Acute necrotizing ulcerative gingivitis. A review of diagnosis, etiology and treatment

Abstract

Vincent's original description of the fusiform-spirochete nature of acute necrotizing ulcerative gingivitis (ANUG) still remains true today, although much additional insight has been gained regarding the etiology, pathogenesis and treatment of the disease. In addition to the historic association of fusiform and spirochete microbes with ANUG, recent findings have also implicated Bacteroides and Selenomonas species. Possible abnormalities in immunological function, such as altered PMN and lymphocyte responsiveness, may be present. Stress, which has long been known to be associated with the disease, appears to play a role through induction of increased cortisol and catecholamine levels. These chemical mediators respectively may compromise the host immune responses and the gingival microcirculation. Cortisol may also serve as a nutrient source for Bacteroides bacteria. Other predisposing factors to ANUG may include smoking and poor oral hygiene. Treatment modalities involve eliminating or reducing the levels of bacterial pathogens by mechanical and antibiotic means, along with attempts at controlling significant psychological and physical precipitating factors.