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Pediatric  Dental  Health

November 10, 2004

Management and Prevention of Dental Caries In Children

There has been remarkable progress in the reduction of tooth decay in the U.S. over the past 30 years. Nevertheless, dental caries continues to be a significant problem for many children. Dental caries continues to be the most common infectious disease of childhood.

During the past few decades, changes have been observed in the prevalence and distribution of dental caries in the population. This disease is endemic in specific sectors of the population, especially the economically disadvantaged. Some children seem to have a mouthful of cavities, while other children have beautiful teeth. Eighty percent of the dental caries is found in only 25 percent of the children. More than half of all children in the U.S. have dental caries by the second grade of school. By the age of 17, approximately 80% of young people have had a dental cavity.

Dental caries is an infectious, communicable disease, which causes destruction of teeth by acid-forming bacteria found in dental plaque. The most important concept to remember is that caries is a dynamic disease process, and not a static problem. Secondly, before a cavity is formed in the tooth, the caries infection can actually be reversed!

Caries progression or reversal is determined by the balance between protective and pathological factors in the mouth. The development of dental caries is a dynamic process: Demineralization of the hard dental tissue by the acidic products of bacterial metabolism – alternating with periods of remineralization.

The development of the carious lesion is episodic, with periods of demineralization alternating with periods of remineralization The lactic acid produced by the cariogenic bacterial dissolve the calcium phosphate mineral of the tooth enamel in a process call demineralization. Baby teeth have thinner enamel than permanent teeth, making them very susceptible to caries.

Dental caries in children is typically first observed clinically as a “white spot lesion.” If the tooth surface remains intact and non-cavitated, then remineralization of the enamel is possible. If the subsurface demineralization of enamel is extensive, it eventually causes the collapse of the overlying tooth surface, resulting in a “cavity.”

Saliva has a critical role in the prevention of dental caries. Saliva provides calcium, phosphate, proteins, lipids, antibacterial substances, and buffers. Saliva buffering can reverse the low pH in plaque, and with a higher pH, calcium and phosphate can be driven back into the tooth enamel. One factor that lowers the risk of cavity formation is normal salivary flow. Anything less than 0.7 ml/minute increases the risk for cavity development.

Early childhood caries is a “virulent” form of dental caries that can destroy the teeth of preschool children and toddlers. Early childhood caries can also be defined as the occurrence of any sign of dental caries on any tooth surface during the first 3 years of a child’s life. Economically disadvantaged children are the most vulnerable to ECC.

Early childhood caries is an infectious disease, and the Streptococcus mutans bacteria is the main causative agent. Not only does S. mutans produce acid, it also thrives in acid. High sugar levels in the mouth increase the acid levels on the teeth. In children with ECC, oral Streptococcus mutans levels routinely exceed 30% of the cultivable dental plaque flora.

The clinical pattern of ECC is rampant and characteristic: First affecting the primary upper anterior teeth, followed by the upper primary molar teeth. The initial appearance of early childhood caries is white areas of demineralization on the surface of the enamel along the gum line of the upper incisor teeth. These white spot lesions progress such that they later become cavities that have been discolored. The mandibular incisors are protected by saliva and the position of the tongue during feeding. The ECC process may be so rapid that the teeth appear to have cavities “from the moment they erupt.”

The first event in the natural history of ECC is primary infection with S. mutans. The second event is the accumulation of S. mutans to pathologic levels, due to prolonged exposure to sugars. The third event is demineralization of enamel, which leads to cavity formation in teeth.

Early infection with S. mutans is a significant risk factor for future development of dental caries. Colonization of an infant’s mouth with this bacteria is usually the result of transmission from the child’s mother. S. mutans can apparently colonize the mouths of infants even before their teeth erupt. Children at high risk for early childhood caries may develop carious lesions on their upper front teeth soon after they erupt into the mouth. As the disease progresses, decay appears on the biting surfaces of the primary upper first molars.

New strategies for combating the infectious component using topical antimicrobial therapy appear promising.

The caries process must be thought of as a dynamic alteration between demineralization and remineralization phases. This represents a competition between the pathologic factors (such as bacteria and carbohydrates) and the protective factors (such as saliva, calcium, phosphate and fluoride). They Keyes diagram (above) shows that cavities are the result of the interaction between a susceptible tooth, a dietary substrate (sugar), a chronic bacterial infection, and time.

