Oral health Early Childhood Caries

Conception to Birth Learning Objectives Early Childhood

Caries  Understand the goal of early intervention and importance of the “dental home”  Define dental caries (tooth decay) Treatment  Differentiate early childhood caries from dental caries generallyearly dental caries from early childhood tooth decay Action Steps  Describe the transmission and colonization of bacteria associated with early childhood tooth decaycaries  Understand the prevalence and consequence of early childhood tooth decaycaries

 Describe conventional treatment for early childhood caries (restorative dentistry)

 Describe emerging treatment (Prevention and disease management for early childhood caries)

In This Section

You will meet the offspring of Mrs. SantosPerez’ daughter, Maria and follow her oral health through her second year of life. You will see the consequences of her lack of dental care. ETC...

Visible plaque on the front Table of Contents teeth, is positively The Child: Maria SantosPerez - 12 Months Why should Maria's physician refer her to a dentist? correlated with The Child: Maria SantosPerez - 33 Months caries Failure of Early Intervention? development What is Dental Caries? by age 3 (28) What is Early Childhood Caries? Prevalence, acuity and consequence of Early Childhood Caries What is the classical treatment? Advances in What is Disease Prevention? the understanding The Child: Maria SantosPerez - 12 Months of dietary influences and Now meet 12 month-old Maria Santos. During Maria’s 12-month well-baby exam at her fluoride on dental disease primary care physician’s office, Mrs. SantosPerez states reports that Maria’s front teeth become “didn’t look right” when they eruptedfirst came in. The health history indicates that Maria was a pre-term infant (i.e.. < 37 weeks gestation) with a low birth weight (i.e.. < instrumental in 2500gm). Her physician takes a brief look, reassures Mrs. SantosPerez that the dental supporting appearanceit may be a “developmental problem” and suggests that if she has further early dental concerns, that she should see consult a dentist. He The primary care provider, intervention unaware of the American Academy of Pediatric’s Infant Oral Health Guidelines (Mike, the link is:

http://aappolicy.aappublications.org/cgi/content/full/pediatrics;111/5/1113 , does not provide oral health risk assessment or counseling and does not facilitate a formal referral as is typically done for other types of services. write a referral letter.

As young as Maria is, both developmental and acquired disease are already evident on careful examination.

Active Disease:

 RED Arrow: thick plaque and decalcification (mineral loss) on primary teeth  BLUE Arrow: shows the gingival tissue as shiny and full, indicating inflammation.

Developmental Findings:

 ORANGE arrows: Notching of incisors  GRAY arrow: eruption hematoma  PINK arrow: atypical eruption sequence  GREEN arrow: anatomical variant of the labial frenum

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The primary components of dental plaque are bacteria, inter-bacterial matrix, and debris. Acid, produced by these many bacterial species (mainly especially the mutans Streptococci)us mutans) is considered the most important activity in the production of tooth decayconcentrates in the plaque and destroys the tooth surface by “decalcifying” the enamel. Plaque may be especially concentrated in surface defects such as those associated with prematurity. Twenty percent of remature children like Maria, being a low birth-weight infant, is at risk for enamel hypoplasia, as 20% of low birth-weight children are affected. E have such enamel hypoplasia which is defined as a deficiency in enamel formation, that manifests clinically as grooves or pits, or a lack of surface enamel (29). These surface irregularities act as “plaque traps” allow for an increased colonization of harmful bacteria and increase Maria’s risk for developing cavities.

Why should Maria’s physician refer her to a dentist?

The goal of an early dental assessment is primary prevention. This may be accomplished with the timely delivery of oral health information, including the conditions that create caries & cavities; its natural progression; and its prevention (read more about "Anticipatory Guidance" later in this module), and the identification of populations at high risk for tooth decay. The traditional approach of treating the effects of tooth decay (i.e.. “drilling and filling”) is beingcan be replaced by disease prevention and disease management if children at high risk of developing cavities can be identified early and effectively.

