CURRENT Diagnosis and Treatment Pediatrics, (Current Pediatric Diagnosis & Treatment) 22nd Edition

17. Oral Medicine & Dentistry

Ulrich Klein, DMD, DDS, MS


Concept of the Dental Home

Analogous to the American Academy of Pediatrics’ (AAP) concept of a “medical home,” the American Academy of Pediatric Dentistry (AAPD) has promoted the concept of a “dental home.” A dental home is best established by referring a child for oral health examination to a dentist who provides care for infants and young children (ie, pediatric dentist) 6 months after the first tooth erupts or by 12 months of age. The primary goal of the dental home is to encourage good oral healthcare habits that will allow the child to grow up free from dental disease. In partnership with the caregivers, the pediatric dentist develops a comprehensive, personalized preventive healthcare program based on an accurate risk assessment for dental disease. The pediatric dentist provides education on age-appropriate oral hygiene techniques and a tooth-friendly diet. Other functions of the dental home include provision of anticipatory guidance on growth and development, provision of comprehensive routine and emergency dental care, and referral to other dental specialists as needed. The dental home has the benefit of promoting continuity of care in a family-centered and culturally appropriate environment, and is associated with fewer emergency visits and reduced treatment costs. A child is less likely to develop dental anxiety if a number of positive experiences precede a less pleasant appointment.

AAPD policies and guidelines: Accessed December 26, 2013.

American Academy of Pediatric Dentistry (AAPD): Policy on the dental home. Pediatr Dent 2013;35 (Reference Manual):24–25.

Perinatal Factors & Oral Health

The perinatal period offers a unique opportunity for oral health counseling from various healthcare providers aimed at women’s self-care as well as future child care. Mothers may be unaware of the consequences of their own poor oral health or that of their children. Cariogenic bacteria can be transmitted vertically from mother to child by licking a pacifier or sharing eating utensils or horizontally between siblings of similar age, from the father, and from children in day care centers. Colonization of the infant with mutans streptococci (MS) is more likely when maternal salivary MS levels are high. The mother’s oral hygiene, snacking habits, and socioeconomic status all have an influence on the infant’s colonization with MS. Anticipatory guidance and dental treatment of the expectant mother can significantly reduce the child’s risk of acquiring MS. Prenatal dental counseling should include education on the importance of regular dental visits and the role of fluoride in maternal and childhood oral health, counseling on appropriate maternal diet, and advice on reduction of MS colonization. Maternal MS levels and the risk of transmission to infants can be reduced by twice-daily rinsing with chlorhexidine digluconate 0.12% for 2 weeks followed by chewing 100% xylitol gum for 5 minutes 3–5 times/d (total dose of xylitol 6–10 g/d) for several weeks.

Delayed dental development is characteristic of preterm infants and is also seen in infants with global developmental delay. Postnatal environmental tobacco smoke exposure increases susceptibility to childhood caries, an association that is independent of age, family income, geographic region, and frequency of dental visits. It is important to advise expectant mothers about this risk. The risk of oral anomalies is higher in preterm and low-birth-weight infants than in full-term infants. These anomalies may include a narrow palate caused by traumatic laryngoscopy or prolonged endotracheal intubation, hypoplasia of the enamel of primary dentition, and crown dilaceration (an angulation, or a sharp bend or curve, in the root or crown of a formed tooth) of the permanent maxillary incisors. The role of palatal protection plates to prevent palatal “grooving” is not clear.

AAPD: Guideline on perinatal oral health care. Pediatr Dent 2013;35 (Reference Manual):131–136.

Infant Oral Health Care

Infant oral health care is the foundation on which preventive dental care is built. Ideally, this begins before caries develops so preventive measures can be implemented. The primary goals for an infant oral health program are: (1) to establish with parents the goals of oral health; (2) to inform parents of their role in reaching these goals; (3) to motivate parents to learn and practice good preventive dental care; and (4) to initiate a long-term dental care relationship with parents. These goals can be achieved through oral examination of the child, risk assessment for oral disease, anticipatory parental guidance, and regular dental health supervision. This approach advances dental care beyond tooth monitoring toward true health promotion. Because pediatricians encounter new mothers and infants earlier than dentists, it is essential that they be aware of the infectious pathophysiology and risk factors for early childhood caries (ECC).

Pediatricians should incorporate oral health into anticipatory guidance by providing information on oral health in their offices and by referring children with special healthcare needs to a pediatric dentist as early as 6 months of age. Referral of healthy infants to establish a dental home should occur no later than 6 months after the first tooth erupts or 12 months of age (whichever comes first).

AAPD: Guideline on infant oral health care. Pediatr Dent 2013;35 (Reference Manual):131–141.

Caries-Risk Assessment

Caries-risk assessment estimates the likelihood of developing carious lesions based on biological and protective factors as well as clinical findings. By 6 months of age, every child should have a caries-risk assessment performed by a pediatric healthcare provider. The Caries Risk Assessment Form (Table 17–1) details risk indicators for the age group 0–3 years old that directly or indirectly influence development of dental caries. Caries management by risk assessment (CAMBRA) is another protocol for a comprehensive evaluation of the child and his/her family and integrates the many factors that contribute to the development of ECC into a practical and individualized strategy for caries control. Although the best predictor of future caries is the incidence of previous caries, this finding is not a practical preventative tool. Additional risk factors include the level of parental education and age of colonization with MS and lactobacilli. The earlier the colonization occurs, the greater the risk of severe decay.

