Necrotizing ulcerative gingivitis (NUG) is a microbial disease of the gingiva in the context of an impaired host response. It is characterized by the necrosis and sloughing of gingival tissue, and it presents with characteristic signs and symptoms.
NUG is usually identified as an acute disease. However, the term acute in this case is a clinical descriptor and should not be used as a diagnosis, because there is no chronic form of the disease. Although the acronym ANUG is frequently used, it is a misnomer.57 NUG often undergoes a diminution in severity without treatment, thereby leading to a subacute stage with milder clinical symptoms. Thus, patients may have a history of repeated remissions and exacerbations, and the condition can also recur in previously treated patients. Involvement may be limited to a single tooth or group of teeth, or it may be widespread throughout the mouth (Figure 17-1).
NUG can cause tissue destruction that involves the periodontal attachment apparatus,39 especially in patients with long-standing disease or severe immunosuppression. When bone loss occurs, the condition is called necrotizing ulcerative periodontitis (NUP) (see Chapter 24).
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.
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
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.
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
Light and electron microscopy have been used to study the relationship of bacteria to the characteristic lesion of NUG. Light microscopy shows that the exudate on the surface of the necrotic lesion contains microorganisms that morphologically resemble cocci, fusiform bacilli, and spirochetes.71 The layer between the necrotic and living tissue contains enormous numbers of fusiform bacilli and spirochetes in addition to leukocytes and fibrin. Spirochetes and other bacteria invade the underlying living tissue.4,12,16,36
Spirochetes have been found as deep as 300 µm from the surface. The majority of spirochetes in the deeper zones are morphologically different from cultivated strains of Treponema microdentium. They occur in non-necrotic tissue before other types of bacteria, and they may be present in high concentrations intercellularly in the epithelium adjacent to the ulcerated lesion and in the connective tissue.35
Smears from the lesions (Figure 17-3) show scattered bacteria (predominantly spirochetes and fusiform bacilli), desquamated epithelial cells, and occasional PMNs. Spirochetes and fusiform bacteria are usually seen with other oral spirochetes, vibrios, and filaments.
Diagnosis is based on clinical findings of gingival pain, ulceration, and bleeding. A bacterial smear is not necessary or definitive, because the bacterial picture is not appreciably different from that of patients with marginal gingivitis, periodontal pockets, pericoronitis, or primary herpetic gingivostomatitis.55 However, bacterial studies are useful for the differential diagnosis of NUG and specific infections of the oral cavity (e.g., diphtheria, thrush, actinomycosis, streptococcal stomatitis).
The microscopic examination of a biopsy specimen is not sufficiently specific to be diagnostic. It can be used to differentiate NUG from specific infections (e.g., tuberculosis) or from neoplastic disease, but it does not differentiate between NUG and other necrotizing conditions of nonspecific origin, such as those produced by trauma or caustic medications.
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.)
|Necrotizing Ulcerative Gingivitis||Primary Herpetic Gingivostomatitis|
|Etiology: interaction between host and bacteria, most probably fusospirochetes||Specific viral etiology|
|Necrotizing condition||Diffuse erythema and vesicular eruption|
|Punched-out gingival margin; pseudomembrane that peels off and leaves raw areas||Vesicles rupture and leave slightly depressed oval or spherical ulcer|
|Marginal gingiva affected; other oral tissues rarely affected||Diffuse involvement of gingiva; may include buccal mucosa and lips|
|Uncommon in children||Occurs more frequently in children|
|No definite duration||Duration of 7 to 10 days|
|No demonstrated immunity||Acute episode results in some degree of immunity|
|Contagion not demonstrated||Contagion|
|Necrotizing Ulcerative Gingivitis||Desquamative Gingivitis||Chronic Destructive Periodontal Disease|
|Bacterial smears show fusospirochetal complex||Bacterial smears reveal numerous epithelial cells and few bacterial forms||Bacterial smears variable|
|Marginal gingiva affected||Diffuse involvement of marginal and attached gingivae and other areas of oral mucosa||Marginal gingiva affected|
|Acute history||Chronic history||Chronic history|
|Painful||May or may not be painful||Painless if uncomplicated|
|Pseudomembrane||Patchy desquamation of gingival epithelium||Generally no desquamation, but purulent material may appear from pockets|
|Papillary and marginal necrotic lesions||Papillae do not undergo necrosis||Papillae do not undergo noticeable necrosis|
|Affects adults of both genders and occasionally affects children||Affects adults, most often women||Generally found in adults, occasionally found in children|
|Characteristic fetid odor||No odor||Some odor present but not strikingly fetid|
|Necrotizing Ulcerative Gingivitis||Diphtheria||Secondary Stage of Syphilis (Mucous Patch)|
|Etiology: interaction between host and bacteria, most probably fusospirochetes||Specific bacterial etiology: Corynebacterium diphtheriae||Specific bacterial etiology: Treponema pallidum|
|Affects marginal gingiva||Rarely affects marginal gingiva||Rarely affects marginal gingiva|
|Membrane removal easy||Membrane removal difficult||Membrane not detachable|
|Painful condition||Less painful||Minimal pain|
|Marginal gingivae affected||Throat, fauces, and tonsils affected||Any part of mouth affected|
|Serologic findings normal||Serologic findings normal||Serologic findings abnormal*|
|Immunity not conferred||Immunity conferred by an attack||Immunity not conferred|
|Doubtful contagiousness||Contagion||Only direct contact will communicate disease|
|Antibiotic therapy relieves symptoms||Antibiotic treatment has minimal effect||Antibiotic therapy has excellent results|
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/>