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Noma is a serious orofacial gangrene originating intraorally in the gingival-oral mucosa complex before spreading extraorally to produce a visibly destructive ulcer. Although cases of noma are now rarely reported in the developed countries, it is still prevalent among children in third world countries, notably in sub-Sahara Africa, where poverty, ignorance, malnutrition, and preventable childhood infections are still common. This review summarizes historical, epidemiological, management, and research updates on noma with suggestions for its prevention and ultimate global eradication. The global annual incidence remains high at about 140,000 cases, with a mortality rate exceeding 90% for untreated diseases. Where the patients survive, noma defects result in unsightly facial disfigurement, intense scarring, trismus, oral incompetence, and social alienation. Although the etiology has long been held to be infectious, a definitive causal role between microorganisms cited, and noma has been difficult to establish. The management of noma with active disease requires antibiotics followed by reconstructive surgery. Current research efforts are focused towards a comprehensive understanding of the epidemiology, and further elucidation of the microbiology and pathogenesis of noma.Although a formidable public health challenge, noma can be prevented with a potential for subsequent global eradication. To achieve both desirable goals, detection of early disease is crucial because these early lesions respond to conventional antibiotic treatments when instituted side by side with nutritional rehabilitation, and obviates the necessity for extensive surgical reconstruction often indicated in late stage disease. The eradication of noma in the developed world in the mid 20thcentury bears out the notion of a similar outcome following effective preventive strategies in Africa. A fundamental and necessary step towards attaining this goal is for the international community to adopt a perception of noma as an urgent global public health challenge. Research effort toward deciphering the microbiology, molecular events, and pathogenesis of noma also should intensify.

— A case of acute ulcerative gingivitis (AUG) with pericoronitis is presented showing how differential dark‐field microscopy can be used to aid in diagnosis and monitor therapy. The AUG site showed a unique flora with dark‐field microscopy, which in this case was shared by the pericoronitis lesion. Metronidazole therapy resulted in a marked change in the flora of both sites. Four days following therapy both sites showed a similar flora to a normal healthy site which remained unaltered throughout the treatment. 1985 Australian Dental Association

The present study was a preliminary histological and immunofluorescent investigation of the edge of the ulcer in acute ulcerative gingivitis. The results of this study show that the lesion is dominated by polymorphonuclear leukocytes, with plasma cells present in the deeper parts. The epithelium on the edge shows widening of the intercellular spaces with destruction of the epithelial cells, accompanied by a heavy infiltrate of PMNs. Both IgG and C3 could be demonstrated between these epithelial cells, although the present study could not establish whether this represented immune complex deposition. The histopathogenesis of AUG therefore seems to involve a PMN infiltration of the epithelium, with subsequent destruction of the epithelium, probably due to the release of hydrolytic enzymes. The presence of the PMNs within the epithelium may involve direct bacterial chemotaxis and/or the activation of complement via the classical or alternative pathways.

SUMMARY: Fusiforms isolated from saliva and gingival debris were allocated on morphological, cultural and biochemical grounds to Fusobacterium nucleatum, F. polymorphum, Leptotrichia buccalis A and L. buccalis B (Hadi & Russell, 1968a). The viable count of such fusiforms increases significantly in both saliva (Hadi & Russell, 1968b) and gingival material (Hadi & Russell, 1969) in cases of acute ulcerative gingivitis (A.U.G.). Few investigations have been made of the nutritional requirements of fusobacteria (Omata, 1953, 1959; Coles, 1968) and no work done on leptotrichiae. The present study was undertaken to determine the vitamin, purine and pyrimidine requirements of oral fusobacteria and leptotrichiae.

A total of 1,179 patients, comprising 737 males and 442 females, with acute ulcerative gingivitis presented at the Stomatological Clinic in Prague during the decade 1958–1967. The relationship between age and season and the incidence of acute ulcerative gingivitis was studied in these subjects. The highest incidence was in females between 16 and 17 years of age and in males 17 to 22 years of age. The incidence in all subjects 15 to 19 years of age was equivalent to 8.3 persons per10,000 inhabitants. The corresponding figures for the age ranges 20–24 and 25–29 were 4.8 and 2.1 respectively. There were three seasonal peaks in incidence. The highest occurred in September and October, the next highest in December and January and the third was in June. The disease was often associated with the common cold.