Table 17–1. Caries-risk assessment for 0–3-year-olds.


The ultimate purpose of this assessment is to develop a caries management protocol. Based on a child’s risk category and extent of parental engagement, interventions include diagnostics (regular recalls and determination of MS levels in saliva), optimization of the protective factors listed above, dietary counseling, and restorative measures as needed.

AAPD: Guideline on caries-risk assessment and management for infants, children, and adolescents. Pediatr Dent 2013;35 (Reference Manual):123–130.

Ramos-Gomez FJ et al: Caries risk assessment appropriate for the age 1 visit (infants and toddlers). J Calif Dent Assoc 2007 Oct; 35:687–702 [PMID: 18044377].


Dental caries is the most common chronic disease of childhood and the most prevalent unmet health need of US children. Dental caries is largely a disease of poverty. Children and adolescents in low-income families account for 80% of patients with tooth decay.

image Pathogenesis

Development of caries requires the interaction of four factors: (1) a host (tooth in the oral environment); (2) a suitable dietary substrate (fermentable carbohydrates); (3) cariogenic microorganisms that adhere to the tooth; and (4) time, measured as the frequency of exposure to fermentable carbohydrates and the duration of acid exposure. The main organisms implicated in the initiation of caries are Streptococcus mutans (MS) and Streptococcus sobrinusLactobacillus acidophilus and Lactobacillus casei are linked to the progression of caries. MS organisms are most commonly passed vertically from mother to child. A “window of infectivity” between ages 19 and 33 months has been described, but colonization can occur as early as 3 months of age. Earlier colonization increases the risk of caries. Dental plaque is an adherent biofilm on the tooth surface that harbors acidogenic bacteria in close proximity to the enamel. As bacteria metabolize sucrose, they produce lactic acid that solubilizes calcium phosphate in tooth enamel and dentin. Demineralization of the dental enamel occurs below pH 5.5 and is the first step in cariogenesis. The flow rate of saliva and its buffering capacity are important modifiers of demineralization. Demineralization of enamel and dentin can be halted or even reversed by redeposition of calcium, phosphate, and fluoride from saliva. If not halted, the carious process penetrates the enamel, advancing through the dentin toward the pulp of the tooth. In response, blood vessels in the pulp dilate and inflammatory cells begin to infiltrate (pulpitis). If the carious lesion is untreated, pulp exposure will occur, triggering invasion of more inflammatory cells and the eventual formation of a small pulp abscess. If this abscess can drain into the oral cavity, the apical tooth tissue may remain vital. However, if the radical pulp becomes necrotic, a periapical abscess develops (Figure 17–1). Although this process may be asymptomatic, it usually causes severe pain, fever, and swelling.


image Figure 17–1. Tooth anatomy and progression of caries.

image Clinical Findings & Treatment

The diagnosis of caries is usually made by visual and tactile oral examination. Radiographs are used to visualize caries on the surfaces between teeth. The initial defect observed on enamel beneath the dental plaque is the so-called “white-spot lesion,” a white, chalky, decalcified area along the gingival margin or on approximated tooth surfaces. Frank carious lesions are light- to dark-brown spots or cavities of varying size on the tooth. A light shade of brown indicates more rampant decay. Arrested caries are almost black in color. In the early stages of decay, the tooth may be sensitive to temperature changes or sweets. Removing the carious tooth structure and filling the early defect with a restorative material can repair the tooth. As decay progresses deeper into the pulp, inflammation and pain increase. Eventually, the entire pulp becomes necrotic, and a choice must be made between root canal therapy (pulpectomy) or removal of the tooth. In the presence of cellulitis or facial space abscess, extraction and antibiotic therapy are the treatments of choice.

Cavitation is the late phase of disease. Filling cavities does not address the underlying pathologic process responsible for tooth decay. Unlike other infections, dental caries cannot be treated by a course of antibiotics. However, a daily dose of chlorhexidine gluconate rinse 0.12% for 2 weeks can significantly reduce the number of cariogenic bacteria in the mouth and delay recolonization for 3–6 weeks. Such treatment is recommended at 3-month intervals for patients with high levels of bacteria. Improvement in risk of dental caries can only be achieved by a sustained reduction in the number of cariogenic oral bacteria and by the creation of a favorable oral environment. Additionally, all active cavities must be restored to eliminate sources of reinfection. A patient and his/her family must be encouraged to change diet and habits of oral hygiene in an effort to prevent further infection. Motivational interviewing has been shown to be more successful in setting these self-management goals than simple or stern recommendations. Regular dental visits, the periodicity of which should be determined by the risk level for developing carious lesions, must be maintained to monitor and reinforce these goals. The concept of prevention through timely and regular parent education, early diagnosis, and prompt intervention offers greater efficiency, better health outcomes, and lower costs than repeated restoration of diseased teeth.

image Caries Prevention

Prevention of dental caries necessitates restoring the delicate balance between pathologic and protective factors. Pathologic factors include cariogenic bacteria and fermentable carbohydrates. Protective factors include salivary flow, and fluoride in food, beverages, drinking water, and oral care products. Saliva provides calcium, phosphate, proteins, antibacterial substances, and buffers to neutralize acid produced by bacteria in plaque.

