Acute Necrotizing Ulcerative Gingivitis


Acute necrotizing ulcerative gingivitis (ANUG) is an endogenous oral infection that is characterized by necrosis of the gingiva. Occasionally, ulcers of the oral mucosa also occur in patients with hematologic disease or severe nutritional deficiencies (see Chapter 16).

ANUG became known notoriously as “trench mouth” during World War I because of its prevalence in the combat trenches, and it was incorrectly considered a highly contagious disease. Since then, studies have shown that the disease is accompanied by an overgrowth of organisms prevalent in normal oral flora and is not transmissible. The organisms most frequently mentioned as working symbiotically to cause the lesions are the fusiform bacillus and spirochetes.
Plaque samples taken from ANUG patients demonstrate a constant anaerobic flora of Treponema spp, Selenomonas spp, Fusobacterium spp, and Bacteroides intermedius.The tissue destruction is thought to be caused by endotoxins that act either directly on the tissues or indirectly by triggering immunologic and inflammatory reactions.
Classic ANUG in patients without an underlying medical disorder is found most often in those between the ages of 16 and 30 years, and it is associated with three major factors:
1. Poor oral hygiene with pre-existing marginal gingivitis or faulty dental restorations
2. Smoking 3. Emotional stress
Systemic disorders associated with ANUG are diseases affecting neutrophils (such as leukemia or aplastic anemia), marked malnutrition, and HIV infection. Malnutrition-associated cases are reported from emergent countries where the untreated disease may progress to noma, a large necrotic ulcer extending from the oral mucosa through the facial soft tissues.
The prevalence of the disease was reported by Giddon and colleagues,who studied the prevalence of ANUG in 12,500 students served by the Harvard University Dental Health Service. About 0.9% of the total sample developed ANUG during the period of study. A 4% prevalence in those students who made use of the dental clinic was observed. Members of the junior class were most often affected. A relation to stress was noted by an increased frequency during examination and vacation periods. Studies of military trainees or college students demonstrated a prevalence of 5 to 7%.
There are three forms of periodontal diseases observed in patients with acquired immunodeficiency syndrome (AIDS): linear gingival erythema (LGE), necrotizing ulcerative gingivitis (NUG), and necrotizing ulcerative periodontitis (NUP).
LGE is an intense red band involving the marginal gingiva that does not resolve with standard oral hygiene procedures. Some cases are believed to be caused by candidal overgrowth, and these cases resolve with antifungal therapy. NUG and NUP are clinically similar to ANUG; the term “NUG” is used when the disease involves only the gingiva, and “NUP”involves a loss of periodontal attachment.There is evidence that, in patients with AIDS, the host response in the gingival crevice is altered. Levels of proinflammatory cytokines such as interleukin-1 β are increased in the gingival crevice of patients with human immunodeficiency virus (HIV), which alters the regulation of neutrophils. This alteration in neutrophil function may explain the increase in NUP-related organisms including fusobacteria and Candida,which results in the rapid necrosis of gingival tissues.A fulminating form of ulcerative stomatitis related to ANUG is noma (cancrum oris), which predominantly affects children in sub-Saharan Africa. This disease is characterized by extensive necrosis that begins on the gingiva and then progresses from the mouth through the cheek to the facial skin, causing extensive disfigurement (Figure 4-17). The major risk factors associated with noma include malnutrition, poor oral hygiene, and concomitant infectious diseases such as measles.Living in close proximity to livestock is also believed to play a role, and Fusobacterium necrophorum,a pathogen associated with disease in livestock, has been isolated from over 85% of noma lesions.The mortality rate without appropriate therapy exceeds 70%.