CHAPTER 31

Oral Health and Dental Disorders

Charlotte W. Lewis, MD, MPH, FAAP

Healthy teeth allow us to consume a variety of foods, from which we obtain essential nutrients. Although physicians receive limited training about teeth, given the common nature of dental problems in children it is important that pediatricians and other pediatric primary care physicians understand and can not only recognize normal and abnormal dental conditions but can implement primary and secondary prevention of dental caries and dental injuries in their practice. Well-child care visits begin in the neonatal period and continue through the end of adolescence, and at every visit opportunities exist to promote oral health and examine oral structures for timely identification of dental problems. Infancy and early childhood are critical times for the establishment of habits, both good and bad, that have the potential to affect lifelong oral health.

Epidemiology

Both dental trauma and dental caries are common in childhood. Approximately one-third of toddlers and preschool-age children and 20% of teenagers experience dental trauma—in young children typically as the result of a fall and in older children most often the result of contact sports. Occlusal abnormalities are also common in children. At least 30% of children are estimated to have moderate to severe orthodontic needs.

Dental caries is the most common chronic disease of childhood. Even so, dental decay disproportionately affects low-income individuals, resulting in earlier onset of caries, more teeth affected, more caries-related complications, and ultimately more tooth loss during adulthood because of caries. Population-based data collected from 2011 through 2014 indicate that 36% of children age 2 through 8 years in the United States had experienced caries in their primary dentition, and 57% of US children age 12 through 19 years had experienced caries in their permanent dentition. Poverty is the most important risk factor for caries, and it also affects access to professional dental care. In 2015 to 2016, the prevalence of dental caries in children age 2 through 19 years in the United States increased as family income decreased (Figure 31.1). Among youth from families living below the federal poverty level, 56.3% had any caries, compared with 34.8% for youth from families with income levels greater than 300% of the federal poverty level. Likewise, the prevalence of untreated dental caries affected 18.6% of youth from families living below the federal poverty level, compared with 7.0% of youth from families with incomes greater than 300% of the federal poverty level.

Alaska Native/American Indian (AI/AN) children have a markedly higher prevalence of caries relative to other populations in the United States. In 2014, 76% of AI/AN children age 2 to 5 years had experienced at least 1 instance of dental caries, with 47% of all AI/AN children in this age group having untreated caries. In contrast, during 2011 to 2014, 24% of all US children between 2 and 5 years of age experienced caries and approximately 11% of children in this age group had untreated caries.

Toothache, a complication of dental caries, afflicts millions of US children. In 2007, 14% of 6- to 12-year-olds had experienced a toothache within the previous 6 months. Toothache disproportionately affects children who are poor or of minority status, or who have special health care needs.

Figure 31.1. Percentage of US children, 2 to 19 years of age, with any caries and untreated caries by family income relative to Federal Poverty Guideline (FPG), 2015–2016.

Adapted from Fleming E, Afful J. Prevalence of total and untreated dental caries among youth: United States, 2015-2016. NCHS Data Brief. 2018;(307):1–8.

Clinical Presentation

Dental development begins in utero. Subsequently, the teeth erupt into the lower (ie, mandibular) portion of the jaw and into the upper (ie, maxillary) jaw. Teeth have a crown and root section (Figure 31.2). The crown is the visible portion of the tooth. The root is that part contained within the socket of the alveolar bone. The outer hard coating of the crown is the enamel. Beneath the enamel is the dentin, which is composed of microtubules for transport of nutrients from the pulp to the outer portions of the tooth. The pulp contains nerves and vascular structures critical for the health and viability of the tooth. Teeth are anchored to the jaw by periodontal ligaments.

Humans have 20 primary or deciduous teeth, which erupt sequentially between approximately 6 and 34 months of age (Figure 31.3A). The first primary teeth to erupt typically are the lower central incisors. These teeth erupt on average at approximately 8 months of age (±1 standard deviation: 6–10 months), after which approximately 1 tooth erupts per month until all primary teeth have erupted, by approximately 24 to 34 months of age. In each quadrant of the mouth, the normal pattern of primary tooth eruption is that the incisors erupt first, after which the first molars, the canines (ie, cuspids), and finally the second molars erupt (Table 31.1). There is variation in the timing of tooth eruption, and normal tooth eruption can vary by 6 months or more from the average age. Occasionally, the eruption process may be preceded by a bluish discoloration to the gum, called an eruption hematoma, which is a benign process. More often, eruption of the primary teeth is associated with more generalized symptoms, such as fussiness and drooling. These symptoms are commonly referred to as teething. Teething does not cause diarrhea, respiratory infections, or true fever, although these conditions may be present coincidentally with tooth eruption in infants.

diarrhea, respiratory infections, or true fever, although these conditions may be present coincidentally with tooth eruption in infants.