Prevention focuses on the establishment and maintenance of good oral hygiene, optimizing systemic and topical fluoride exposure, and eliminating high frequency or prolonged exposure to simple sugars in the diet. Prevention is the foundation for the establishment of a “dental home” by 1 year of age. The concept of the "dental home" as advocated by the American Academy of Pediatric Dentistry (Mike: The link is www.aapd.org/media/Policies_Guidelines/P_DentalHome.pdf ) is derived from the American Academy of Pediatrics concept of the "medical home." This concept states that “the primary health care of infants, children, and adolescents should be accessible, continuous, comprehensive, family centered, coordinated, compassionate, and culturally effective. It should be delivered or directed by well-trained child health specialists who provide primary care and help to manage and facilitate essentially all aspects of pediatric care” (25).

Every child should have an examination and oral health risk assessment by 12 months of age by a dentist or qualified pediatric health care professional. (26) The Caries Risk Assessment Tool (CAT), provided by the American Academy of Pediatric Dentistry (27), was designed to assist both dental and nondental other health professionals in assessing the risk of tooth decay in infants, children and adolescents. The CAT can be used to Perhaps the single determine the relative risk of caries of the patient. Questions directed at dietary practices, strongest fluoride exposure, oral hygiene, utilization of dental services, socioeconomic status and general level of health can help determine if a child is at low, moderate or high risk for predictor of dental disease. disease acquisition and Using the CAT, and Maria’s history (low socioeconomic status and no usual source progression, is of dental care) and exam findings (thick plaque, areas of demineralization and frequency gingivitis), Maria would be considered at high risk for dental disease. (rather that quantity or It is too late for Maria to gain the advantage of primary prevention and some aspects of source) of anticipatory guidance, as she already exhibits overt signs of dental disease. Maria, fermentable however, is not too late for disease suppression. With proper diet control and the carbohydrates application of topical fluoride, Maria may have avoided surgical intervention if timely care is (e.g. obtained. Unfortunately, without a timely dental referral to a dentist who will provide sweetened disease management services, disease progression is inevitable. milk, juice, soda). The referral was never made from Maria’s physician to a dentist and Mrs. SantosPerez failed to negotiate the dental care systems to seek care on her own.

The Child: Maria SantosPerez - 33 Months

Maria is now 33 months old and has presented with her mother to the local health center dental clinic, because, according to Mrs. SantosPerez, Maria has “been up all night, crying about her teeth”. (See image of Maria's teeth at left, click to enlarge)

Dental History - in the last 2 months, Maria has become increasingly irritable at mealtimes. It began as whining with cold or sweet foods, and has progressed to crying when biting with the front teeth. For the last 3 nights Maria has awoken from sleep and Mrs. SantosPerez was has been able to console her with her usual bottle of apple juice. Last night, she was inconsolable and required pain medicine (“oral numbing gel”)(“baby Tylenol” to help her sleep.

Mrs. Santos did not take Maria to the dentist before, as her local dentist doesn’t except medicaid and she is aware of the unpredictable wait and long hours for walk-in “emergencies” at the health center. Additionally, Mrs. SantosPerez, aware of Maria’s problem, had elected to “wait it out” in part because of her physician’s statement that the poor appearance of the teeth represented a “developmental problem” and in part because she stated that her physician said it was a “developmental problem” and she felt since these are “baby teeth”, that they will “just fall out, so why bother fixing them sooner or later”. Failure of Early Intervention?

Tooth decay in the primary teeth, has significant functional and disease progression consequences:

Disease: Since the mouth (rather than any single tooth or tooth surface) is the locus of disease, and not all the primary teeth are replaced simultaneously, disease in the primary teeth will spread toset the stage for decay in the incoming permanent teeth. Dental disease impacts all these new teeth as they become available, and because the exchange takes so long (until age 12-13 years), children that have untreated, active oral disease are at an increased risk for more generalized, ongoing and often severe tooth decay.

Child: As can be seen in Maria’s case, early childhood tooth decay in the primary teeth, if not cared for, results in chronic pain, infection and sleeplessness nights. It may also lead to poor weight gain, the inability to eat (2) and may affects the overall quality of a child’s daily life. (30)

Dentition: Loss of primary teeth impairs mastication, affects the development of the craniofacial system, and results in loss of arch space for the succeeding permanent teeth to “grow in” (erupt) into the proper position. This is the reason that failure to maintain the primary dentition intact leads directly to orthodontic problems as the permanent teeth replace them.

Maria is diagnosed with severe early childhood caries or “(early childhood tooth decay)”.

What is Dental Caries?

