Pediatric Clinics of North America

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Figure 1. Pit and fissure sealants in place on two permanent upper molars. The sealant is adhesively bonded to the tooth enamel and prevents fermentable carbohydrate from entering the narrow pits and fissures in which cariogenic bacteria reside.
Recommendations for parents include:

Prescribe fluoride supplements if needed.

Establish a dental home for the patient at approximately 1 year of age.

Ensure that the child's dentist evaluates the teeth for developmental defects and for the need for pit and fissure sealants.


Assessing an infant's or toddler's risk for dental caries is an essential component of an oral health program. Disease risk assessment is a systematic evaluation of the presence and intensity of etiologic and contributory disease factors. This assessment is designed to provide an estimation of an individual's disease susceptibility and to aid in targeting preventive and treatment strategies. In the case of dental caries, risk assessment information can be divided into three categories ( Table 3 (Table Not Available) ). [45] Category I comprises markers of disease that are provided by the patient and parent through the history and physical examination. The presence of many of these markers can be determined by the pediatrician. Category II comprises disease markers and the single true risk factor for dental caries, the presence of MS. Some of the items in Category II can be appreciated by pediatricians, but most require dental training or technologies not likely to be present in a pediatric office. Determination of Category III markers requires the use of technologies that are not practical for clinical use at this time.


(Not Available)

Adapted from Moss ME, Zero DT: An overview of caries risk assessment, and its potential utility. J Dent Educ 59:932, 1995; with permission.

Among the data from Category I, pediatricians can make a general assessment of caries risk for a child through the patient's demographic data. The socioeconomic status of the family is a risk marker because dental caries is increasingly a disease of people of low socioeconomic status. Eighty percent of the dental caries in children in the United States can be found in approximately 25% of the population, and this portion of the population is typically children of poverty. [19] [32] [66] Caries rates in some communities are also higher among some racial and ethnic groups, in particular African Americans, Hispanics, and Native Americans. [32] [33] The patient's age indicates whether transmission of MS is likely to have taken place. [10] Lower maternal education levels also have been associated with dental caries risk. [20]

A child's medical history, well known to the pediatrician, can provide valuable information. Prematurity and very low birthweight are associated with the presence of enamel defects, often subclinical, that can predispose teeth to caries at an early age. An increased risk also exists for children who have taken syrup-based medications on a long-term basis. A child's dental history, which might not be well known to the pediatrician, may provide substantial information. A history of early childhood caries is one of the best indicators of future dental disease, so pediatricians should routinely evaluate the dentition for obvious carious lesions or evidence of dental restorations.

Behavioral factors include oral hygiene habits, feeding practices, and dietary preferences. A diet rich in fermentable carbohydrates, frequent snacking, constant use of a "tippy" cup filled with fruit juice, bottle use at sleeptime, and prolonged at-will breastfeeding have all been associated with early childhood caries. [20] [27] [30] Parental inattention to oral hygiene practices are another marker for potential dental disease. [26] Patients with an impaired ability to maintain oral hygiene are at higher risk; this category of patients includes infants, toddlers, and young children, all of whom must rely on a caregiver for tooth-cleaning procedures. Others in this category include physically challenged and developmentally disabled individuals. Older children undergoing orthodontic treatment or wearing other types of intraoral appliances are also at a higher risk. Such appliances provide difficult-to-clean niches for plaque growth.

Other risk factors in Category I that may not be as readily available to pediatricians include the mother's oral health status. High levels of maternal dental caries [63] or a poor gingival condition [55] have been associated with higher levels of dental disease in the offspring. The child's fluoride exposure, although important in assessing resistance to tooth decay, is not always easily quantified. More detail is provided in the discussion on supplemental fluoride.

Data from Category II are more likely to be obtained in a pediatric dental office. A plaque index measures in a relatively standardized way the amount of plaque present on the teeth. High plaque levels have been associated with an increased risk for dental caries. [42] [43] Diet histories are used to assess the cariogenicity of the diet and to provide the basis of recommendations for dietary changes. Salivary MS and lactobacilli assays can be easily done with commercially available kits and incubators (Cultura Incubator, Dentocult-SM, and Dentocult-LB, Ivoclar Vivadent, Amherst, NY), although they are not in wide use at this time. Such tests not only indicate whether transmission of MS has occurred but also provide a quantitative measure of the infection, another factor in caries risk determination. [27] Salivary flow rate, although relatively easy to assess, is not routinely done, nor are assays of salivary buffering capacity, which requires special equipment.