Humoral antibodies and cell-mediated immunity in patients with acute ulcerative gingivitis were investigated using antigens from Odontomyces(Actinomyces) viscosus, Fusobacterium fusiforme, Veillotiella alcalescens and Bacteroides melaninogenicus. There were no differences in serum antibody levels between patients and control subjects on the first day of attendance and up to one month after the disease started. Serum and salivary IgA estimations failed to show a significant difference between patients and controls. Cell-mediated immunity measured by the lymphocyte transformation test, yielded significantly different results between patients and controls. An immune pathogenesis for acute ulcerative gingivitis has been postulated to account for the immunological findings.

The prevalence of acute ulcerative gingivitis in Nigerian children aged 2–6 years was—Ibadan City 11.7%, Abebeyun 11.7%, Igun 1.7%, Akufo 26.9% and Uboma 12.6%. Two of the 63 individuals with acute ulcerative gingivitis had cancrum oris simultaneously. The age range of the children with acute ulcerative gingivitis was 2 years to 12 years. Seventeen of the 50 houses visited in Ibadan City with children aged 2–6 years had one or more children with acute ulcerative gingivitis. Of the 98 rural households with children aged 2–6 years, 20 had one or more children with acute ulcerative gingivitis. In Ibadan City 73 per cent of the children with acute ulcerative gingivitis lived in a house where another child had the infection.

Quantitative estimations of fusiforms were made on saliva from “normal” subjects and from cases of acute ulcerative gingivitis (A.U.G.). It was found that the mean viable count of fusiforms in saliva of patients with A.U.G. (1.79 × 106 per ml) was significantly higher (P < 0.001) than that found in saliva of “normal” subjects (2.72 × 105 per ml). Fusobacterium nucleatum was predominant in both cases, accounting for about 75 per cent of the total fusiforms. Strain B of Leptotrichia buccalis apparently showed a disproportionate increase in saliva from A.U.G. compared with “normal” conditions (from 1.8 to 7.1 per cent of the total fusiforms).

material from the gingival crevice. J . Periodont. 33:3, July 1962. 16. Hirt , A . , Ansorge, J . , and Markstahler, H . : Luminescenz mikroskepische untersuchungen an der lebenden Frosch und Ratten leben. Die Ausscheidung von Fluorescein und Trypaflavin. Zeikschr. f. Anat. v. Entwicklgesch, Band 109, 1-32, 1939. 17. Krasse, B. and Brill, N . : Effect of consistency of diet on bacteria in gingival pocket in dogs. Odont. Revy. 11:1 52-165, 1960. 18. Krasse, B., and Egelberg, J . : The relative proportions of sodium, potassium, and calcium in gingival pocket fluid. Acta Odont. Scandinav. 20:2, 143152, Tune 1962. 19. Parfitt, G. J . : A five year longitudinal study of the gingival condition of a group of children in England. J . Periodont. 28:1, 26-32, January 1957.

A trial was conducted to compare the effectiveness of povidone iodine and chlorhexidine gluconate with buffered peroxyborate in the treatment of acute ulcerative gingivitis. After 20 patients had entered the trial and 11 had required additional therapy with metronidazole to control their symptoms, the study was terminated. Those patients receiving peroxyborate all showed a satisfactory improvement in clinical signs and symptoms. One patient each receiving povidone iodine or chlorhexidine reported a symptomatic improvement, although gingival ulceration was still apparent at 1 week. The remaining patients all required metronidazole therapy to control their symptoms. Povidone iodine and chlorhexidine gluconate therefore cannot be recommended for the treatment of acute ulcerative gingivitis.

The use of nitrimidazine in the treatment of acute ulcerative gingivitis. A double-blind controlled trial

Study of gingival biopsy specimens from patients with acute ulcerative gingivitis showed that immune complex formation has no role in the pathogenesis of this disease.

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