Dental caries, better known as “tooth decay”, is the disease process that leads to the loss of tooth mineral and eventually, to cavitation of the tooth surface (“cavity”). It is a dieto- bacterial, infectious, transmissible, oral disease. Three things are required for dental caries activity to become established and progress: one or more susceptible tooth surfaces, "cariogenic“ (decay causing) bacteria, and fermentable carbohydrates (particularly sucrose).

Early childhood caries is better known as early childhood tooth decay. “Tooth Decay” refers to both the process and result of dental caries.

1. Dental “caries”: refers is the proper name for to the disease process that leads to dental cavities (the word “caries” is always a singular noun) 2. Dental cavitiesCavities: are the the resultant holes in the teeth that result from dental caries 3. Deep Dental Decalcification is the: loss of tooth mineral or first from the surface enamel which marks the first clinical signs of dental caries and the first step in cavity formation

4. Tooth decay: includes all of the above

What is Early Childhood Caries?

Early Childhood Caries (ECC) or early childhood tooth decay, previously termed “nursing caries” or “baby-bottle tooth decay”, is a particularly virulent form of tooth decay, that affects the teeth of infants and preschool children. Its formal definition, as stated by the American Academy of Pediatric Dentistry (AAPD), is based on the age of the child when decalcifications or cavities are first noted. ECC is diagnosed when any child younger than “71 months” demonstrates any sign of tooth decay or prior treatment for tooth decay. Severe ECC is diagnosed when a young child has evidence of tooth decay on multiple teeth. Since AAPD’s definition was adopted in 2003, greater attention has been placed on younger-and-younger children so that any child under age three with any sign of tooth decay should be considered to have the severe form of ECC.

(MIKE: This definition is from http://www.aapd.org/media/Policies_Guidelines/D_ECC.pdf)

ECC Etiology: The process of ECC is the same as the generic process of tooth decay: a combination of acidogenic bacteria that metablize simple carbohydrates into acid thereby producing an environment on the tooth surface that decalcifies tooth structures until they are so weakened that they collapse into a “cavity.” What distinguishes ECC and especially Severe-ECC (S-ECC) from ordinary tooth decay is its aggressiveness. This enhanced pathogenesis is primarily predicated on the contribution of specific “cariogenic” (decay causing) bacteria in the dental plaque. (Dental plaque is the sticky white or yellowish film of bacteria, bacterial products, and debris that forms on tooth surfaces, especially along the gum line where it is least disturbed by eating and brushing). In particular, the plaque that causes ECC and S-ECC is richer in bacteria of the mutans streptococci group as these bacteria are the most efficient and effective in initiating the caries process. Children with ECC have “mutans” levels in plaque that typically exceed 30% of the plaque’s bacterial composition (31-33) while young children without ECC have plaque with mutans that compromises less than 1% of cultivable flora (34). Based on over 35 years of experimental and clinical studies, the mutans streptococci have been implicated as the primary infectious agent for caries initiation.

It results from an overgrowth of specific organisms that are a part of dental plaque (sticky white or yellow film found on the tooth surface) . Although numerous types of bacteria live in the mouth, tooth decay results from the overgrowth of specific cariogenic (decay causing) organisms. Studies demonstrate that children with early childhood tooth decay, have Streptococcus mutans (S. mutans), counts that exceed 30% of the cultivable plaque flora (31-33). Conversly, in children with negligible to no caries activity, S. mutans comprises less than 1% of total cultivable flora (34). Thus, S. mutans have been implicated as the most likely infectious etiologic agents of tooth decay (35).

Transmission and Colonization: Infants’ teeth are colonized with bacteria, including those that promote caries, shortly after the eruption of the first primary dentition teeth at approximately 6 to 30 months of age. Colonization requires direct transmission of saliva from the primary caregiver, typically the mother, to the child. This transmission occurs whenever and however saliva is “shared,” for example by using the same spoon to taste and feed a baby, by maternal cleaning of a pacifier in her own mouth before passing it to the child, by using saliva to clean around a baby’s mouth, or during play through which the baby picks up maternal saliva on its hand or face and transfers the saliva to its own mouth. As with other infectious conditions, the “success” of transmission depends on three factors:

1. The Source, i.e. the titer of the inoculum: in this case the concentration of mutans streptococci in the mother’s or caregiver’s saliva; 2. The Transmission, i.e. the efficiency of the transfer: in this case the frequency of transmission from mother/caregiver to child; 3. The Receiver, i.e. the ability of the target to receive the pathologic bacteria: in this case the presence of teeth in the child ’s mouth coupled with the availability of sugar in the child’s diet to support the transfe r.

