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Summary Background Fresh noma (cancrum oris) occurs predominantly in children <4 years of age. The key risk factors are poverty, malnutrition and infections. Evolution from an intraoral inflammation to a grotesque oro-facial gangrene is very rapid. Objective We assessed potential relationship between the occurrence of fresh noma and linear growth retardation (LGR) which is prevalent in deprived Third World infants/children between ages 3 and 30 months. LGR is attributed to malnutrition and chronic immunostimulation by environmental antigens. Design Anthropometric evaluation of children (n = 91) with fresh noma, ages 0–8 years, in relation to US National Center for Health Statistics Reference values was carried out. Age-matched noma-free, poor village children (n = 151) from similar communities as noma cases, and elite urban children (n = 132) served as control groups. Heights and weights were measured and the height for age (HAZ), weight for age (WAZ) and weight for height (WHZ) scores calculated as indices of stunting, underweight and wasting respectively. Serum level of interleukin (IL)-18, a multifunctional cytokine, was also measured. Results In the age groups 0–4 and 4–8 years, the percentages of noma children <−2.0SD were 91% and 67% respectively. The corresponding values for the village children were 37% and 24% and significantly different (P < 0.001) from the noma group. Only 7% of the elite children aged 4–8 years were stunted. Low body weight and wasting were prominent features of village and noma groups, but more marked in the latter. Associated with noma was a profound increase (P < 0.001) in IL-18 in comparison with urban controls, and a 34% non-statistically significant increase relative to the village control group. Among other functions, IL-18 induces several pro-inflammatory cytokines and the matrix metalloproteinases, influences long bone growth, and consequently may be relevant to growth retardation seen in poor village children and noma victims. Conclusion These results suggest that occurrence of fresh noma was probably programmed very early in life by malnutrition and chronic infections resulting from replacement of breast milk with contaminated, inferior substitutes. Although not investigated, we speculate that children with fresh noma might also be victims of intrauterine growth retardation as noma is most prevalent during the infantile phase of child growth which starts at mid-gestation and tails off at 4 years.