A. Changes in Lifestyle

Oral hygiene practices should start soon after birth. The infant’s gums should be cleaned daily using a moist, soft cloth. Once the teeth erupt, oral hygiene must be practiced in earnest, particularly in children assessed as high risk. A small amount of fluoridated toothpaste (“smear layer”) should be used on a small, soft toothbrush designed for infants. Because of a lack of manual dexterity in children younger than 8 years of age, parents need to brush for them twice daily and assist with flossing. Another important parental task is reducing the amount of substrate available to the bacteria by limiting the consumption of sugar-containing infant formulas, beverages, and snacks. Each such exposure produces an acidic oral environment for up to 30 minutes. The primary care physician and his/her team play an invaluable role in disseminating this information during early well-baby visits.

B. Fluorides

Fluorides are safe and effective in caries prevention through three topical mechanisms of action: inhibition of bacterial metabolism by interfering with enzyme activity; inhibition of demineralization; and enhancing remineralization. Fluoride can be applied professionally or by the patient under parental supervision. Although more than half the US population has access to fluoridated community water, an increasing number of families consume processed water with unknown fluoride content. Fluorides affect the dentin and enamel of both erupted and unerupted teeth. Systemic effects are achieved by oral ingestion from sources such as fluoridated drinking water or fluoride supplements. Fluoridated toothpaste and mouth rinses deliver topical benefits. Table 17–2 shows the current ADA recommendations for dietary fluoride supplementation for children at high caries risk. They should be taken daily to maximize the caries risk prevention benefit. For children at low caries risk, dietary fluoride supplements are not recommended. The child’s true exposure to fluoride must be evaluated before supplements are prescribed to avoid the mottled enamel (dental fluorosis) produced by excessive fluoride. Because children younger than 6 years of age cannot expectorate reliably, parents must monitor the use of fluoridated toothpaste, ensuring that only a “pea-sized” amount of the product is used at each brushing. Several factors are associated with a high risk for caries—orthodontic appliances, decreased salivary function, gastroesophageal reflux disease, cariogenic diet, physical inability to properly clean the teeth, mother or siblings with caries, personal history of caries. Children with these risk factors should be considered for additional topical fluoride therapy to supplement oral hygiene measures.

Table 17–2. Dietary fluoride supplementation schedule for children at high caries risk.


Infants who consume concentrate infant formulas as the main source of nutrition may incur an increased risk for enamel fluorosis in the permanent dentition if those formulas are reconstituted with optimally fluoridated drinking water. It is important that practitioners evaluate all sources of fluoride intake when advising parents about the use of fluoridated toothpastes or prescribing fluoride supplements.

Berg J et al: Evidence-based clinical recommendations regarding fluoride intake from reconstituted infant formula and enamel fluorosis: a report of the American Dental Association Council on Scientific Affairs. J Am Dent Assoc 2011 Jan;142(1):79–87 [PMID: 21243832].

C. Other Adjunctive Measures

Consumption of beverages sweetened with artificial sweeteners instead of sugar can help reduce the intake of fermentable carbohydrates. While chewing gum helps to clean food debris from teeth and increases salivary flow, these beneficial effects are lost when sugar-containing gum is used. The AAP considers chewing gum a choking risk in smaller children. A significant reduction of salivary MS by the polyol sweetener xylitol has been described, but a dose of at least 5–10 g/d for adults and 5–7.5 g/d for toddlers aged 6–36 months with exposure times lasting several minutes three times daily are required to produce this effect. Topical application of 8 g/d xylitol syrup in 9–15-month-old children twice per day for 12 months during primary tooth eruption could prevent up to 70% of dental caries. However, unclear labeling of the ingredients in xylitol-containing products makes the exact determination of the dose difficult and the high cost of foods containing xylitol limits its widespread use.

AAPD: Policy on the use of Xylitol in caries prevention. Pediatr Dent 2013;35 (Reference Manual):45–47.

Featherstone JD: The science and practice of caries prevention. J Am Dent Assoc 2000 Jul;131(7):887–899 [PMID: 10916327].

Early Childhood Caries

Formerly termed “baby bottle tooth decay” or “nursing bottle caries,” early childhood caries (ECC) is a particularly virulent and rapidly progressive form of caries that begins on the smooth surfaces of the teeth soon after eruption. Lack of adequate preventive care as well as poor feeding habits, such as the frequent consumption of liquids containing fermentable carbohydrates from a nursing bottle, frequent sipping from a no-spill sippy cup, taking a bottle to bed, and breast-feeding in combination with other carbohydrates, place children at high risk for ECC. It is uncertain whether ad libitum breast-feeding increases the risk for developing caries. ECC typically involves the maxillary incisors but any other teeth may be affected.

ECC is defined as one or more decayed (d), missing (m), or filled (f) tooth surfaces (s) in any primary tooth in a child younger than 71 months of age. Any sign of smooth-surface caries in a child younger than 3 years is termed severe ECC (S-ECC). From 3 to 5 years, one or more decayed, missing, or filled smooth surfaces in maxillary front teeth or a total dmfs score of 4 or higher must be present to make a diagnosis of S-ECC. By age 5 years, a dmfs score of 6 or higher must be present to constitute S-ECC. Children with S-ECC are at higher risk for new carious lesions, more frequent hospitalizations, and emergency department visits. They are absent more often from school, may have below-normal height and weight gain, and have a diminished oral health-related quality of life. Although S-ECC can affect all children, it is 32 times more likely in children who consume sugary foods and whose mothers are of low socioeconomic status and education level.

