Caries

Dental caries remains a highly prevalent disease among children, both in the primary and permanent dentition. The risk of early childhood caries is increased in babies who sleep with bottles, who graze (rather than eating at discrete mealtimes), and whose parents have untreated caries.

Bacteria, especially the Streptococcus mutans group, are typically transmitted from mother to infant soon after the eruption of the primary teeth. These bacteria colonize tooth surfaces and form plaques above and below the gingival margin. Caries result when these bacteria ferment sucrose from ingested dietary carbohydrate, producing organic acids on the tooth surface. These acids lead to the destruction of the hydroxyapatite crystals that give the enamel its structure, making the enamel more and more porous and eventually causing breakdown of the tooth surface (Figure 34-3). These areas of breakdown can erode through the enamel and dentin into the pulp, where an inflammatory response raises the pressure in the pulp chamber and can cause compression, and thus ischemia, of the pulp vessels. This is known as pulp necrosis.

Figure 34-3 Dental caries.

When pulp necrosis extends into the periapical region, a periapical abscess can form and can erode the alveolar bone or involve other teeth. An abscessed tooth may be tender and mobile, with soft tissue swelling or purulence. It can result in cellulitis and impair development of an underlying permanent tooth.

Caries prevention can be accomplished through appropriate anticipatory guidance. In addition to promoting healthy dietary habits (minimal juice at meals only, no carbonated beverages, discontinuing bottle use at 1 year of age, and never putting baby to bed with a bottle), providers can educate parents on proper dental hygiene and fluoride supplementation. From the first tooth eruption to age 24 months, parents should clean the child’s teeth twice a day without toothpaste. Starting at age 2 years, the teeth may be brushed using standard flouride-containing toothpaste. Children younger than 6 years of age may swallow too much toothpaste and should be supervised while brushing.

In low concentrations, fluoride protects against caries by promoting enamel mineralization; in addition to fluoridated toothpaste, many children are exposed to fluoride supplementation in community water supplies. This supplementation is thought to have dramatically reduced the prevalence of caries among children. However, in higher concentrations in children, fluoride can cause fluorosis, a condition in which the enamel is hypomineralized, increasing its porosity. The clinical manifestations range in severity from white flecks to severe pitting and mottling.

Periodontal Infections

Gingivitis is an inflammatory response to bacteria that live in the sulcus between the enamel and the gingiva. The gingiva may be edematous and erythematous and may also bleed and ulcerate. Long-term gingivitis may result in tissue hypertrophy. It is highly prevalent in children and adolescents, and poor dental hygiene is usually causative.

Periodontitis evolves from gingivitis with bacterially induced destruction of the tooth’s surrounding and supportive structures. There are several forms of periodontitis. Chronic periodontitis is the most common, but it is not usually diagnosed until adulthood. Several rare but aggressive forms exist in children. Clinical manifestations include tooth mobility and loss of attachment, gingival recession, periodontal bone loss, and tooth loss.

Ankyloglossia

Uncommonly, children may be born with a short lingual frenulum, known as ankyloglossia or “tongue-tie” (Figure 34-4). Tongue movement may be restricted, and the close attachment of the frenulum to the tongue may cause the tip of the tongue to appear to have a mild cleft (“heart-shaped tongue”). The condition is more prevalent in boys than in girls. It does not usually affect speech or feeding, and the frenulum often lengthens as the child grows. In some cases, the short lingual attachment may impair a child’s ability to clear food from the buccal side of the teeth, which may promote bacterial growth and tooth decay. A frenulectomy may be required in the case of true disability.

Figure 34-4 Lesions of the oral soft tissues.

Geographic Tongue

This benign condition is characterized by irregular red patches on the tongue, with yellow, gray, or white margins (see Figure 34-4). The filiform papillae are absent in these areas. The lesions typically spontaneously resolve and then subsequently appear elsewhere on the tongue, giving the condition its other name of “migratory glossitis.”

