CHAPTER 7 NEW INSIGHTS INTO EARLY CHILDHOOD CARIES AND STRATEGIES FOR PREVENTION
The previous century was marked by the development of the scientific method with the consequent explosion of information and an understanding of the underlying biologic processes. The new millennium has harnessed the information through new technology; new understanding has led to new clinical insights. Every dental school attempts to link the basic biologic sciences with the diagnosis and treatment of dental disease. This chapter traces the embryologic development of dental enamel, speculates about the relationship of embryologic development and dental caries, describes the public health impact of early childhood caries, and suggests strategies for prevention.
Enamel formation of the primary teeth begins with the incisors at approximately 11 to 14 weeks of fetal life.1,2 The initial phase consists of matrix formation followed by calcification. These two processes begin in utero and are completed by the third postnatal month. Because enamel is a relatively stable structure, defects of the enamel of the primary teeth involving its matrix secretion or maturation, or both, can act as a permanent record of insults occurring during the prenatal or early postnatal periods. Birth itself leaves its mark on the developing teeth. The change from intrauterine life to extrauterine life causes the formation of the neonatal line.3 This is a narrow line of hypoplasia, seen in the crowns of the primary incisors near the gingiva and in the primary molars in the middle portion of the crown. In a child born through a normal delivery, the neonatal line is seen only microscopically; however, after complicated deliveries the neonatal line is likely to be macroscopic and visible to the naked eye. A wide range of conditions may contribute to these hypoplastic or hypocalcified defects. Systemic maternal disorders associated with enamel hypoplasia of the dentition of the fetus or neonate include diabetes, kidney disease, and viral or bacterial infections. Systemic disorders of the neonate may include premature birth, Rh incompatibility, allergies, tetany, gastroenteritis, malnutrition, infectious diseases, and chronic diarrhea.4–8 Some researchers have suggested that a common factor in all these conditions—both maternal and fetal or neonatal—is transient hypocalcemia, which may be a predisposing factor for dental caries. Others maintain that linear enamel hypoplasia is a predisposing factor to dental caries.9 A possible correlation between hypoplastic defects and dental caries was proposed as early as four decades ago.10,11 However, hypoplastic dental defects may be difficult to distinguish from caries caused by excessive bottle nursing, especially when the caries is subsequent to the defect.12
Dental caries is the most prevalent childhood dental disease. In the 1980s studies of children up to age 12 in Western countries showed a dramatic decline in the prevalence of dental caries and an increasing number of children with caries-free dentitions.13,14 However, a more recent study warned that the 50% caries-free characterization of U.S. schoolchildren was mythical because it failed to consider decayed primary teeth and it inappropriately averaged in children who were too young to have experienced decay.15 When decay in primary teeth is also considered, roughly half of children have already experienced decay before first grade. It has been observed that the prevalence of dental caries continues to increase steadily with age until five of every six high school graduates are affected. In light of such opposing opinions, a review of some basic aspects of dental caries is in order.
Dental caries is caused by the demineralization of the dental enamel by organic acids that are the outcome of the metabolism of carbohydrates by microorganisms in the mouth. It is a multifactorial disease, involving four main factors:
Saliva is a major factor influencing the development or inhibition of dental caries. Saliva is to the tooth enamel what blood is to body cells. Just as body cells depend on the bloodstream to supply nutrients, remove waste, and protect the cells, enamel depends on saliva to perform similar functions. The beneficial actions of saliva include the following:
Children as young as 6 months to 3 years old are already at risk for a distinctive pattern of dental caries known as early childhood caries (ECC), baby-bottle tooth decay (BBTD), or nursing bottle caries. ECC is seen in epidemic proportions in developing countries and among disadvantaged children in Western countries.31 Because it is so prevalent, ECC requires special attention from both clinical and public health perspectives.
Early childhood caries is the term now recommended by the Centers for Disease Control and Prevention to describe a unique pattern of carious lesions in infants, toddlers, and preschool children. This term now covers the previously used terms baby-bottle tooth decay and nursing caries that describe a form of rampant caries of the primary dentition caused by prolonged use of a bottle of milk or other liquid including carbohydrates.12,31 Clinically, the decay is first found in the maxillary primary incisors; later it spreads to the maxillary molars, mandibular molars, and rarely the mandibular incisors. It has been postulated that this pattern of caries is related to the following factors:
The contents of the feeding bottles must be considered in cases of ECC. Most studies have reported that these bottles all contain some form of sugar.33–36 How, for example, does milk affect the occurrence of ECC? Cow’s milk and mother’s milk contain lactose, composed of glucose and fructose, both of which enhance cariogenic bacteria colonization and acid production.37–39 Some studies report on ECC in children who were fed with cow’s milk only and some on ECC in children who were only breast-fed.40–42 It has also been found that the high concentrations of calcium and phosphate in milk are caries protective.33,43–46 Apparently, under normal diet conditions milk is not cariogenic and may even provide some protection against caries. However, the diets of most children with ECC are not normal; prolonged exposure to milk leads to its stagnation around the necks of the teeth, especially the maxillary incisors, leading to high acidity (low pH) and subsequent enamel demineralization.47 In addition to having sweet liquids from bottles, affected children are often given pacifiers dipped in sweets; an association has been established between the use of these comforters and ECC.48–50
It is difficult to determine the exact prevalence of ECC because every survey is seriously limited. Preschool-age children with ECC are less available for dental examination than are older children. In addition, those children who are examined may not necessarily represent the general population of this age. Instead, the population of children seen at a given dental clinic may be biased because their parents believed that their children had a dental problem.40 Selection of survey samples from mother-child centers or from child health centers could skew the sample into a particular socioeconomic class.51 In addition, because the patterns of infant feeding habits are largely culturally and ethnically influenced, survey samples of children from such cultural or ethnic backgrounds will be similarly skewed.52 For all these reasons it is difficult to make an analogy from the prevalence of ECC in one country with its prevalence in another country.53–55
The reported prevalence of ECC may also be influenced by the fact that infants are difficult to examine. Not every pediatric dentist knows that a thorough dental examination of an infant requires that the infant lie with his or her head on the dentist’s lap with the legs on the mother. Furthermore, the infant’s distress and crying may trouble an inexperienced examiner so much that the examination may be superficial at best.