Parents should be counseled to eliminate saliva-sharing activities and not to put infants to sleep with a bottle containing fermentable carbohydrates. After eruption of the first tooth, ad libitum breast-feeding should be discontinued and regular oral hygiene measures such as twice-daily use of fluoridated toothpaste, both in optimally fluoridated and fluoride-deficient communities, should be implemented. Infants should be weaned from the bottle at about 1 year of age and encouraged to drink from a uncovered cup mainly as part of a snack or meal. Frequent consumption of cariogenic liquids from a bottle or no-spill training cup should be avoided. The AAP recommends limiting juice to 4–6 oz/day for children 1–6 years of age.

Preventive strategies focused on the pregnant woman should start in the prenatal and perinatal periods. Maternal malnutrition during the third trimester, low birth weight, and systemic illness in the neonatal period can lead to tooth hypoplasia, which makes teeth more susceptible to caries. Later, motivational interviewing may help parents to reduce deleterious feeding habits and to adopt lifestyle changes within their family that address the multifactorial etiologies of early childhood caries.

AAPD: Policy on Early Childhood Caries (ECC): classifications, consequences, and preventive strategies. Pediatr Dent 2013;35 (Reference Manual):50–52.

AAPD: Policy on early childhood caries (ECC): unique challenges and treatment options. Pediatr Dent 2013;35 (Reference Manual):53–55.

Salone LR, Vann WF Jr, Dee DL: Breastfeeding: an overview of oral and general health benefits. J Am Dent Assoc 2013 Feb; 144(2):143–151 [PMID: 23372130].

Preventive Dental Treatment (Fluoride Varnish) by Physicians for High-Risk Populations

Since parents are more likely to take their very young child to a physician for well-child visits than to a dentist for oral health counseling, some states have established formal programs to entice medical offices to provide preventive dental services. These include dental screening, risk assessment, and referrals to dentists as needed, parent counseling about their child’s oral health, and applications of fluoride varnish (ICD-9-CM Diagnosis Code V07.31: Need for Prophylactic Fluoride Administration). The latter consists of a resin base in which fluoride (5% NaF) is suspended. Its sticky nature allows for extended contact time of the fluoride with the tooth surface. Many studies have demonstrated the safety and efficacy of fluoride varnishes and have described a significant reduction in the decay rate of smooth surfaces as well as pits and fissures. A report from a medical office-based preventive dental program in North Carolina found that it was successful in reducing caries-related treatments for children up to 6 years of age by 17%. Multiple fluoride varnish applications at the time of tooth emergence seemed to be most beneficial.

The varnish in single-dose packages (0.3–0.5 mL) should be stirred vigorously before application and the contents of larger tubes (5 mL) massaged to redissolve any precipitated fluoride. The former are preferable because consistent availability of fluoride cannot be guaranteed with multidose packages. The average amount of varnish needed depends on the number of teeth present and ranges from 0.1 mL for infants to 0.3 mL for preschool children. Teeth should be dried with gauze before application of the varnish with a small brush. It will set quickly to a dull yellow film upon contact with saliva. Caregivers should be instructed not to brush or floss and to give their child only soft foods until the next morning in order to provide the fluoride enough time for absorption into enamel.

Miller EK, Vann WF Jr: The use of fluoride varnish in children: a critical review with treatment recommendations. J Clin Pediatr Dent 2008;32(4):259–264 [PMID: 18767454].

Pahel BT, Rozier RG, Stearns SC, Quiñonez RB: Effectiveness of preventive dental treatments by physicians for young Medicaid enrollees. Pediatrics 2011 Mar;127:e682–e689 [PMID: 21357343].


The sagittal and vertical maxillomandibular relationships are different at birth. An anterior open bite is considered physiologic before the onset of tooth eruption. The infant’s mouth is more triangularly shaped and its oral cavity is small and totally filled by the tongue due to a small and slightly retrognathic lower jaw. This newborn’s pseudo micrognathia is due to ventral positioning of the fetus and will generally correct after birth by physiologic suckling.

Sucking Pads

Frequent breast-feeding can lead in some babies to formation of a lip callus (“sucking or suckling pad”) at the midline of the upper lip. Since it does not bother the mother or the child, it should not be removed. It will generally go away within the baby’s first year.

Within the cheek of newborns wedged between masseter and buccinator and related to the facial nerve and parotid duct there is a buccal fat pad that is completely enclosed within a distinctive capsule. These “suckling pads” are supposed to strengthen and support the cheek during the act of suckling.

The mouth of the normal newborn is lined with an intact, smooth, moist, shiny mucosa (Figure 17–2). The alveolar ridges are continuous and relatively smooth. Within the alveolar bone are numerous tooth buds, which at birth are mostly primary teeth.


image Figure 17–2. Normal anatomy of the newborn mouth.


Hard tissue formation of primary teeth begins at approximately 4 months’ gestation. At birth, all 20 primary teeth are calcified. The central maxillary incisors are almost completely calcified while only the cusp tips of the maxillary and mandibular second molars are calcified. There is a trace of enamel on the first four permanent molars at birth.

The primary teeth usually begin to erupt at around 7 months of age. On rare occasions (1:3000), natal teeth are present at birth or neonatal teeth erupt within the first month. These are most commonly (85%) mandibular primary incisors. They can be “real” primary teeth (90%) or supernumerary teeth (10%) and should be differentiated radiographically. Although the preferred approach is to leave the tooth in place, supernumerary and hypermobile immature primary teeth should be extracted. On occasion, such teeth must be smoothed or removed if their sharp incisal edge causes laceration of the tongue (Riga-Fede disease). If such teeth cause difficulties with breast-feeding, pumping and bottling the milk is initially recommended while the infant is conditioned not to “bite” during suckling.


