Infections of the Oral Cavity

Dental Caries

In the United States, caries are the most common chronic disease of childhood and are 5 times more common than asthma. Caries of primary teeth commonly are referred to as caries of early childhood. Plaque-related bacteria colonize the tooth surface and produce a weak acid during their carbohydrate metabolism. Acid production lowers local pH and results in demineralization of the tooth with efflux of calcium, phosphorus, and carbonate. Tooth colonization with cariogenic bacteria is a key factor for development of caries. Bacterial 16S sequence analysis has shown association of S. mutans, S. salivarius, Streptococcus sobrinus , and Streptococcus parasanguinis with early stages of caries, and Veillonella species were predictive of future caries among children without history of caries. Lactobacilli are strongly associated with more advanced stages of caries. With progression of caries severity there is loss of healthy microbial community diversity. The major reservoir from which infants acquire cariogenic bacteria is from their primary care giver, usually the mother. Caries can affect any part of the tooth. In children, coronal caries typically have been found in the pits and fissures of the occlusal surfaces of molars and premolars. Food retention occurs less frequently at interproximal sites and the gingival margins except in infants who fall asleep drinking a bottle of milk or juice. In early childhood the disease develops over smooth surfaces. Treatment consists of restoration of the affected tooth augmented by preventive methods such as fluoride treatments, flossing, tooth brushing, meticulous removal of the biofilm, placement of sealants, and avoidance of sugary snacks and drinks. Maternal oral health education has had mixed impact on childhood caries.

Pericoronitis

Pericoronitis is an acute localized infection associated with operculum of the gum overlying partially erupted teeth or impacted wisdom teeth. The third molars (wisdom teeth) often are affected especially when their eruption is hindered by lack of space. The tissue around the tooth becomes red, edematous, and tender to touch, but the underlying bone usually is not involved. The patient reports continuous pain that ranges from dull to throbbing to intense, often radiating to the mouth, ear, throat, or floor of the mouth. Other symptoms can include swelling of the cheek, trismus, dysphagia, and foul breath smell. Systemic manifestations can include fever, chills, and submandibular, submental, or cervical lymphadenopathy. Treatment consists of gentle débridement, irrigation under the operculum, and a systemic antibiotic effective against mouth flora, along with incision and drainage if infection spreads into soft tissue.

Pulpitis and Periapical Abscess

Pulpal infection most frequently results from caries. Demineralization and destruction of the enamel is followed by invasion of the pulp to produce localized or generalized pulpitis . In early stages of infection ( reversible pulpitis) patients typically complain of tooth sensitivity to percussion and thermal changes, especially cold drinks. Pain stops abruptly when the stimulus is withdrawn. The ongoing inflammation and built-up pressure lead to pulp necrosis described as irreversible pulpitis. Complications of pulpitis include spread of infection to the adjacent periodontal ligaments and invasion of the alveolar bone condition called periapical abscess . Serious complications of periapical infections are rare. Among 75 cases of pulpitis, 16S rDNA sequencing revealed Lactobacillus genus as the most abundant bacteria causing reversible and irreversible pulpitis. However, in some cases infection spreads, causing abscesses in the submaxillary triangle or in the parapharyngeal or submasseteric space. In the maxilla, periapical infection can manifest in the soft tissues of the face. Infection also can extend to the infratemporal space including the sinuses and from there to the central nervous system, causing subdural empyema, brain abscess, or meningitis.

The most common organisms isolated from infected pulp include aerobic, facultative anaerobic organisms (i.e., S . salivarius , other alpha-hemolytic streptococci, nonhemolytic streptococci) and anaerobic streptococci, anaerobic gram-negative bacilli, Actinomyces spp., Propionibacterium spp., Veillonella spp., and others. Treatment consists of elimination of infected pulp (root canal treatment) or extraction of the tooth. Cochrane literature review found no evidence to support antibiotic use for treatment of pulpitis alone. There was no difference in pain perception or analgesic use among 40 patients with irreversible pulpitis randomly assigned to penicillin or placebo arm. Antibiotic therapy is indicated if drainage cannot be performed or the infection has spread to surrounding soft tissues. Penicillin usually is adequate; amoxicillin-clavulanate or clindamycin are effective against β-lactamase producing anaerobes.