Pediatricians interested in gathering data on caries risk in young children can use much of the information in Category I, especially the demographic data, including the parents' dental histories. Additional information about the patient's medical history, previous dental treatment (if any), and dietary or feeding habits may help practitioners to make a general determination about a child's risk for dental disease. Fine tuning the risk determination beyond low risk versus high risk is not easily done.


Water Fluoridation

In the 1900s, McKay, practicing in Colorado, noticed that many of his dental patients exhibited an unusual intrinsic enamel discoloration, termed Colorado brown stain by area residents. McKay also noted that individuals with this type of mottled enamel had low levels of dental caries. Subsequent investigations determined that water-borne fluoride was responsible for the mottling and the caries resistance. Epidemiologic studies were conducted in the 1930s in several midwestern communities with differing levels of fluoride in the water supply to determine the relationships between fluoride concentrations in drinking water, dental fluorosis (replacing the term mottling), and dental caries. (An example of dental fluorosis is shown in Fig. 11 in article by Wright earlier in this issue). Those studies led to the findings that communities with water fluoride levels of approximately 1 mg/L (part per million) demonstrated the best compromise between caries reductions and community fluorosis levels. At that level, fluorosis in the population was mild in severity and low in prevalence. Subsequent studies determined the relationship between mean annual temperature and mean water consumption in various locales. Based on those data, recommendations were developed for artificially fluoridating water supplies at a flouride level between 0.7 (warmer climates) to 1.2 (cooler climates) mg/L.

In the 1940s, full-scale prospective trials of artificial water fluoridation began in four pairs of cities in the United States and Canada. Each pair of communities was carefully selected after matching on many demographic, socioeconomic, and health parameters. Before the studies, the fluoride level in each city was negligible. Artificial fluoridation to a level of 1.0 ppm to 1.2 ppm was begun in one city in each pair in 1945. Sequential cross-sectional surveys were conducted for 13 to 15 years. Among the multitude of variables studied, the only significant difference found was a 50% to 65% decrease in dental caries in the fluoridated communities. The prevalence and severity of fluorosis in each intervention city was comparable with those of communities with naturally occurring fluoride at a level of 1.0 mg/L. These studies ushered in an era of community water fluoridation that continues today and that resulted in sharp decreases in dental caries in the United States over the latter half of the twentieth century. This modality of fluoride delivery is extremely cost-effective, with estimates of per capita cost ranging from a few cents to a few dollars per year, depending on community size.

Contemporary Exposure to Fluoride

At the time of the initial fluoridation studies, an individual's exposure to the ion was limited to naturally occurring fluoride. Except in communities with high natural fluoride levels or artificial fluoridation, these levels were low. In the intervening years, however, the disparity in fluoride exposure has decreased between optimally fluoridated and fluoride-deficient communities. Exposure to fluoride in fluoride-deficient communities has increased through three primary sources: (1) fluoridated dentifrice; (2) foods and beverages processed in optimally fluoridated communities; and (3) fluoride supplements. This increase in fluoride exposure in fluoride-deficient communities has been termed the halo effect because of the concomitant reductions in caries in these locales. Today the caries-reduction benefits of optimal fluoridation are approximately 20% to 40% compared with some fluoride-deficient communities in contrast to the 50% reductions reported in the 1950s. This change is caused by an improvement of the dental health in residents of fluoride-deficient communities compared with 50 years ago. At the same time, the prevalence of fluorosis in fluoride-deficient communities has increased to levels approximating the prevalence in optimally fluoridated communities. [60] Most of this fluorosis is scored as mild and is not considered by most authorities to be cosmetically objectionable or to pose a public health concern. The halo effect does, however, make it difficult to accurately determine an individual's exposure to fluoride by simply assessing the fluoride concentration of the municipal or well water supply.