Noticeable but small maxillary and mandibular labial frena should be present (Figure 17–3). The “persisting tectolabial frenum” that is observed in 25% of all children tends to diminish in size with normal development. Its physiological purpose is to provide greater support to the upper lip during breast-feeding. Several small accessory frena may also be present farther posteriorly. In rare cases, as in oral-facial-digital syndrome, there are multiple thick tightly bound frena. Decisions about surgical correction should be based on the ability to maintain the child’s gingival health and are best left until the late preteen years. Many thick frena do not require correction.


image Figure 17–3. The frena.

The tongue is connected to the floor of the mouth by the lingual frenum (Figures 17–3 and 17–4). This connection should not impede the free movement of the tongue. If the attachment is tight and high up on the alveolar ridge (Figure 17–5), it may restrict movement and interfere with the child’s ability to produce “t,” “d,” and “l” sounds. This condition is called ankyloglossia (tongue-tie). Surgical correction may be indicated if the tongue cannot touch the maxillary incisors or the roof of the mouth. Earlier intervention (at age 3–4 years) is better than later, but there is usually no urgency for surgery in the neonatal period unless the child has difficulty latching on properly to the mother’s nipple and causes her pain during nursing. Frenotomy can be carried out as early as at 10 days of age to provide, in most cases, real, immediate, and sustained improvement in breast-feeding.


image Figure 17–4. Normal position of lingual frenum.


image Figure 17–5. Ankyloglossia (tongue-tie) in a 6-wk old, before (A) and after (B) the release surgery.

Berry J, Griffiths M, Westcott C: A double-blind, randomized, controlled trial of tongue-tie division and its immediate effect on breastfeeding. Breastfeed Med 2012 Jun;7(3):189–193 [PMID: 21999476].

Cleft Lip & Palate

The palate of the newborn should be intact and continuous from the alveolar ridge anteriorly to the uvula (see Figure 17–2). Cleft lip and palate are common defects with an incidence of 0.28–3.74 in 1000 live births globally. Incidence varies widely among races and ranges from 1 in 500 among Navaho Native Americans and Japanese to more than 1 in 800 in Caucasians and 1 in 2000 in African Americans. The cleft of the palate can be unilateral or bilateral (Figure 17–6). It can involve only the alveolar ridge, or the ridge and entire palate. Cleft palate may also present as an isolated submucous cleft or as bifid uvula. Although clefts present superficially as a cosmetic problem, they cause complex functional problems such as oro-antral communication and disruption of the maxillary alveolar ridge with significant associated dental problems, such as irregularities in tooth numbers, delayed eruption, and malocclusion. They disturb the muscle arrangement of the perioral and the soft palate muscles by interrupting their continuity across the midline. As a result, feeding, swallowing, speech, and ventilation of the middle ear are negatively affected.


image Figure 17–6. Types of clefts.

Children with cleft lip and palate should be referred as soon as possible to a multidisciplinary cleft palate team for comprehensive assessment of their medical status, feeding problems, general development, dental development, hearing, facial esthetics, and overall functioning. The dental needs of children with cleft palate are extensive, and treatment may begin immediately after birth with fabrication of a palatal obturator as a feeding aid. Nasoalveolar molding should be performed to lengthen the columella and to guide the protruding greater segment (in unilateral clefts) or the premaxilla (in bilateral clefts) back into the oral cavity, thus making surgical lip closure easier when it is performed, usually after 10 weeks of age. Palate closure to approximate the muscles of the soft palate, which is intended to restore its proper function and to facilitate the acquisition of normal speech without nasality, follows at 12–18 months of age. The associated scar formation causes significant dentofacial growth disturbance. Orthodontic treatment aims to address the sagittal and transverse maxillary growth deficits as well as the frequent irregularities in tooth eruption and position. Between 8 and 10 years of age, an alveolar bone graft is indicated to add bony support to the central incisor adjacent to the cleft and to enable eruption of the lateral incisor and canine on the cleft side. In some patients, orthognathic surgery to reposition the maxilla anteriorly and mandible posteriorly is needed in late adolescence after cessation of growth to complete their successful rehabilitation.

Other Soft Tissue Variations

Minor oral soft tissue variations can occur in newborns. Small, 1–2 mm round, smooth, white, or grayish lesions are sometimes noted on the buccal and lingual aspects of the alveolar ridges or the midpalatine raphe. The latter, called Epstein pearls, are remnants of epithelial tissue trapped along the raphe during fetal growth. The former, Bohn nodules, are remnants of mucous gland tissue. Both are benign, require no treatment, and usually disappear a few weeks after birth.

Some newborns may have small intraoral lymphangiomas on the alveolar ridge or the floor of the mouth. A dentist familiar with neonates should evaluate these and any other soft tissue variations that are more noticeable or larger than those just described.


Normal Eruption

Primary teeth generally begin to erupt at about 7 months of age, but a gestational age of < 37 weeks or a birth weight < 2500 g increases the mean eruption times by 1 month. The mandibular incisors usually erupt before the maxillary incisors. The first teeth may appear as early as age 3–4 months or as late as age 12–16 months. Many symptoms are ascribed to teething, but any association with fever, upper respiratory infection, or systemic illness is probably coincidental rather than related to the eruption process. Attributing fever to teething without thorough diagnostic evaluation for other sources has resulted in missing serious organic disease.

