
@Article{,
AUTHOR = {Reshma S. Phillips, Cyril O. Enwonwu, William A. Falkler},
TITLE = {Pro- <i>versus</i> anti-inﬂammatory cytokine proﬁle in African children with acute oro-facial noma (<i>cancrum oris</i>, noma)},
JOURNAL = {European Cytokine Network},
VOLUME = {16},
YEAR = {2005},
NUMBER = {1},
PAGES = {70--77},
URL = {http://www.techscience.com/ECN/v16n1/66239},
ISSN = {1952-4005},
ABSTRACT = {Fresh noma is a severe orofacial necrosis with an astonishingly rapid development. It is seen mainly
in malnourished children less than 4 years old from developing countries. Cytokines play a central role in oral
mucosal inﬂammation. We therefore studied the relevance of circulating cytokines to noma, and the key
microorganisms associated with the lesion. Nigerian village children with acute noma (n=68) and their
neighborhood village (n=63) as well as urban (n=45) counterparts of comparable age and free of overt infections
were evaluated for serum cytokine levels by ELISA. Oral bacteria were studied by polymerase chain reaction.
Evaluation of random cases of the village and noma children showed marked depletion (p<0.05 or 0.001) of the
plasma antioxidant micronutrients (retinol, ascorbic acid, zinc) as well as albumin and blood hemoglobin in the
latter, relative to the former group. Concentrations of the circulating, pro-inﬂammatory cytokines (IL-18, IL-6,
IL-12, IL-8, IFN-γ) and the soluble inhibitors (TNFR-p55, TNFR-p75 and IL-1ra) were signiﬁcantly higher
(p< 0.01 or 0.001) in noma children than in the healthy urban children, but less so when compared to their
neighborhood village counterparts. The increase in levels of the anti-inﬂammatory/regulatory cytokines (IL-4,
IL-10 and TGF-β) was less marked relative to the pro-inﬂammatory cytokines. Bacteria observed at the highest
frequencies in noma lesions were P. intermedia (83%), T. forsythensis (83%), P. gingivalis (50%), C. rectus (50%)
and T. denticola (50%). We conclude that noma is an immunopathological response to potent bacterial factors
resulting in uncontrolled production of cytokines and possibly other, still unknown, inﬂammatory mediators.},
DOI = {}
}