Mucocele

This painless pseudocyst results from trauma to the duct of a minor salivary gland, usually in the lower lip or cheek (e.g., from lip biting). Ranging in size from 1 mm to several centimeters, it is usually smooth, soft, and bluish to translucent, filled with mucin from the damaged duct (see Figure 34-4). It may spontaneously drain as a result of the patient’s unroofing the lesion with his or her teeth; however, surgical excision may be required, in which case the entire underlying gland must be removed to prevent recurrence.

Ranula

Similar in appearance and pathophysiology to a mucocele, a ranula is a mucous cyst on the floor of the mouth. Rarely, it may herniate through the mylohyoid muscle to involve the submandibular region and neck. It must be removed by surgical excision.

Traumatic Ulcers

These lesions are usually single, painful, and located on the lateral tongue, buccal mucosa, lips, or gingiva. Treatment is symptomatic relief, and healing is usually complete within 1 to 3 weeks. A special case is Riga-Fede disease in infants, who sustain traumatic ulceration on the ventral surface of the tongue as a result of rubbing the tongue against the mandibular incisors.

Aphthous Ulcers

These recurrent and painful ulcers, also known as canker sores, occur in up to one-third of children. Their cause is unclear, but viruses, T-cell dysfunction, trauma, and genetic predisposition have been implicated. They appear as white necrotic areas surrounded by a red margin, usually on the buccal and labial mucosa (see Figure 34-4). They usually resolve completely within 10 to 14 days. Differential diagnosis consideration should include recurrent traumatic ulcers from child abuse, oral manifestations of inflammatory bowel disease, secondary herpetic ulcers, neutropenic ulcers, and PFAPA (periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis) syndrome.

Candidiasis

Thrush caused by the overgrowth of Candida spp. (mostly Candida albicans) occurs in 2% to 5% of normal newborns; it is also common in immunocompromised children and those who have used antibiotics or steroids. It presents as pseudomembranous white plaques on the buccal mucosa, palate, and tongue (see Figure 34-4). These plaques may be wiped away to reveal underlying raw, painful, erythematous mucosa. Treatment with an oral suspension of nystatin is usually effective; most clinicians recommend a course of 2 weeks or until 2 to 3 days after symptoms have resolved. For immunocompromised children or those who do not respond to nystatin, systemic fluconazole should be considered. Any objects that the infected child has regularly put in his or her mouth, such as pacifiers and toothbrushes, should be discarded.

Primary Herpetic Gingivostomatitis

Primary herpes simplex virus (HSV) infection presents with clusters of painful vesicles surrounded by erythema, which are primarily located on the gingiva, hard palate, and anterior tongue and extend to the vermilion border of the lips (see Figure 34-4). These vesicles may have a red halo, may ulcerate, and may become secondarily infected with bacteria. Other symptoms may include fever, lymphadenopathy, arthralgia, headache, and drooling or dehydration resulting from the pain associated with swallowing. Diagnosis is made by unroofing a vesicle with a sterile needle and sending vesicular fluid for viral culture, polymerase chain reaction, direct immunofluorescence, or Tzanck smear. Treatment with acyclovir within 3 days of symptom onset shortens the length of symptoms and the period of viral shedding. After primary HSV infection, recurrence may occur because the virus remains latent within the trigeminal ganglion until a flare is triggered by stress, sunlight, cold, trauma, or immunosuppression.

Enterovirus Infections

Herpangina, usually caused by the Coxsackie A virus in summer and early fall, manifests as painful vesicles on the tonsils and soft palate. It is distinguished from HSV stomatitis by its predilection for the posterior oropharynx. It can be associated with headache, vomiting, abdominal pain, and fever. Treatment is supportive, and resolution is usually spontaneous after 3 to 5 days.

Hand, foot, and mouth disease, often caused by the Coxsackie A and B viruses in the spring and early summer, manifests with vesicles similar in appearance to herpangina; however, children may also have vesicles on the palate, tongue, buccal mucosa, hands, feet, buttocks, and sometimes genitalia. It may also be associated with fever and resolves spontaneously in several days.