Common treatment for teething pain is the application of topical anesthetics or teething gels that are available over the counter. Most contain benzocaine or, less commonly, lidocaine. If improperly used, they can cause numbness of the entire oral cavity and pharynx. Suppression of the gag reflex can be a serious side effect. Systemic analgesics such as acetaminophen or ibuprofen are safer and more effective. Chewing on a teething object can be beneficial, if only for distraction purposes.

Occasionally, swelling of the alveolar mucosa overlying an erupting tooth is seen during teething. This condition appears as localized red to purple, round, raised, smooth lesions that may be symptomatic but usually are not. Treatment is rarely needed, as these so-called eruption cysts or eruption hematomas resolve with tooth eruption.

Delayed Eruption

Premature loss of a primary tooth can either accelerate or delay eruption of the underlying secondary tooth. Typically, early eruption occurs when the permanent tooth is in its active eruption stage and the overlying primary tooth is removed within 6–9 months of its normal exfoliation. If loss of the primary tooth occurs more than 1 year before expected exfoliation, the permanent tooth will likely be delayed in eruption owing to healing, which results in filling in of bone and gingiva over the permanent tooth. The loss of a primary tooth may cause adjacent teeth to tip or drift into the space and lead to space loss for the underlying permanent tooth. Placement of a space maintainer can prevent this.

Other local factors delaying or preventing tooth eruption include supernumerary teeth, cysts, tumors, overretained primary teeth, ankylosed primary teeth, and impaction. A generalized delay in eruption may be associated with global developmental delays, endocrinopathies (hypothyroidism or hypopituitarism), or other systemic conditions (eg, cleidocranial dysplasia, rickets, or trisomy 21).

Ectopic Eruption

If the dental arch provides insufficient room, permanent teeth may erupt ectopically and cause a usually painless partial or complete root resorption in the adjacent primary tooth. This phenomenon is more common in the maxilla, with ectopic eruption of the maxillary first permanent molar being the most frequent. In the mandible, lower incisors may erupt lingually and thus the primary predecessor may be retained. Parental concern about a “double row of teeth” may be the reason for the child’s first dental visit. If the primary teeth are not loose, the dentist should remove them to allow their successors to drift into proper position.


Impaction occurs when a permanent tooth is prevented from erupting. Although crowding is the most frequent reason, an over-retained primary or supernumerary tooth is another cause. The teeth most often affected in the developing dentition are the maxillary canines. Generally, they are brought into correct alignment through surgical exposure and orthodontic treatment.

Variations in Tooth Number

Failure of teeth to develop—a condition called hypodontia—is rare in the primary dentition, but occurs with an incidence of 5:100 in the permanent dentition. The most frequently missing teeth are the third molars followed by the lateral maxillary incisors and mandibular second premolars. Oligodontia, a condition in which only a few teeth develop, occurs in patients with ectodermal dysplasias. Tooth agenesis is likely caused by several independent defective genes, which can act alone or in combination with other genes. It can occur in isolated cases, but often occurs in combination with cleft lip/cleft palate as part of the phenotype of over 200 syndromes.

Occasionally, supernumerary teeth are present, most typically in the maxillary incisor area, distal to the maxillary molars, or in the mandibular bicuspid region. Mesiodentes are peg-shaped supernumerary teeth situated at the maxillary midline that occur in about 5% of individuals. If they hinder eruption of adjacent permanent incisors, their timely removal is recommended.

Dean JA, Avery DR, McDonald RE: McDonald and Avery’s Dentistry for the Child and Adolescent, 9th ed. Maryland Heights, MO: Mosby Elsevier.


Periodontal disease involves a tooth’s supporting structures: bone, gingiva, and periodontal ligaments (Figure 17–7). It begins as inflammation of the gingival tissue adjacent to a tooth. Bacterial accumulation in the gingival sulcus causes irritation and inflammation. This initial phase, called dental plaque-induced disease, is found almost universally in children and adolescents. Systemic conditions, alterations in hormone levels (insulin, gonadotropin), certain medications, and malnutrition can intensify the inflammatory response to plaque. Generally, this condition responds well to removal of bacterial deposits and improved oral hygiene.


image Figure 17–7. Periodontal disease.

Periodontitis is characterized by loss of attachment and destruction of bone. Patients with localized aggressive periodontitis typically have severe alveolar bone loss around permanent first molars and incisors, whereas the generalized form involves other teeth as well. The prevalence is 0.2% in Caucasians, but higher (2.5%) in African Americans, and tends to run in families. Functional defects, such as defects in neutrophil chemotaxis, phagocytosis, and antibacterial activity increase the risk of periodontitis. Actinobacillus actinomycetemcomitans in combination with Bacteroides-like species are implicated in this disease. Treatment consists of combined surgical and nonsurgical root debridement plus antibiotic therapy.

Periodontitis as a manifestation of systemic disease can be associated with hematological (acquired neutropenia, leukemias) or genetic disorders, such as Down-, Papillon–Lefèvre-, Chediak–Higashi-, hypophosphatasia-, and leukocyte adhesion deficiency syndromes. The incidence of necrotizing periodontal diseases is lower (1%) in North America than in developing countries (2%–5%). Necrotizing periodontal disease is characterized by interproximal ulceration and necrosis of the dental papillae, rapid onset of dental pain, and often fever. Predisposing factors include viral infections (including human immunodeficiency virus [HIV]), malnutrition, emotional stress, and systemic disease. The condition usually responds rapidly to treatment consisting of mechanical debridement with ultrasonic scalers, improved oral hygiene, and metronidazole and penicillin for febrile patients.

AAPD: Endorsement; periodontal diseases of children and adolescents. Pediatr Dent 2013;35 (Reference Manual):338–345.