The diagnosing criteria of ECC are somewhat controversial; some researchers claim that a minimum of one infected incisor is a sufficient criterion for diagnosing the condition.53 Others maintain that a minimum of two teeth is required, whereas some believe that at least three infected maxillary incisors are required.48,52,56
It is generally accepted that the prevalence of ECC in predominantly Western-type cultures is about 5%.35,40,48,51–56 In certain populations a higher prevalence has been found. In the United States, Hardwick and colleagues57 reported a 21% prevalence of ECC for urban Hispanic children younger than 5 years. Barnes and colleagues58 reported a 16% prevalence for urban children and a 37% prevalence for rural Hispanic children. In a preliminary study of children of Mexican-American migrant workers, Weinstein and colleagues59 found a 29.2% prevalence of ECC among infants age 27.6 months on the average. In a subsequent study the same research group found that in a sample of children with an average age of 17.1 months, 7% had at least one maxillary incisor with decay and more than 30% had at least one incisor with a white spot lesion.60 A study among Arizona infants and toddlers reported a more complex pattern of prevalence, associated with age: among 13- to 24-month-olds, caries was most prevalent on the buccal and lingual surfaces of the maxillary central incisors (approximately 4% in the 19- to 24-month-olds). In children age 25 to 27 months, caries of the maxillary central incisors was most prevalent on the mesial and distal surfaces (nearly 6%), and among 31- to 33-month-olds, prevalence on these surfaces was nearly 10%. Caries of the lateral incisors showed a similar pattern of change with age, except that the distal surface was consistently the least prevalent.32
ECC has a predictable progression. Initially the teeth are seen to have white spots that are usually decalcification lesions, which may become frank lesions or caries within 6 months to 1 year. Such decalcification lesions do not necessarily progress to cavities because the process may be reversed and the teeth may become remineralized.61 Undetected, and thus unchecked, early ECC causes severe problems for the child, who may be in considerable pain and may have difficulty eating and talking. The disease is also a serious threat to the health of other primary teeth and subsequently to the health of the permanent dentition. An association between ECC and failure to thrive (FTT) has been found.62 However, the results of this study do not distinguish clearly whether ECC had caused the FTT or whether the FTT, caused by various general systemic conditions, was itself a predisposing factor in the development of ECC.
The results of a pilot study indicate a strong correlation between BBTD and maternal diseases or complications during pregnancy or delivery.63 This study compared the pregnancies of the mothers of two groups of age-matched children with similar eating and feeding habits—they all were fed from bottles containing sweet liquids. Compared with the pregnancies of mothers of children with healthy teeth, the pregnancies of the mothers of children with ECC involved more cases of vaginal bleeding, premature uterine contractions, episodes of viral or bacterial infections, and other indications of high-risk pregnancies. There were also more instrumental deliveries (vacuum or forceps) and cesarean sections. Therefore it seems clear that children born of high-risk pregnancies are more likely to have ECC than are children of normal pregnancies.
The biology of ECC may be modified by factors unique to young children: the implantation of cariogenic bacteria associated with feeding and oral hygiene in early childhood.64 ECC is known to be characterized microbiologically by dense oral populations of mutans streptococci (MS).65 It is suggested that the development of ECC occurs in three stages. The first stage is characterized by the primary infection of the oral cavity with MS. The second stage is characterized by the accumulation of these organisms to pathologic levels as a consequence of frequent and prolonged exposure to cariogenic substrate. The third stage is characterized by a rapid demineralization and cavitation of enamel, resulting in rampant caries.66 It has been demonstrated that colonization by MS is stable over time. Over a 2-year period, levels of MS were fairly stable; high levels of infection tended to stay high and were associated with subsequent development of caries.67
Furthermore, none of the teeth with undetectable levels of MS developed caries. This indicates that children with ECC are highly susceptible to the development of caries in later years when compared with caries-free children.
The traditional perception of blaming the bottle containing sweetened liquid as responsible per se for ECC must be reconsidered. Most studies have only asked the question, “Did your child ever go to bed with the bottle?” Few studies have investigated related behaviors, such as whether the child quickly finishes the bottle or whether the child uses the bottle ad lib. during the day. The method of bedtime bottle use also has been found to influence caries risk. If the bottle is removed after feeding, no increased caries risk is noted. However, if the bottle remains in the bed, the child is at greater risk of developing ECC compared with those children who had no nighttime bottle.68 These questions touch the time factor mentioned previously and must be considered whenever disease progression is discussed. Nevertheless, the bottle still must be considered as a risk factor, and to eliminate the baby bottle as a cause of or at least a risk factor for ECC would be premature.69
A recent study on caries among Arizona infants and toddlers has revealed some interesting findings: Use of an infant feeding bottle was common; nearly 45% of 13- to 36-month-olds reported still using a bottle. Those children currently using a bottle were more likely to have a prior history of sleeping with a bottle than those who were no longer using the bottle.32