NUG/P = Necrotizing Ulcerative Gingivitis/Periodontitis, Types V A (NUG) and V B (NUP)
Ulcerative gingivitis is usually an acute, painful, rapidly progressing inflammation of the gingiva, which may enter a sub-acute or chronic stage. Without treatment, this disease usually develops quickly into localized ulcerative periodontitis. It seldom occurs as a generalized process, nor is its severity always identical. It may be quite advanced in anterior segments, while the premolars or molars are not affected at all, or only mildly so. The reasons for this remain unknown (oral hygiene? ischemia? locally predominating pathogenic bacteria? plaque-retentive areas? tooth type?). Probing depths are usually shallow because gingival tissue is lost to necrosis as attachment loss proceeds. Secondary ulceration of other oral mucosal surfaces is rarely observed, and only in severe cases (AAP 1996e). Caution: Ulceration can represent an early oral symptom in HIV-positive patients and AIDS victims (p. 151).
Ulcerative gingivitis/periodontitis has become less common in recent decades than earlier (exception: HIV-positive and AIDS patients). In the younger population, the morbidity has been variously reported between 0.1–1%.
The etiology of NUG is not completely understood. In addition to plaque and a previously existing gingivitis, the following local and systemic predisposing factors are suspected:
Poor oral hygiene
Predominance of spirochetes, fusiforms and P. intermedia, and occasionally Selenomonas and Porphyromonas in the plaque
Smoking (local irritation by tar products)
Poor general health, psychic stress, alcohol
Smoking: nicotine as a sympatheticomimetic, and carbon monoxide (CO) as a chemotaxin (p. 216)
Age (15–30 years)
Season of the year (September/October and December/January; Skâch et al. 1970)
NUG/P patients usually exhibit similar life styles and habits: The teeth do not occupy a high position in the patient’s consciousness. They are usually young adults, heavy smokers (tobacco: high content of tar and nicotine), exercise poor oral hygiene, and become interested in treatment only during acute, painful exacerbations.
The clinical course is acute, but fever occurs only seldom. Within only a few days, interdental papillae may be lost to ulceration. The acute phase may gravitate into a chronic interval stage if host resistance improves (see pre-disposing factors) or through self-treatment (rinsing with a disinfectant mouthwash). Untreated ulcerative gingivitis exhibits a high recurrence rate, and may develop rapidly into ulcerative periodontitis (attachment loss with shallow pockets!).
Therapy: In addition to local debridement, the early stages of treatment should be supported with medicaments. Topical application of ointments containing cortisone or antibiotics, or metronidazol may be effective. In severe cases, systemic metronidazol (e.g., Flagyl) may be prescribed (see Medicaments, p. 287). After reduction of the acute symptoms in advanced cases, surgery to correct gingival contours may be indicated.
The clinical and histopathologic pictures in NUG are correlated. The histopathology of NUG is, however, significantly different from that of simple gingivitis.
As a consequence of the acute reaction, an enormous number of PMNs transmigrate the junctional epithelium in the direction of the sulcus and the col. In contrast to the situation in simple gingivitis, PMNs also migrate toward the oral epithelium and the tips of papillae, which undergo necrotic destruction. The ulcerated wound is covered by a clinically visible, whitish pseudomembrane that consists of bacteria, dead leukocytes and epithelial cells as well as fibrin. The tissue subjacent to the ulcerated areas is edematous, hyperemic and heavily infiltrated by PMNs. In long-standing disease, the deeper tissue regions will also contain lymphocytes and plasma cells. Within the infiltrated area, collagen destruction progress rapidly.
Spirochetes and other bacteria often penetrate into the damaged tissues (Listgarten 1965, Listgarten & Lewis 1967).