Orofacial Trauma

Orofacial trauma most often consists only of abrasions or lacerations of the lips, gingiva, tongue, or oral mucosa (including the frena), without damage to the teeth. Lacerations should be cleansed, inspected for foreign bodies, and sutured if necessary. Occasionally, radiographs of the tongue, lips, or cheeks are needed to detect tooth fragments or other foreign bodies. All patients with facial trauma should be evaluated for jaw fractures. Blows to the chin are among the most common childhood orofacial traumas. They are also a leading cause of condylar fracture in the pediatric population. Condylar fracture should be suspected if pain or deviation occurs when the jaw is opened.

Tooth-related trauma affects any or all of the dental hard tissues and the pulp, the alveolar process, and the periodontal tissues. The range of luxation injuries includes concussion; subluxation; intrusive, extrusive, and lateral luxation; and avulsion. Figure 17–8 demonstrates the different luxation injuries, and Figure 17–9 shows the different degrees of tooth fractures.


image Figure 17–8. Patterns of luxation injuries.


image Figure 17–9. Patterns of crown fractures.

The least problematic luxation injuries are concussion (no mobility) and subluxation (mobility without displacement). Unless mobility is extensive, this condition can be followed without active intervention, but pulp vitality should be periodically assessed.

Primary Teeth

The peak age for injuries to primary teeth is toddlerhood. Any treatment must include measures to ensure the integrity of the permanent teeth. Parents should be advised of any permanent tooth complications such as enamel hypocalcification or crown-root dilaceration caused by intrusion injuries of primary maxillary front teeth. An intrusive luxation is usually observed for a period of time to discern whether the tooth will spontaneously reerupt (see Figure 17–8). Severe luxations in any direction are treated with extraction. Avulsed primary teeth are not replanted. In a root fracture, the crown and apical fragment are generally extracted. The latter should be left for physiologic resorption if its retrieval would result in potential damage to the permanent tooth.

Permanent Teeth

Because the prognosis for viability worsens rapidly as time outside the mouth increases, an avulsed permanent tooth should be replanted into its socket, ideally as soon as possible at or near the accident scene following gentle rinsing with clean water. The patient should seek emergency dental care immediately thereafter. Hank’s balanced salt solution is the best storage and transport medium for avulsed teeth that are to be replanted at a distant emergency clinic. The next best storage media in decreasing order are milk, saline, saliva (buccal vestibule), or water. The commercially available FDA-approved Save-a-Tooth kit should be part of first-aid kits in schools and sports facilities.

Intrusions of permanent teeth are corrected with surgical or orthodontic repositioning. Lateral and extrusive luxations are generally repositioned and splinted for up to 3 weeks. Root canal treatment is necessary in the majority of injuries. Factors to consider during treatment planning are root development (open or closed apex) and the extent of the luxation. Pulp necrosis; surface, inflammatory, and replacement resorption; or ankylosis may occur at any time during the healing process and determine the long-term outcome. All luxated and replanted teeth need to be followed regularly by a dentist.

Save-a-Tooth® Emergency Tooth Preserving System: Accessed March 2013.

The Dental Trauma Guide—Your Interactive Tool to Evidence-based Trauma Treatment: Accessed March 2013.

Other Dental Emergencies

Dental emergencies other than trauma are usually associated with pain or swelling due to infection resulting from advanced caries. Odontogenic pain usually responds to acetaminophen or ibuprofen. Topical medications are of limited value.

A localized small swelling confined to the gingival tissue associated with a tooth is usually not an urgent situation. This “gumboil” or parulis represents an infection that has spread outward from the root of the tooth through the bone and periosteum. Usually it will drain and leave a fistulous tract. Facial cellulitis results if the infection invades the facial spaces. Elevated temperature (> 38.8°C), difficulty swallowing, and difficulty breathing are signs of more serious infection. Swelling of the midface—especially the bridge of the nose and the lower eyelid—should be urgently evaluated as a potential dental infection. Depending on the clinical situation and the patient’s overall health, treatment choices range from treating or extracting the offending tooth/teeth with or without antibiotic coverage to achieve drainage. Occasionally, treatment is delayed for several days while antibiotics are prescribed to contain the spread of the infection. Hospitalization is a prudent choice for younger children with severe facial cellulitis especially if other risk factors are present—dehydration, airway compromise, or possible noncompliance. Inpatient treatment consists of intravenous antibiotics such as clindamycin or ampicillin-sulbactam (Unasyn) with incision, drainage, and removal of the source of infection.


The antibiotics of choice for odontogenic infection are penicillin and clindamycin. The need for antibiotics—usually a 5- to 7-day course—depends on the severity of the infection and the patient’s medical status.

Patients with certain medical conditions are at risk for bacteremia-induced infections and require prophylactic antibiotic coverage prior to invasive dental manipulation. These include children with artificial heart valves, previous infectious endocarditis, certain repaired or nonrepaired congenital heart conditions, or compromised immunity. For nonvalvular devices such as indwelling vascular catheters and cardiovascular implantable electronic devices, antibiotic coverage is indicated only at the time they are placed. Hydrocephalus shunts with vascular access (eg, ventriculoatrial, ventriculocardiac, ventriculovenous) may cause bacteremia-induced infections and therefore require antibiotic prophylaxis, whereas the nonvascular type (ventriculoperitoneal) does not.

