, et al, Bacterial, behavioral and environmental factors associated with early childhood caries. J Clin Pediatr Dent 26(2):165-73, 2002.
18. Kelly M and Bruerd B, The prevalence of baby bottle tooth decay among two native American populations. J Public Health Dent 47(2):94-7, 1987.
19. Tsubouchi J, Tsubouchi M, et al, A study of dental caries and risk factors among Native American infants. ASDC J Dent Child 62(4):283-7, 1995.
20. Berkowitz RJ and Jones P, Mouth-to-mouth transmission of the bacterium Streptococcus mutans between mother and child. Arch Oral Biol 30(4):377-9, 1985.
21. Berkowitz RJ, Turner J, and Green P, Maternal salivary levels of Streptococcus mutans and primary oral infection of infants. Arch Oral Biol 26(2):147-9, 1981.
22. Berkowitz RJ and Jordan HV, Similarity of bacteriocins of Streptococcus mutans from mother and infant. Arch Oral Biol 20(11):725-30, 1975.
23. Caufield PW and Griffen AL, Dental caries. An infectious and transmissible disease. Pediatr Clin North Am 47(5):1001-19, v, 2000.
24. Caufield PW, Ratanapridakul K, et al, Plasmid-containing strains of Streptococcus mutans cluster within family and racial cohorts: implications for natural transmission. Infect Immun 56(12):3216-20, 1988.
25. Caufield PW, Wannemuehler YM, and Hansen JB, Familial clustering of the Streptococcus mutans cryptic plasmid strain in a dental clinic population. Infect Immun 38(2):785-7, 1982.
26. Mattos-Graner RO, Li Y, et al, Genotypic diversity of mutans streptococci in Brazilian nursery children suggests horizontal transmission. J Clin Microbiol 39(6):2313-6, 2001.
27. Kohler B, Bratthall D, and Krasse B, Preventive measures in mothers influence the establishment of the bacterium Streptococcus mutans in their infants. Arch Oral Biol 28(3):225-31, 1983.
28. Isokangas P, Soderling E, et al., Occurrence of dental decay in children after maternal consumption of xylitol chewing gum, a follow-up from 0 to 5 years of age. J Dent Res 79(11):1885-9, 2000.
29. Dasanayake AP, Caufield PW, et al, Transmission of mutans streptococci to infants following short term application of an iodine-NaF solution to mothers’ dentition. Community Dent Oral Epidemiol 21(3):136-42, 1993.
30. Cook HW, Duncan WK, et al, The cost of nursing caries in a Native American head start population. J Clin Pediatr Dent 18:139-42, 1994.
31. Wright JT, Cutter GR, et al, Effect of conventional dental restorative treatment on bacteria in saliva. Community Dent Oral Epidemiol 20(3):138-43, 1992.
32. Berkowitz RJ, Moss M, et al, Clinical outcomes for nursing caries treated using general anesthesia. ASDC J Dent Child 64(3):210-1, 228, 1997.
33. Almeida AG, Roseman MM, et al, Future caries susceptibility in children with early childhood caries following treatment under general anesthesia. Pediatr Dent 22(4):302-6, 2000.
34. Jordan HV and DePaola PF, Effect of prolonged topical application of vancomycin on human oral Streptococcus mutans populations. Arch Oral Biol 22:193-9, 1977.
35. Loesche WJ, Hockett RN, and Syed SA, Reduction of dental decay in rampant caries individuals following short term kanamycin treatment. J Dent Res 56:254-67, 1977.
36. Lynch H and Milgrom P, Xylitol and dental caries: An overview for clinicians. J Cal Dent Assoc, in press, 2003.
37. Caufield PW and Wannamuehler YM, In vitro susceptibility of Streptococcus mutans 6715 to iodine and sodium fluoride, singly and in combination at various Ph values. Antimicrob Agents Chemother 22:115-9, 1982.
38. Tanzer JM, Brown AT, et al, In vitro evaluation of three iodine-containing compounds as antiplaque agents. Antimicrob Agents Chemother 12:107-13, 1977.
39. Gibbons RJ, DePaola PF, et al, Interdental localization of Streptococcus mutans as related to dental caries experience. Infect Immun 9:481-8, 1974.
40. Caufield PW and Gibbons RJ, Suppression of Streptococcus mutans in the mouth of humans by a dental prophylaxis and topically-applied iodine. J Dent Res 58:1317-26, 1979.
41. Lopez L, Berkowitz R, et al, Topical antimicrobial therapy in the prevention of "early childhood caries" a follow-up report. J Ped Dent 24(3):204-6, 2002.
To request a printed copy of this article, please contact: Pamela DenBesten, DDS, Department of Growth and Development, Box 0640, UCSF, San Francisco, CA 94143-0640 or pkdb@itsa.ucsf.edu.
Legends
Figure 1a. Initial stages of early childhood caries where the maxillary incisors are primarily affected.
Figure 1b. Extensive early childhood caries affecting all maxillary teeth and mandibular posterior teeth. The lower incisors are protected by the tongue and are caries-free.