Streptococcus mutans is the major cariogenic bacterium. S. mutans forms glucan and levan polymers that are adhesive. The bacteria, along with the polymers, work together to form a biofilm – called dental plaque. The bacteria use a substrate (sugar) to produce acids that dissolve dental enamel. Repeated demineralization by these acids leads to dental cavities.

S. mutans has been highly associated with dental caries. The proportion of S. mutans in plaque associated with ECC can be 30% to 50% of the total viable bacterial counts in dental plaque. In contrast, S. mutans usually constitutes less than 1% of the plaque flora in non-caries active children. Lactobacilli are highly acidogenic microorganisms, associated more with deep cavities in dentin than with the initiation of the disease. Lactobacilli counts alone are not considered reliable enough in predicting dental caries activity, however.

The causes of caries are multifactorial, and the individual risk factors associated with ECC are therefore not necessarily causative.
  • Frequent intake of carbohydrate-rich or sugary foods enables the cariogenic bacteria to maintain a low pH on the surfaces of the teeth.
  • Night- time bottle feeding, or prolonged use of a sippy cup, can lead to early childhood caries. The flow of saliva is decreased during sleep, so clearance of the sugary liquid from the oral cavity is slowed down.
  • The earlier that a child’s mouth is infected with Mutans streptococci, the greater the risk for future caries development.
  • Children who already have one or more dental cavities are considered high risk for developing more.
  • A low fluoride level on the surface of the teeth reduces the remineralization process and increases the risk for caries.
  • When the saliva flow is below 0.7 ml/minute, the saliva cannot wash carbohydrates off the dental surface. In addition, low salivary buffering capacity, low salivary IgA, low salivary calcium, and low salivary phosphate reduce the potential for neutralization of acids in the dental plaque.
  • Finally, a low socioeconomic status can reduce interest in oral hygiene and a healthy diet.

    Effective dental care requires early identification of children at high risk for dental caries, so that they may receive early and intensive intervention. Caries risk assessment is one of the most important goals of a child’s first oral examination. The goal of caries risk assessment is to deliver patient-specific diagnostic, preventive, and restorative services – based on the needs of each individual child. Caries risk describes the status of the whole patient. It can be defined as the likelihood of a child getting a new cavity.

    Universal preventive strategies for all children are no longer appropriate. Since dental caries is no longer pandemic, but rather confined to a specific subset of children and tooth morphology types – a new risk assessment strategy is required. The nonexclusive contributory disease model of caries has three components: “Environment,” “genetic,” and “infectious agent.” In this model, any component may contribute to formation of a cavity – but does not necessarily cause it. Environmental factors include: Sugar consumption, fluoride exposure, oral hygiene practices, and socioeconomic status.

    Inherited disorders that affect dental development or salivary flow may increase the risk of dental caries.

    Streptococcus mutans levels above 500,000 colony-forming units per milliliter of saliva are associated with higher levels of smooth surface caries in the child. The higher the mother’s own level of S. mutans, the greater the likelihood of transmitting the bacteria to the infant. The best predictor of future caries activity is actually the child’s past caries experience.

    Completing a clinical investigation for dental caries is another important goal during a child’s first oral examination.
    During the dental examination, the presence of open cavities and fillings represents the prevalence of the disease - which is the most important indicator of the balance between resistance factors and caries inducing agents.
    The incidence of the disease must also be evaluated. Caries incidence may be determined by observing the speed at which existing lesions enlarge, or by observing the development of new carious lesions between two clinical examinations. The placement of new restorations within a short period of time indicates a high caries risk in the past.

    During the initial dental examination, the number of teeth and restorations should be noted. The number of cavities, and their active or inactive status should be noted: Dark hard tissues indicate inactive dental lesions. The presence of lesions on smooth dental surfaces indicates a high caries risk situation. Furthermore, the development of carious lesions with minimal plaque deposits indicates a very high risk for caries!

    Decalcifications should be carefully examined, charted in the record, and demonstrated to parents as evidence of pre-cavitation caries activity. Decalcifications usually appear as discrete white spots. These lesions are amenable to home hygiene and fluoride varnish treatment.