Early-Onset Periodontitis

Juvenile (aggressive) periodontitis is a particularly destructive form of periodontitis seen in adolescents. Its localized form is characterized by rapid bone loss affecting the first molar and incisor teeth. The generalized form is rapidly progressive, affecting other teeth. Plaque is minimal, and specific defects in neutrophil chemotaxis and phagocytosis were demonstrated among 75% of patients. DNA probes and primers have revealed anaerobic organisms such as A . actinomycetemcomitans, P . gingivalis, Prevotella intermedia, T . denticola, and T . forsythia . Treatment consists of systemic antibiotics. Narrow-spectrum antibiotics such as penicillin, amoxicillin, cephalexin, and macrolides are not effective against increasing number of β-lactamase–producing anaerobes. Antibiotics that include β-lactamase inhibitor (i.e., clavulanate sulbactam) or clindamycin offer excellent coverage against the majority of aerobic and anaerobic oral pathogens. The decision whether to use narrow- or broader-spectrum antibiotic should be individualized.

Herpes Simplex Virus (HSV) Gingivostomatitis

HSV gingivostomatitis is the most recognized viral infection of the oral cavity. Primary infection with HSV-1 occurs throughout childhood, most commonly between the ages of 6 months and 5 years, and during adolescence and results in seropositivity in up to 90% of adults. ^, Up to 90% of children with primary HSV infections are asymptomatic. After primary infection, HSV remains dormant in the trigeminal ganglion and reactivates after stressful stimuli (i.e., cold, trauma, sunlight, intercurrent illness). Recrudescent disease has been estimated to occur in up to 40% of seropositive individuals. HSV infection is ubiquitous and acquired from symptomatic and asymptomatic people with primary or recurrent infection. Infections with HSV-1 usually result from direct contact with infected oral secretions. The incubation period for HSV infection beyond the neonatal period is 2 days to 2 weeks. In primary infection, vesicles appear on the first day of illness in 85% of symptomatic children and can persist for 7–18 days. Primary symptomatic infections are accompanied by fever, lymphadenopathy, malaise, pharyngitis, and anorexia. Gingiva are red, swollen, and bleeding. Small vesicles surrounded by red halo on the gingiva and anterior lingual and buccal mucosa rapidly rupture and coalesce giving rise to ulcerations. HSV gingivostomatitis is painful, and children commonly refuse to swallow, resulting in drooling. Differential diagnosis includes coxsackievirus infection (herpangina), erythema multiforme, pemphigus vulgaris, acute necrotizing ulcerative gingivitis (ANUG), and most commonly, aphthous stomatitis.

Complications of HSV gingivostomatitis include dehydration, herpetic whitlow or herpetic keratitis from autoinoculation, and secondary bacteremia with oral flora. ^, Recurrent HSV orolabial lesions occurs in one-third of individuals with prior HSV infection. Reactivation lesions typically are found around the gingiva, the hard palate, and vermilion border of the lip (“cold sore”). A prodrome of tingling, burning, and itching occurs 12–36 hours prior to the eruption of the vesicles. Viral shedding persisted for a mean of 7 days (range 2–12 days) among 36 untreated immunocompetent children in one study.

Treatment of HSV gingivostomatitis usually is palliative, with hydration and pain control. Topical application of diphenhydramine, simethicone (Maalox), and bismuth subsalicylate (Kaopectate) and viscous lidocaine frequently are prescribed; however, their usefulness and benefit have been questioned. Systemic analgesics (i.e., ibuprofen, paracetamol, acetaminophen) should be strongly considered to ease pain and improve intake and hydration.

A randomized, double-blind treatment trial in children using oral acyclovir during early stages reduced the duration of symptoms, improved healing, and reduced infectivity. A systematic review showed weak evidence that oral acyclovir offered treatment benefit. In general, most experts would treat patients (with oral acyclovir or valacyclovir) who come to attention early (within 96 hours of the onset of symptoms) or who have severe disease. Valacyclovir offers benefit of better bioavailability and less frequent dosing regimen compared with acyclovir. Chronic suppressive therapy can be used to reduce recurrences, such as in patients with facial, periorbital, or ocular lesions or very frequent episodes. Among healthy subjects, combination of early topical acyclovir 5% plus hydrocortisone 1% cream (ME-609) was more effective in reducing progression to ulcerative HSV lip lesions and reduced the size of the lesions compared with topical acyclovir alone or placebo.