The primary caregiver of the infant, frequently the mother, has been shown to be the most likely source of inoculation of an infant’s dental flora. There are no studies that explain absolutely how transmission occurs, however, examples include cleaning the baby's pacifier in the mother's mouth before giving it to the baby, sharing utensils or pre-chewing the baby's food. Transmission and colonization of S mutans depends on the magnitude of the innoculum. Higher levels of S mutans are associated with untreated tooth decay, thus, infants of mothers with untreated tooth decay are at higher risk of acquiring the bacteria (36) Acid Production and Demineralization: Decay causing bacteria ingest sugar and other fermentable carbohydrates from the child’s diet and produce acid as a by-product, causing a drop in the plaque pH. The acid attacks the outer surface of the tooth (enamel) for approximately 20 minutesafter each food exposure (longer for sticky foods), resulting in mineral loss (demineralization). This is a highly sophisticated and dynamic process that is influenced by these bacterias’ capacities to store carbohydrate substrate both intracellularly and extracellularly in the plaque for later metabolism into acid. For this reason, the decay process can continue unabated for an extended time between meals or snacks (although the greatest “decay attack” occurs during and for approximately 20 minutes after eating).

“White Spot lesions” - Clinically, this isthese areas of demineralization are the first visually detectable stage signs of tooth decay. They are chalky white smooth patches or linear markings that most frequently form along the gum line where plaque is most abundant – starting on the maxillary incisors (upper front teeth). As they may be hidden under plaque, white spot lesions are most readily seen when the plaque is first wiped away using a corner of a washcloth or gauze square. (Finger cots made of terrycloth are available for cleaning babies’ teeth.) Not all white spots are early lesions of tooth decay as some are developmental. Demineralized white spots resulting from tooth decay are unique in their flat appearance, shape, location, and association with plaque.. It is an area of demineralization, characterized by a chalky, white appearance. Although white spot lesions represent loss of mineral from the tooth, the loss is localized mainly in the subsurface of the enamel. The enamel surface in thise incipient lesion is essentially intact and amenable to remineralization. THIS STAGE IS REVERSIBLE IF CAUGHT IN TIME.

“Cavities” - When demineralization exceeds remineralization as a result of frequent or prolonged acid attacks, the result is a breakdown of the enamel, and the formation of a hole or “cavity” in the tooth surface. This is a late-stage sign of tooth decay. Cavities, unlike white spot lesions, are not reversible, but can be arrested with intense diet control and oral hygiene and high frequency topical application of fluoride through a variety of products including toothpaste, rinses, and varnishes.

“Progression” – If the caries process is not suppressed or the cavity not repaired, the hole will continue to expand in depth and width. As it deepens, it moves inexorably toward the dental pulp (nerve) causing increased pain frequency and severity. When the pulp is directly affected by the caries process it dies and subsequently becomes infected. This infection first occurs within the nerve chamber of the tooth and then spreads beyond the tooth’s root-end into the bone and soft tissues of the mouth and face. Unchecked, the infection can drain into the mouth (creating a parulis or fistula) or spread further into the neck, midface, and cranium. For this reason, draining abscesses and facial cellulites (infection of the cheek or other facial tissues) are common presenting signs of ECC. Numerous case reports of children presenting to the emergency room with facial cellulites “of unkown origin” turn out to be caused by dental infections.

Prevalence, acuity and consequence of Early Childhood Caries Despite it being easily preventable, ECC continues to be a public health issue. Dental caries affects approximately 1/5th of preschoolers, ½ of second graders (3, 36) 80% of tooth decay is concentrated in 25% of children (37). Low income children, who suffer the most from dental disease, have the least access to care. Dental disease, untreated, results in pain, infection, and may inhibit general growth and development (2).

Maria's reality

Low income pre-schoolers are about twice as likely to experience caries, twice as likely to experience dental pain, have more than twice the extent of dental disease, and are about twice as likely to have insurance coverage because of Mmedicaid, but are only ½ as likely to have a dental visit because of lack of access (CDHP 38)

To find out how Maria is treated and what the options are for managing her overall oral health, click on the link or picture below.

Continue to... Part III: Treatment