Antibiotic prophylaxis is generally not indicated for dental patients with pins, plates, screws, or other orthopedic hardware that is not within a synovial joint. Likewise, most patients with total joint replacements do not routinely require antibiotic prophylaxis, but for them, as well as for the management of patients at high risk and those with Harrington rods or external fixation devices, consultation with the child’s physician is advised. Special consideration is also warranted when higher risk dental procedures are performed within 24 months of implant surgery, on immunocompromised patients with total joint arthroplasty, or those who have had previous joint infections.

AAPD: Guideline on antibiotic prophylaxis for dental patients at risk for infection. Pediatr Dent 2013;35 (Reference Manual): 276–278.

Wilson W et al: Prevention of infective endocarditis: guidelines from the American Heart Association. J Am Dent Assoc 2008 Jan;139(Suppl):S3–S24 [PMID: 18167394].


Children With Cancer

The most common source of systemic sepsis in the immunosuppressed patient with cancer is the oral cavity. Therefore, a dentist knowledgeable about pediatric oncology should evaluate children with cancer soon after diagnosis. The aim is to educate the patient and caregivers about the importance of good oral hygiene and to remove all existing and potential sources of infection, such as abscessed teeth, extensive caries, teeth that will soon exfoliate, ragged or broken teeth, uneven fillings, and orthodontic appliances, before the child becomes neutropenic as a consequence of chemotherapy. Younger patients have more oral problems than adults. After an initial evaluation and before the initiation of cancer therapy, a dental treatment plan should be developed in discussion with the medical team. Preventive strategies include reduction of refined sugars, fluoride therapy, lip care, and patient education. Chemotherapeutic drugs and local irradiation are cytotoxic to the oral mucosa, which becomes atrophic and develops mucositis. Oral pain may be severe and often leads to inadequate food and fluid intake, infections in the oral cavity, and an increased risk of septicemia. Meticulous oral hygiene reduces the risk of severe mucositis.

The pediatric oncology patient should be monitored throughout therapy to screen for infection, manage oral bleeding, and control oral pain. These patients can experience spontaneous oral hemorrhage, especially when the platelet count is less than 20,000/μL. Poor oral hygiene or areas of irritation can increase the chances of bleeding. Children receiving radiation therapy to the head and neck may develop xerostomia if salivary glands are in the path of the beam of radiation. Customized fluoride applicators and artificial saliva in combination with close follow-up are used to manage xerostomia aggressively to avoid rapid and extensive destruction of the teeth. Children receiving hematopoietic stem cell transplantation may require longer periods of immunosuppression. During the neutropenic phase of pretransplant conditioning, mucositis, xerostomia, oral pain, oral bleeding, and opportunistic infections may occur. Oral graft-versus-host disease as well as oral fungal and herpes simplex virus infections can be seen during the subsequent initial engraftment and hematopoietic reconstitution period. Long-term dental follow-up includes management of salivary dysfunction and craniofacial growth abnormalities from total body radiation and treatment of oral graft-versus-host disease.

Pediatric oncology patients need regular care by a dentist familiar with young children and their growth and development. Oral and maxillofacial growth disturbances can occur after therapy. Late effects of therapy include such morphologic changes as microdontia, hypocalcification, short and blunted roots, delayed eruption, and alterations in facial bone growth.

da Fonseca MA: Dental care of the pediatric cancer patient. Pediatr Dent 2004;26:53–57 [PMID: 15080359].

Children With Bleeding Disorders

Children with some genetic or acquired disorders of coagulation may require clotting factors before and after invasive dental procedures, including local block anesthesia. Oral surgical procedures on any child with a bleeding disorder should be planned in concert with the child’s hematologist. Patients with hemophilia A and factor VIII antibodies (inhibitors) requiring surgery should be admitted to a hospital. Some patients with very mild factor VIII deficiency or von Willebrand disease type 1 may respond to DDAVP (1-deamino-8-D-arginine vasopressin), whereas von Willebrand types 2 and 3 require cryoprecipitate. Antifibrinolytic medications such as ε-aminocaproic and tranexamic acid are used successfully after dental treatment. Topical medications such as Gelfoam and thrombin can be used to control postoperative bleeding. Patients receiving anticoagulant therapy should generally not undergo dosage reduction before surgical dental treatment because the risk of embolic complications is much higher than bleeding complications in those whose anticoagulant therapy is continued. However, the dentist is advised to consult with the hematologist to obtain the most recent INR (international normalized ratio) results and to discuss the most appropriate level of anticoagulation.

Children With Type 1 Diabetes

The incidence of caries is not increased in diabetic children if metabolic control is good. However, they are at higher risk for periodontal disease that usually starts at puberty with mild gingivitis, gum bleeding, and gingival recession. Care must be taken not to disturb the regular cycle of eating and insulin dosage. Anxiety associated with dental appointments can cause a major upset in glycemic control. Postoperative pain or pain from dental abscess can disrupt their routine oral intake, necessitating adjustment of insulin doses.


A child’s dentist usually initiates the referral to an orthodontist. For any child with a cleft palate or other craniofacial growth disorder, referral is indicated when maxillary permanent incisors are starting to erupt. Other localized problems such as anterior and/or posterior crossbites and disturbances associated with the eruption of maxillary and mandibular front teeth should be addressed early to restore proper function and normal craniofacial growth. Significant arch length deficiency that results in severe crowding requires early decisions on how to guide the developing dentition through extractions of multiple primary and permanent teeth (ie, serial extraction sequence). Likewise, pronounced discrepancies in anterior-posterior skeletal jaw relationships warrant early evaluation by an orthodontist.