    The role of diet in ECC disease is critical. Consumption of sucrose is one of the most important factors leading to caries development. Children with early childhood caries often experience frequent or prolonged consumption of sugary liquids.

    Sucrose, glucose, and fructose contained in fruit juices are easily metabolized by S. mutans bacteria to form acids which slowly dissolve teeth. Bottles and sippy cups containing juice greatly increase the risk of developing ECC.

    Determination of oral MS bacterial levels can be done using a laboratory facility, or a chairside kit.

    When using a laboratory facility, the stimulated saliva is collected after chewing on paraffin for 5 minutes. It is then transported in a special medium to the laboratory. After incubation on selective medium agar plates, the MS colonies on the plates are counted. The results are expressed as colony forming units (CFU) per ml of saliva.

    When using a chairside kit for determining MS levels, the choices include an agar kit or a Strip Mutans test. One example of the agar kit is “Cariescreen.” An example of the Strip Mutans test is the “Dentocult Strip Mutans.” All of these kits need to be incubated for 48 hours before they can be read. Caries risk threshold is usually set for values ≥ 100,000 CFU/ml of saliva.

    Salivary flow and composition can also affect the health of oral soft and hard tissues. The clearance of acid metabolites by saliva is an important defense mechanism against hard tissue demineralization. To measure the flow of saliva, the child is asked to chew a paraffin tablet for 1 to 2 minutes, and to swallow the saliva. The timer then starts. The child is then asked to chew the paraffin for 5 minutes, frequently spitting saliva into a graduated test tube. When the time is up, the amount of secretion is recorded in milliliters, and the flow rate is calculated in ml/min. Normal stimulated salivary flow in adults is greater than 1.0 ml/min.

    The salivary buffer systems act as regulator of oral pH and thereby act to control the remineralization-demineralization process. This capacity is based on the phosphate system, as well as the carbonic acid and bicarbonate systems. Inorganic phosphate is the most concentrated buffer of non-stimulated saliva, while carbonic acid and bicarbonate are the most important in stimulated saliva.

    In the past the treatment for dental caries was to “drill and fill.” Restorative dentistry unfortunately has little long-term impact on oral S. mutans levels. Diet counseling and educating parents about undesirable feeding practices has also had minimal success in decreasing ECC in high-risk groups of children. Optimal long-term results can only be achieved by treatment of the underlying caries process.

    The modern approach to caries management is the “medical model.” The medical model treats the underlying caries process, and has 4 steps:
    1) Gaining control of the bacterial infection.
    2) Reduction of risk levels.
    3) Remineralization of teeth.
    4) Long term follow-up.

    1) Gaining control of the bacterial infection:
    The control of S. mutans is accomplished in two phases: Caries control, followed by chemotheraputic medication. We will start with caries control – treating the cavitated lesions with glass ionomer cements.

    1a) Caries control:
    The goal of caries control is to reduce the bacterial burden in the mouth of the child. Minimally invasive caries control, also called Atraumatic Restorative Treatment, reduces both the current and future treatment expenses. This mechanical measure will enable the subsequent chemotherapy to be more effective. At caries control visits, the teeth are excavated with spoon excavators and glass ionomer cement is used to seal the teeth. The dentist can be confident that the caries control process has been successfully managed when caries excavation is complete and parents are engaged in managing their child’s disease.

    1b) Chemotheraputic medication:
    The second phase of gaining control of the oral bacteria involves chemotheraputic antibacterial therapy. A combination of fluoride varnish and chlorhexidine application is used to lower the Mutans streptococci count.

    Fluoride varnish can be used alone, or in combination with other antimicrobial agents. The varnishes contain 5% sodium fluoride (NaF) at 22,600 ppm of fluoride. There is a mean caries reduction of 38% when fluoride varnish is used in caries prevention. In an aggressive preventive program, varnish can be applied 3 times within a 10 day period. This is followed by another varnish application every 3 months for the first year. The NIH consensus statement on caries notes that only fluorides and chlorhexidine gluconate are proven antimicrobial treatments for dental caries.

    Another successful antibacterial therapy against cariogenic bacteria is treatment with a chlorhexidine gluconate rinse or gel. The 0.12% chlorhexidine gluconate can be applied to toddlers’ teeth twice a day for 14 days. It is applied at least 30 minutes after the use of toothpaste because the sodium lauryl sulfate contained in most toothpastes will neutralize chlohexidine gluconate. It has a long history of safety. If the bacterial challenge is extremely high, only chlorhexidine can successfully deal with the infection.