Figure 31.2. Tooth anatomy.

Figure 31.3. A, Primary dentition. B, Permanent dentition.

^a Upper: Maxillary.

^b Lower: Mandibular.

The primary teeth are replaced by the permanent teeth (Figure 31.3B), which begin erupting at approximately 6 years of age. Permanent and primary teeth are present during the mixed dentition phase, which occurs between 6 and 13 years of age (Table 31.2). During early mixed dentition, the permanent dentition looks large and awkward relative to the remaining primary teeth, and transient malpositioning of the teeth may occur. Normally, the adult mouth has 32 permanent teeth; the last teeth to erupt are the third molars, commonly referred to as “wisdom teeth,” which emerge at approximately 17 to 21 years of age.

Variations from normal in number of teeth are not uncommon. Hypodontia refers to the presence of fewer than normal teeth. The most common teeth to be congenitally absent are the third molars, second premolars, and maxillary lateral incisors. Congenital absence of a central incisor is distinctly uncommon and should raise concern for the presence of other midline defects. Several teeth may be missing in disorders such as Down syndrome or ectodermal dysplasia. Anodontia is the congenital absence of teeth. Extra teeth are called supernumerary teeth. Children may be born with teeth already erupted, known as natal teeth. Teeth that erupt shortly after birth are referred to as neonatal teeth if their eruption occurs in the first month after birth. These teeth are usually incisors, and at least 90% represent normal dentition rather than supernumerary teeth. The presence of natal or neonatal teeth may be familial and, rarely, may be suggestive of an underlying syndrome. In addition to variations in number, teeth may also demonstrate variations in color and structure resulting from abnormalities in tooth development, trauma, or extrinsic factors.

^a Upper: Maxillary.

^b Lower: Mandibular.

The relationship of the maxillary to the mandibular dentition has functional and aesthetic implications. Malocclusion is an abnormal relationship between the upper and lower teeth and may be developmental, genetic, or environmental in etiology. Children with craniofacial disorders often have significant occlusal problems and facial asymmetries necessitating early referral for care by a craniofacial team. Other children may have milder malocclusion requiring orthodontic care. Normal occlusion, or class I occlusion, occurs when the maxillary incisors are slightly in front of the mandibular incisors and the posterior molars interdigitate (Figure 31.4). Class II occlusion occurs when the maxillary teeth project too far anteriorly from the mandibular teeth. This may be associated with an overjet, commonly known as “buck teeth,” which can predispose to dental injury when children fall. Class III occlusion, or under-bite, occurs when the mandibular teeth are anterior to the maxillary teeth. Other common forms of malocclusion include an anterior open bite, whereby the posterior teeth come together but an opening exists between the top and bottom anterior teeth, and a crossbite, which occurs when some of the upper molars are located inside the lower molars during occlusion.

Dental injuries can be classified into tooth concussion, subluxation, luxation, avulsion, and fracture. A concussed tooth follows a blow that leaves the tooth tender but not displaced or mobile. Subluxation is loosening of a tooth after injury without displacement. With luxation, or displacement of the tooth from its normal position, the tooth is dislodged from its usual location; the tooth may not be mobile at all if it has been forced into adjacent bone. Luxation injuries usually result in damage to the periodontal ligament, threatening the future viability of the tooth. Intrusion is a form of luxation; it occurs when a tooth is driven into the bone, fracturing the alveolar socket. An intruded tooth may not be visible at all; alternatively, only the very distal aspect of the crown may emerge from the gingiva. Complete loss of the tooth from the socket is referred to as an avulsion.

Figure 31.4. Classes of occlusion. Class I is considered most desirable from a functional and aesthetic perspective.

Dental fractures may affect the tooth crown, tooth root, and/or the alveolar bone. Fracture of the crown with no loss of tooth structure— that is, a crack exists in the tooth but no piece of tooth has broken off—is a dental infraction. Usually, these are initially asymptomatic. Dental follow up is needed for an infraction because the crack may allow passage of bacteria into the pulp, which can result in pulpal necrosis. Fractures involving the tooth crown, with loss of tooth structure, are classified depending on the site of the fracture. Fractures through the enamel (Ellis class I) or dentin (Ellis class II) are considered uncomplicated dental fractures. Fractures that involve the pulp (Ellis class 3), the root, or the alveolar bone are classified as complicated dental fractures.

