Abstract

Noma (cancrum oris) is a gangrenous disease of unknown etiology affecting the maxillo-facial region of young children in extremely limited resource countries. In an attempt to better understand the microbiological events occurring during this disease, we used phylogenetic and low-density microarrays targeting the 16S rRNA gene to characterize the gingival flora of acute noma and acute necrotizing gingivitis (ANG) lesions, and compared them to healthy control subjects of the same geographical and social background. Our observations raise doubts about Fusobacterium necrophorum, a previously suspected causative agent of noma, as this species was not associated with noma lesions. Various oral pathogens were more abundant in noma lesions, notably Atopobium spp., Prevotella intermedia, Peptostreptococcus spp., Streptococcus pyogenes and Streptococcus anginosus. On the other hand, pathogens associated with periodontal diseases such as Aggregatibacter actinomycetemcomitans, Capnocytophaga spp., Porphyromonas spp. and Fusobacteriales were more abundant in healthy controls. Importantly, the overall loss of bacterial diversity observed in noma samples as well as its homology to that of ANG microbiota supports the hypothesis that ANG might be the immediate step preceding noma.

Highlights

  • Noma, known as cancrum oris, is a gangrenous disease that typically affects soft as well as hard tissues of the maxillo-facial region

  • In an attempt to better understand the etiology of noma, the authors of the study used microarrays to assess the bacterial microbiota of gingival fluids sampled from 413 healthy and diseased children

  • Results obtained show reduced bacterial diversity and abundance in samples obtained from diseased patients compared to samples obtained from healthy donors, sharing identical social situation

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Summary

Introduction

Known as cancrum oris, is a gangrenous disease that typically affects soft as well as hard tissues of the maxillo-facial region. In 1998, the World Health Organization estimated a global yearly incidence of 140,000 cases [2], but the exact prevalence of the disease is not really known due to distance of villages from medical centers in numerous countries affected by noma. Falkler [10] suggested that multiple factors such as malnutrition, weakened immune functions and prior viral infections (measles, Herpesviridae), all worsened by poor oral hygiene, could play in unison to reduce host resistance and promote the development of oral ulcers. These lesions would serve as entry sites for the microorganism(s) responsible for the disease. Potential bacterial candidates include Fusobacterium necrophorum and Prevotella intermedia [10,11,12,13]

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