    2) Reduction of risk levels:
    Step two in the medical model is reduction of the risk levels for patients. First, sugar intake must be reduced. A dietary assessment can identify when sugar consumption needs to decreased . Increasing fluoride use at home will also reduce the risk of dental caries.

    3) Remineralization of teeth:
    Step three in the medical model of caries management is the reversal of active caries site by remineralization. There are four parts to this step:
    a)Fluoride varnish is applied 3 times in a 10 day period.
    b)Fluoride is applied at home. A fluoridated dentifrice is used twice daily. Application of 1.1% NaF gel by toothbrush is recommended for very high risk children with dentin caries.
    c)Xylitol gum is recommended.
    d)A source of calcium, such as cheese, is also recommended.

    4) Long term follow-up:
    The last step in the medical model is long term follow-up at home and in the dental office. The office recall frequency should be every 3 months for high risk patients and every six months for low risk cases. Caries activity and risk are re-evaluated at the dental recall visits.

    1) First, the most important component in the treatment of the caries disease is prevention. Understanding the balance between pathological factors and protective factors is the key to successful prevention of caries.
    2) Second, any preventive program for ECC must involve the participation of the parent or caregiver.
    3) Third, preventive activities must art at an early age.

    There are three principal ways to prevent ECC:
  • Community-based programs
  • Home-care methods
  • Professional dental measures

    Professional dental measures are conducted mostly at a dental office. The goal of primary prevention is to decrease or postpone the transmission of Mutans streptococci from mother to child. Preventive therapy should be based on the risk factors for a particular child.

    Chemotheraputic treatment of caries is based on the use of two well-known agents (fluoride and chlorhexidine) to achieve selective antimicrobial control of carious microflora. Fluoride and chlorhexidine have an antimicrobial action against MS that is significantly higher than that which they have against other noncariogenic bacterial species.

    The systemic and topical use of fluoride is the most effective measure to prevent dental caries. Fluoride, the key agent in battling caries, works primarily by topical action: inhibition of demineralization and enhancement of remineralization. Twice daily exposure to topical fluoride via fluoridated toothpaste is a major component of caries prevention therapy. Fluoride varnish may be applied with a soft brush, and reapplication is recommended every 3 to 6 months.

    The anticaries action of fluoride results from two different mechanisms.
  • First, the fluoride ion is incorporated into the hard tissues of the tooth, strengthening its crystalline structure.
  • Second, the fluoride ion is able to interfere with the metabolism of cariogenic microorganisms, reducing both their number and pathogenicity. Fluoride inhibits enolase, an enzyme which bacteria need to metabolize carbohydrates.

    The differential sensitivity of MS to chlorhexidine makes selective chemotheraputic treatment of caries possible. When chlorhexidine is used in high risk subjects, significant reduction (50%) in children of new lesion development can be obtained. Chlorhexidine varnish seems promising, because the concentration of chlorhexidine, and the frequency of chemotheraputic treatment are the most important factors to prolong MS suppression. EC40 and Chlorzoin are two European chlorhexidine varnishes used for the prevention of dental caries.

    There is one other chemotheraputic agent for caries which is currently being researched: providine-iodine. Ten percent provodine-iodine solution may be applied to the teeth of infants at high risk for ECC. Iodine may be appropriate as long as the infant is not allergic to it. Iodine kills all of the bad dental bacteria for three to four months.

    It is now realized that the most important action mechanism of fluoride takes place on the enamel surface of the tooth. Fluoride inhibits the loss of minerals and promotes the remineralization process. Apart from water fluoridation, fluoride varnish seems to be the most suitable and documented fluoride regimen for the infant.

    Fluoride varnish contains 2.26% fluoride ion. The actual amount of fluoride used per treatment is 5-11 mg. The volume of fluoride varnish per treatment (0.2 – 0.5 ml) is significantly less than the probable toxic value for a 10 kg child (2.0 ml). The plasma fluoride concentration after varnish application is barely measurable. Therefore, fluoride varnish is very safe for use on infants’ teeth!