Caries may occur any time after eruption of the teeth. Early childhood caries (ECC), a more general term referring to what in the past was called “baby bottle tooth decay” or “nursing bottle caries,” disproportionately affects children of low socioeconomic status. The pattern of decay seen in ECC is different from that seen in the teeth of older children and adults. Typically, ECC first affects the maxillary incisors and spares the lower incisors. This pattern of decay is hypothesized to result from prolonged and frequent exposure of the teeth to sweet liquids, such as falling asleep with a juice bottle in the mouth, whereby the beverage pools around the upper incisors but the lower teeth are protected by the overlying tongue. In its earliest stages, ECC appears on physical examination as white, chalky, opaque areas at the gum line (ie, white spot lesions). At this early stage, the lesion is potentially reversible if remineralization can occur, such as by applying fluoride varnish to the white spots.

In older children, the pit and fissure surfaces of the molars are the likely sites of dental decay. Fermentable carbohydrates, particularly those of a sticky nature, become embedded in these surfaces and are not easily reached by the bristles of a toothbrush. This allows for prolonged action of acid-producing bacteria and subsequent caries formation. As decay invades through the layers of the tooth, it eventually reaches the pulp, resulting in inflammation and necrosis. The infection may then spread around the tooth apex, forming a periapical abscess or fistula. Dental infection can progress to involve the maxilla or mandible and then move into the fascial planes of the head and neck, producing abscess, facial cellulitis, or less commonly, airway obstruction.

Pathophysiology

Hypodontia may be familial or occur secondary to an underlying syndrome. However, failure of 1 tooth to erupt is more commonly caused by another tooth in the path of eruption or insufficient space in the dental arch. Defects of tooth structure have a variety of causes. Development of the primary teeth is predominantly subject to prenatal influences. The permanent teeth begin to develop in utero and mineralize after birth, making them susceptible to prenatal and postnatal exposures. Medications, infection, jaundice, metabolic disorders, and irradiation may adversely affect normal tooth formation or mineralization. Intrauterine infection, for example, with rubella, cytomegalovirus, or syphilis, may adversely affect tooth structure. A dental infection involving a primary tooth (eg, a periapical abscess) can damage the developing permanent tooth bud, resulting in a mal-formed permanent tooth.

Discolored teeth may be the result of intrinsic or extrinsic factors. Fetal or early childhood (ie, before age 8 years) exposure to tetracy-cline can cause intrinsic staining of the permanent teeth. Exposure to high levels of fluoride during early childhood can cause fluorosis of the permanent dentition. Fluorosis, when it occurs in the United States, is usually mild, characterized by white striations on the permanent teeth. Children with mild fluorosis have teeth that are more resistant to dental decay. Teeth more severely affected by fluorosis may display hypoplastic enamel that is prone to staining; however, moderate and severe dental fluorosis is rare in the United States.

Inherited enamel or dentin defects may cause abnormal color of the teeth. These conditions may be isolated to the teeth, as in the case of dentinogenesis imperfecta, or as part of a systemic disorder, such as congenital erythropoietic porphyria. A single dark tooth is usually nonvital or has bled within the tooth structure after dental trauma. Extrinsic staining is superficial and is usually the result of poor oral hygiene; smoking; chewing tobacco or betel nuts; certain beverages such as coffee, tea, or wine; or medications, such as liquid iron supplements.

Malocclusion can be caused by tooth crowding, an underlying craniofacial condition, abnormal jaw growth relationship, or malpositioning of the teeth. One of the more common causes of malocclusion results from prolonged sucking of a digit (usually the thumb) or pacifier. The most common types of malocclusion associated with digit sucking are anterior open bite, overjet, and posterior crossbite.

Dental decay results from bacterial action on teeth. Streptococcus mutans and Lactobacillus species, among other bacteria, produce acids as end products of carbohydrate metabolism. These acids dissolve the calcium-phosphate mineral of a tooth’s enamel during the process of demineralization. If not reversed through remineralization, the tooth’s structure continues to break down until part of it collapses, resulting in a cavity. A balance of caries-promoting and caries-inhibiting factors is constantly in play. Intraoral factors that inhibit caries include normal salivary production and regular fluoride exposure; those that promote caries are frequent intake of carbohydrates, particularly simple sugars, and xerostomia (ie, dry mouth).

A variety of caries risk factors exist, some of which deserve specific mention. On a population level, children in families with low income and AN/AI children are at high risk for caries (Box 31.1). Children with developmental disabilities are also at higher risk than the general population, in part because of limited access to qualified dentists. On a family level, several genes have recently been discovered that influence caries risk. Parental oral hygiene habits, specifically less than twice daily toothbrushing by parents as well as recent maternal tooth loss from caries, increase caries risk in offspring. On an individual level, inadequate exposure to fluoride, frequent ingestion of sweetened beverages and food, use of medications that cause xerostomia, a history of caries in the previous 3 years, and visible plaque seen on oral examination are all associated with an increased risk of caries.

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