History.

NUG is characterized by its sudden onset, sometimes after an episode of debilitating disease or acute respiratory tract infection. A change in living habits, protracted work without adequate rest, poor nutrition, tobacco use, and psychological stress are frequent features of the patient’s history.

Oral Signs.

Characteristic lesions are punched-out, craterlike depressions at the crest of the interdental papillae that subsequently extend to the marginal gingiva and rarely to the attached gingiva and oral mucosa. The surface of the gingival craters is covered by a gray, pseudomembranous slough that is demarcated from the remainder of the gingival mucosa by a pronounced linear erythema (Figure 17-1, A). In some cases, the lesions are denuded of the surface pseudomembrane, thereby exposing the gingival margin, which is red, shiny, and hemorrhagic. The characteristic lesions may progressively destroy the gingiva and the underlying periodontal tissues (see Figure 17-1, B).

Spontaneous gingival hemorrhage or pronounced bleeding after the slightest stimulation are additional characteristic clinical signs (see Figure 17-1, B and C). Other signs that are often found include a fetid odor and increased salivation.

NUG can occur in otherwise disease-free mouths, or it can be superimposed on chronic gingivitis or periodontal pockets. However, NUG or NUP does not usually lead to periodontal pocket formation, because the necrotic changes involve the junctional epithelium; a viable junctional epithelium is needed for pocket deepening (see Chapter 20). It is rare in edentulous mouths, but isolated spherical lesions occasionally occur in the soft palate.⁵⁶

Oral Symptoms.

The lesions are extremely sensitive to touch, and the patient often complains of a constant radiating, gnawing pain that is intensified by eating spicy or hot foods and chewing. There is a “metallic” foul taste, and the patient is conscious of an excessive amount of “pasty” saliva.

Extraoral and Systemic Signs and Symptoms.

Patients are usually ambulatory and have a minimum of systemic symptoms. Local lymphadenopathy and a slight elevation in temperature are common features of the mild and moderate stages of the disease. In severe cases, there may be high fever, increased pulse rate, leukocytosis, loss of appetite, and general lassitude. Systemic reactions are more severe in children. Insomnia, constipation, gastrointestinal disorders, headache, and mental depression sometimes accompany the condition.

In very rare cases, severe sequelae such as gangrenous stomatitis and noma have been described.1,2,17,31

Clinical Course.

The clinical course can vary. If untreated, NUG may lead to a progressive destruction of the periodontium as well as gingival recession accompanied by an increase in the severity of systemic complications.29,49

Histopathology.

Microscopically, the NUG lesion is a nonspecific acute necrotizing inflammation of the gingival margin that involves both the stratified squamous epithelium and the underlying connective tissue. The surface epithelium is destroyed and replaced by a meshwork of fibrin, necrotic epithelial cells, polymorphonuclear leukocytes (neutrophils) (PMNs), and various types of microorganisms (Figure 17-2). This is the zone that appears clinically as the surface pseudomembrane. At the immediate border of the necrotic pseudomembrane, the epithelium is edematous, and the individual cells exhibit varying degrees of hydropic degeneration. In addition, there is an infiltration of PMNs in the intercellular spaces.

The underlying connective tissue is markedly hyperemic, with numerous engorged capillaries and a dense infiltration of PMNs. This acutely inflamed zone appears clinically as the linear erythema beneath the surface pseudomembrane. Numerous plasma cells may appear in the periphery of the infiltrate; this is interpreted as an area of established chronic gingivitis on which the acute lesion became superimposed.²⁸

The epithelium and connective tissue alterations decrease as the distance from the necrotic gingival margin increases, blending gradually with the uninvolved gingiva.

It is noteworthy that the microscopic appearance of NUG is nonspecific. Comparable changes result from trauma, chemical irritation, or the application of caustic medications.

Differential Diagnosis.

NUG should be differentiated from other conditions that resemble it in some respects, such as herpetic gingivostomatitis (Table 17-1); chronic periodontitis; desquamative gingivitis (Table 17-2); streptococcal gingivostomatitis; aphthous stomatitis; gonococcal gingivostomatitis; diphtheritic and syphilitic lesions (Table 17-3); tuberculous gingival lesions; candidiasis, agranulocytosis, and dermatoses (pemphigus, erythema multiforme, and lichen planus); and stomatitis venenata. Treatment options for these diseases vary dramatically, and improper treatment may exacerbate the condition. In the case of primary herpetic gingivostomatitis, early diagnosis may result in treatment with antiviral drugs that would be ineffective for NUG, whereas the treatment of a case of herpes with the debridement required for NUG could exacerbate the herpes. (See Chapter 19 for descriptions of most of these conditions.)

Streptococcal gingivostomatitis is a rare condition that is characterized by a diffuse erythema of the gingiva and other areas of the oral mucosa.⁴² In some cases, it is confined as a marginal erythema with marginal hemorrhage. Necrosis of the gingival margin is not a feature of this disease, and there is no notable fetid odor. Bacterial smears show a preponderance of streptococcal forms, which were identified as Streptococcus viridans, but other studies report findings of group A β-hemolytic streptococcus.³⁷

Agranulocytosis is characterized by a marked decrease in the number of circulating PMNs, lesions of the throat and other mucous membranes, and ulceration and necrosis of the gingiva that may resemble that of NUG and that occurs most commonly after chemotherapy in cancer patients or in patients with leukemia. The oral condition of patients with agranulocytosis is primarily necrotizing, but it lacks the severe inflammatory reaction seen with NUG. Blood studies serve to differentiate between NUG and the gingival necrosis associated with agranulocytosis.

Vincent’s angina is a fusospirochetal infection of the oropharynx and throat as distinguished from NUG, which affects the marginal gingiva. Patients with Vincent’s angina have a painful membranous ulceration of the throat, with edema and hyperemic patches breaking down to form ulcers that are covered with pseudomembranous material. The process may extend to the larynx and the middle ear.

NUG in the patient with leukemia is not produced by leukemia itself, but it may result from the reduced host defense mechanisms seen with leukemia. In addition, NUG may be superimposed on the gingival tissue alterations caused by leukemia. The differential diagnosis consists not of distinguishing between NUG and leukemic gingival changes but rather of determining whether leukemia is a predisposing factor in the mouth of a patient with NUG. For example, if a patient with necroti/>