    Fluoride varnish is available under the trade names Durafluor and Duraphat. Fluoride varnish is recommended for use in preschool age children because of its ease of application, and it equivalency to APF gel systems. The varnish is applied with a small soft brush, and reapplication is recommended every 3 to 6 months. Data show an overall reduction of caries incidence after fluoride varnish applications, ranging from 18% to 70%, compared with untreated control subjects.

    Fluoride incorporated during tooth development is insufficient to play significant role in caries protection. Fluoride is needed regularly throughout life to protect teeth against caries. Fluoride in solution, from topical sources, enhances remineralization by speeding up the growth of a new surface in the partially demineralized subsurface crystals in the carious dental lesion.

    Recommendations for fluoride supplementation can be made based on the fluoride content of the water, the child’s age, and the child’s caries risk. The risk of dental fluorosis is highest during the period of enamel maturation, from 1 to 3 years of age.

    The most important ask for today’s dentist is to identify the high caries-risk child before the clinical manifestations of the disease become apparent, and then to provide individualized protection to that child. The preventive process must begin early in infancy to ensure a child’s oral health.

    The purpose of the first dental visit is to assess individual risk, and to educate the parent or caregiver about reducing such risk. A clinical examination is an essential part of a child’s first dental visit, and as an important part of risk assessment. A correct and efficient diagnostic investigation must include the identification and evaluation of risk factors.

    An initial oral evaluation should occur within 6 months of the eruption of the first primary tooth, and no later than 12 months of age. The best way to accomplish a dental examination on an infant is the “knee-to-knee” method. The dentist and caregiver should sit knee-to-knee facing each other. The child’s legs should be placed around the parent’s waist, and the child’s head is placed in the cradle formed by the dentist’s lap. The dentist should look for early signs of dental caries. White spot lesions represent the early clinical manifestations of the caries process. These chalky lesions represent decalcified enamel, and this finding places the child at high risk for developing cavities.

    Anticipatory guidance is another important element that must be incorporated into the child’s first dental visit. Anticipatory guidance refers to sharing with parents or caregivers information about the child’s current oral health status, as well as future needs. When preventive information is provided to parents, it must be easily understood and easily used. The information must as a clear as possible. Diet counseling is an integral part of anticipatory guidance. Bottle-fed infants should not be put to sleep with the bottle. Nocturnal breast-feeding should be discouraged after the first upper incisor erupts. Only 6 ounces of fruit juice should be consumed by infants each day.

    During the first dental visit, a variety of information needs to be gathered which will be used in the “non-exclusive contributory disease model” of dental caries. The required information falls into three categories: environmental factors, infectious agent and genetic factors.

    1) Environmental factors are noted:
    Existing dental caries, estimated sugar intake, estimated fluoride exposure, socioeconomic status, oral hygiene practices, and dietary habits are recorded.

    2) Infectious agents can be assessed using microbial sampling, such as the Dentocult SM Strip for assaying MS levels in the mouth.

    3) Genetic factors can be evaluated, including:
    Salivary flow, salivary buffering capacity, and tooth morphology disorders.

    Xylitol is a naturally occurring, low-calorie sugar substitute with anticariogenic properties. It is a sugar alcohol, derived mainly from birch and other hardwood trees. Xylitol contains 40% fewer calories than sucrose. Data from recent studies indicate that xylitol can reduce the occurrence of dental caries in young children.

  • The American Academy of Pediatric Dentistry, the American Dental Association, and the Academy of General Dentistry recommend that children visit a dentist within six months of the eruption of the first tooth, and no later than 12 months of age.
  • Infants should not be put to sleep with a bottle. Breast-feeding at night should be avoided after 12 months of age.
  • Infants should be weaned from the bottle at 12-14 months of age.
  • Consumption of juice from a bottle or sippy cup should be avoided. Juice should be offered to a child only in a cup. Infants and toddlers should drink no more than 6 ounces of juice per day.
  • Cleansing of the baby teeth should be started by the time of eruption of the first primary tooth. A small piece of clean gauze or a small toothbrush can be used.

    An article on the WHO Collaboration Centre site discusses the basic steps in Atraumatic Restorative Treatment. ART is an important component of caries control. It is an extremely important component of caries management in high risk populations of children.

    Atraumatic Restorative Treatment

    Copyright ©2004 Daniel Ravel DDS, FAAPD

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