Fluoride Mechanisms of Action

At the time of the water fluoridation trials, and for some time afterward, investigators assumed that fluoride exerted its anticaries activity by becoming incorporated into developing enamel. The presence of fluoride in enamel results in a crystalline structure that is resistant to acid dissolution. Other studies purported that fluoride exposure during dental development results in the formation of posterior teeth with shallower pits and fissures that are therefore less susceptible to decay. [18] Some controversy exists on these issues, but most authorities now agree that the systemic effect of fluoride is minor. [38]

Greater importance is now given to the topical effects of fluoride. Topical contact of fluoride with teeth occurs through the intake of foods and beverages containing the ion, use of fluoridated dentifrice, and perhaps more importantly through salivary secretion of fluoride that has been systemically absorbed. Topical effects are mediated through direct contact with teeth and through the effects of fluoride on bacterial plaque. Dental caries begins with demineralization of enamel through repeated exposure of acid produced by plaque bacteria as they metabolize fermentable carbohydrate. The early lesion begins below the enamel surface and appears clinically as chalky white enamel ( Fig. 2 ). This white spot lesion can be remineralized as long as the surface enamel layer remains intact. The presence of low levels of fluoride in the oral environment promotes remineralization. Cycles of demineralization and remineralization occur constantly. As fluoride is taken up by the lesion during the remineralization process, the lesion is strengthened and becomes more acid resistant than the original intact enamel.

Figure 2. A white spot lesion on the mesial proximal surface of primary lower molar now visible because of the exfoliation of the adjacent primary molar. The white spot represents an area of enamel that has been demineralized by the organic acids produced by plaque bacteria. As long as the surface enamel remains intact, as it is in this example, it is possible to remineralize the lesion.
Fluoride in the oral environment also is absorbed by dental plaque and becomes concentrated to levels that can disrupt bacterial enzyme systems, decreasing the acidogenicity and aciduricity of plaque bacteria. Plaque also serves as a reservoir of bound fluoride that is released as free fluoride during a pH decrease. Free fluoride ions then can participate in the remineralization process.

Supplemental Fluoride

Dietary fluoride supplements were developed as a means of providing fluoride to individuals who resided in fluoride-deficient communities. They represented an attempt to provide a daily dose of fluoride equivalent to the intake of individuals who resided in optimally fluoridated communities. Early supplementation schedules were somewhat awkward, requiring that sodium fluoride tablets be dissolved in water that was used for drinking and cooking. This rationale was also based on the earlier assumption that the anticaries mode of action of fluoride was primarily systemic. Subsequent schedules began the practice of supplementing with a daily dose of fluoride based on the age of the patient and the fluoride content of the drinking water supply. Clinical studies documented caries reductions of 15% to 30% in individuals in fluoride-deficient communities who consumed dietary supplemental fluoride. Dietary fluoride supplements can approximate the caries protection only of water-borne fluoride, given their relatively high-dose, low-frequency nature. By contrast, exposure to fluoridated water is a low-dose, high-frequency regimen.

In several studies over the past 30 years, fluoride supplements have been associated with mild fluorosis. [1] [50] The severity of fluorosis was low, and it was most often found in children who began supplementation before the age of 6 years. Findings of this sort have prompted reductions in the fluoride-dosage schedules over the years. The current schedule, adopted in 1994, is shown in Table 4 . No studies are available to document the fluorosis rates associated with the new schedule, but it is reasonable to assume that the risk for fluorosis is lower.



Fluoride Concentration of Primary Drinking Water Source, mg/L (ppm)

< 0.3

0.3- 0.6

> 0.6

Birth to 6 mo

0 *



6 mo to 3 y




3 y to 6 y




6 y to at least 16 y




*Dose in mg fluoride ion.

