Gingivitis

Poor oral hygiene results in the accumulation of dental plaque at the tooth-gingival interface that activates an inflammatory response, expressed as localized or generalized reddening and swelling of the gingiva. More than half of American school children experience gingivitis. In severe cases, the gingiva spontaneously bleeds and there is oral malodor. Treatment is proper oral hygiene (careful toothbrushing and flossing); complete resolution can be expected. Fluctuations in hormonal levels during the onset of puberty can increase inflammatory response to plaque. Gingivitis in healthy children is unlikely to progress to periodontitis (inflammation of the periodontal ligament resulting in loss of alveolar bone).

Aggressive Periodontitis in Children (Prepubertal Periodontitis)

Periodontitis in children before puberty is a rare disease that often begins between the time of eruption of the primary teeth and the age of 4 or 5 yr. The disease occurs in localized and generalized forms. There is rapid bone loss, often leading to premature loss of primary teeth. It is often associated with systemic problems, including neutropenia, leukocyte adhesion or migration defects, hypophosphatasia, Papillon-Lefèvre syndrome, leukemia, and histiocytosis X. In many cases, however, there is no apparent underlying medical problem. Nonetheless, diagnostic work-ups are necessary to rule out underlying systemic disease.

Treatment includes aggressive professional teeth cleaning, strategic extraction of affected teeth, and antibiotic therapy. There are few reports of long-term successful treatment to reverse bone loss surrounding primary teeth.

Aggressive Periodontitis in Adolescents (Localized Juvenile Periodontitis)

Aggressive periodontitis in adolescents is characterized by rapid alveolar bone loss, especially around the permanent incisors and 1st molars. Overall prevalence in the United States is <1%, but the prevalence among African-Americans is reportedly 2.5%. This form of periodontitis is associated with a strain of Aggregatibacter (Actinobacillus) bacteria. In addition, the neutrophils of patients with aggressive periodontitis can have chemotactic or phagocytic defects. If left untreated, affected teeth lose their attachment and can exfoliate. Treatment varies with the degree of involvement. Patients whose disease is diagnosed at onset are usually managed by surgical or nonsurgical debridement in conjunction with antibiotic therapy. Prognosis depends on the degree of initial involvement and compliance with therapy.

Teething

Teething can lead to intermittent localized discomfort in the area of erupting primary teeth, irritability, low-grade fevers, and excessive salivation; many children have no apparent difficulties. Treatment of symptoms includes oral analgesics and ice rings for the child to “gum.” Similar manifestations can also arise when the 1st permanent molars erupt at about age 6 yr.

Cyclosporine- or Phenytoin-Induced Gingival Overgrowth

The use of cyclosporine to suppress organ rejection or phenytoin for anticonvulsant therapy, and in some cases calcium channel blockers, is associated with generalized enlargement of the gingiva. Phenytoin and its metabolites have a direct stimulatory action on gingival fibroblasts, resulting in accelerated synthesis of collagen. Phenytoin induces less gingival hyperplasia in patients who maintain meticulous oral hygiene.

Gingival hyperplasia occurs in 10-30% of patients treated with phenytoin. Severe manifestations can include gross enlargement of the gingiva, sometimes covering the teeth; edema and erythema of the gingiva; secondary infection, resulting in abscess formation; migration of teeth; and inhibition of exfoliation of primary teeth and subsequent impaction of permanent teeth. Treatment should be directed toward prevention and, if possible, discontinuation of cyclosporine or phenytoin. Patients undergoing long-term treatment with these drugs should receive frequent dental examinations and oral hygiene care. Severe forms of gingival overgrowth are treated by gingivectomy, but the lesion recurs if drug use is continued.

Acute Pericoronitis

Acute inflammation of the flap of gingiva that partially covers the crown of an incompletely erupted tooth is common in mandibular permanent molars. Accumulation of debris and bacteria between the gingival flap and tooth precipitates the inflammatory response. A variant of this condition is a gingival abscess due to entrapment of bacteria because of orthodontic bands or crowns. Trismus and severe pain may be associated with the inflammation. Untreated cases can result in facial space infections and facial cellulitis.

Treatment includes local debridement and irrigation, warm saline rinses, and antibiotic therapy. When the acute phase has subsided, extraction of the tooth or resection of the gingival flap prevents recurrence. Early recognition of the partial impaction of mandibular 3rd molars and their subsequent extraction prevents these areas from developing pericoronitis.

Necrotizing Periodontal Disease (Acute Necrotizing Ulcerative Gingivitis)

Necrotizing periodontal disease, in the past sometimes referred to as “trench mouth,” is a distinct periodontal disease associated with oral spirochetes and fusobacteria. It is not clear, however, whether bacteria initiate the disease or are secondary. It rarely develops in healthy children in developed countries, with a prevalence in the United States of <1%, but is seen more often in children and adolescents from developing areas of Africa, Asia, and South America. In certain African countries, where affected children usually have protein malnutrition, the lesion can extend into adjacent tissues, causing necrosis of facial structures (cancrum oris, or noma).

Clinical manifestations of necrotizing periodontal disease include necrosis and ulceration of gingiva between the teeth, an adherent grayish pseudomembrane over the affected gingiva, oral malodor, cervical lymphadenopathy, malaise, and fever. The condition may be mistaken for acute herpetic gingivostomatitis. Dark-field microscopy of debris obtained from necrotizing lesions demonstrates dense spirochete populations.

Treatment of necrotizing periodontal disease is divided into an acute management with local debridement, oxygenating agents (direct application of 10% carbamide peroxide in anhydrous glycerol qid), and analgesics. Dramatic resolution usually occurs within 48 hr. If a patient is febrile, antibiotics (penicillin or metronidazole) may be an important adjunctive therapy. A 2nd phase of treatment may be necessary if the acute phase of the disease has caused irreversible morphologic damage to the periodontium. The disease is not contagious.