The benefit of supplemental fluoride can be maximized and the risk can be minimized by appropriate prescribing of supplements, which entails:

Determination of the fluoride concentration in the child's primary drinking water source, which might not be tap water in the home. Many families use bottled water, which usually has low levels of fluoride [39] [59] [65] ; however, some contain significant concentrations of the ion. Households with reverse osmosis water-filtration systems have a reduced level of fluoride in the tap water. Point-of-use filtration systems, such as charcoal filters, typically do not remove fluoride. Most well water in the United States is deficient in fluoride, but in some areas of the country, fluoride occurs naturally in ground water sources. Finally, some children may spend most of their days in a day-care setting or at a relative's house, and the primary source of drinking water may come from that location, not the home. Whatever the case, the primary drinking water source should be assayed for fluoride content. This analysis may be provided by some local or state health departments, schools of dentistry, or through commercial sources (FluoriCheck, Omnii Products, West Palm Beach, FL).

Appropriate prescribing. Fluoride supplements should not be prescribed for children younger than 6 months or whose primary drinking water contains significant levels (> 0.6 mg/L) of fluoride.

Education of the parents and caregivers. Parents who do not understand the potential benefits of supplemental fluoride are less likely to fill and properly use the prescriptions with their children. The trade-off of a risk of mild fluorosis for reduced caries experience must be considered by pediatricians and discussed with the parents. Consideration of a child's risk factors for caries may assist in this decision.

Fluoride supplements are available as drops, tablets, and lozenges that deliver 0.25 mg, 0.5 mg, or 1.0 mg fluoride ion to match the doses indicated in Table 4 . Drops should be placed on the infant's tongue once daily between feedings. Tablets and lozenges should be administered after tooth brushing, preferably just before bedtime. They should be sucked or chewed for 1 or 2 minutes before swallowing to maximize contact with the teeth. Supplemental fluoride is also available in combination with vitamins. No evidence suggests that the fluoride in these products is any less effective in caries prevention than is fluoride alone; however, in some cases, the vitamin and fluoride dose requirements of the child may be incompatible with the combinations available. In such cases, it may be necessary to resort to separate supplements to avoid prescribing too much or too little of either component in combination products.

The FDA bans manufacturers of fluoride supplements from claiming that the use of supplemental fluoride by pregnant women will convey a caries-protective effect to their offspring. The only placebo-controlled, double-blind study to investigate this practice in a fluoride-deficient community found no additional benefits to prenatal supplementation when the offspring received postnatal supplements and brushed with a fluoridated dentifrice. [36]

Fluoride-containing Dentifrices

Fluoride-containing dentifrices, introduced in the 1950s, constitute approximately 95% of the dentifrice market in the United States. Most products sold in the United States contain approximately 1000 to 1100 mg/kg (ppm) fluoride, although some dentifrices with higher concentrations (1500 mg/kg flouride) have been introduced. Trials of at least 2 years' duration with fluoridated dentifrice have resulted in median caries reductions in the order of 15% to 30%. [29] [46] Regular use of fluoride-containing toothpaste over a lifetime probably provides decay protection equivalent to that of fluoridated drinking water. The combination of the two provides additional protection. [49]

Because some children enjoy the taste of toothpaste and ingest it deliberately, parents should be cautioned to keep these products out of the reach of young children. Additional vigilance is required with dentifrices that are flavored to appeal to children because they may encourage young patients to use more toothpaste at each brushing, thereby increasing the risk for ingestion. [3] [37]

Fluoride-containing Mouthrinses

Fluoridated mouthrinses, initially prescription-only products, became available over the counter in the 1980s. These products contain 0.05% sodium fluoride, a concentration equivalent to approximately 1 mg fluoride per teaspoonful. Prescription mouthrinses may be ingested, but over-the-counter products are intended for topical use only. They are unsuitable for use by children whose swallowing reflex is not fully mature. Fluoridated mouthrinses have been shown to be effective in individuals and groups at high risk for dental caries, but the rationale for their routine use by most children is questionable. [4]

Professionally Applied Fluoride Compounds

Dentists routinely apply high-concentration (12,300-22,600 mg/kg) fluoride gel, foam, or varnish to their patient's teeth once or twice yearly to provide protection against decay. Although investigators originally thought that the fluoride from these products entered enamel crystals, research has shown that professionally applied fluoride forms a layer of calcium fluoride-like material on the enamel surface. When the oral pH decreases, fluoride is released and made available to remineralize early developing carious lesions.

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