Bionutrition and Oral Cancer in Humans

Enwonwu, Cyril O.; Meeks, Valli

doi:10.1177/10454411950060010401

Cited by 67 publications

(42 citation statements)

References 119 publications

(144 reference statements)

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“…Additionally, the plasma zinc levels found in the children with noma (Table 3) were in the range usually associated with biochemical and clinical alterations resulting from zinc depletion. 45 Some reports have examined the cellular and molecular effects of nutrient deficiencies, 56 particularly with reference to diseases of the oral cavity; 57,58 therefore, these will not be detailed here. Vitamin A and zinc deficiencies in the human are characterized by diminished cell-mediated immunity, as well as an early breakdown in the integrity of epithelial tissues, including pathologic alterations of the oral mucosa.…”

Section: Discussionmentioning

confidence: 99%

Pathogenesis of cancrum oris (noma): confounding interactions of malnutrition with infection.

Enwonwu¹,

Falkler²,

Idigbe³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

107

129

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Abstract. This study showed that impoverished Nigerian children at risk for cancrum oris (noma) had significantly reduced plasma concentrations of zinc (Ͻ 10.8 mol/L), retinol (Ͻ 1.05 mol/L), ascorbate (Ͻ 11 mol/L), and the essential amino acids, with prominently increased plasma and saliva levels of free cortisol, compared with their healthy counterparts. The nutrient deficiencies, in concert with previously reported widespread viral infections (measles, herpesviruses) in the children, would impair oral mucosal immunity. We postulate, subject to additional studies, that evolution of the oral mucosal ulcers including acute necrotizing gingivitis to noma is triggered by a consortium of microorganisms of which Fusobacterium necrophorum is a key component. Fusobacterium necrophorum elaborates several dermonecrotic toxic metabolites and is acquired by the impoverished children via fecal contamination resulting from shared residential facilities with animals and very poor environmental sanitation.

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Section: Discussionmentioning

confidence: 99%

Pathogenesis of cancrum oris (noma): confounding interactions of malnutrition with infection.

Enwonwu¹,

Falkler²,

Idigbe³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

107

129

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“…127,128 These data suggest that low BMI may be a biomarker of chronic nutritional deficiencies secondary to chronic alcohol and tobacco use, at least in developed countries. 130 In the IARC Multinational case-control study, risk of oral cancer increased with declining tertiles of BMI in neversmokers and ever-smokers as well as in neverdrinkers and ever-drinkers. 103 In comparison to the studies noted above, a large proportion of the IARC study population was enrolled from developing countries where chronic nutritional deficiency states may be independent of alcohol and tobacco consumption.…”

Section: Diet and Body Mass Indexmentioning

confidence: 99%

Current topics in the epidemiology of oral cavity and oropharyngeal cancers

2007

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Oral cancer incidence rates rose dramatically during the twentieth century in the United States and Europe, especially among individuals under the age of 60 years. Although influenced by age, sex, and country of origin, incidence trends were most strongly affected by elevated risk among individuals born after approximately 1915. This cohort effect was indicative of strong behavioral influences on oral cancer risk. In this article, associations between oral cancer risk and established behavioral risk factors including alcohol and tobacco use are reviewed. Additionally, possible associations between oral cancer risk and oral hygiene, diet, nutritional status, and sexual behavior as well as the influence of genetic factors on oral cancer risk are considered. Special emphasis is placed on evaluating possible risk differences in individuals above and below the age of 45 and in users and nonusers of alcohol and tobacco. Oral squamous cell carcinomas arise from several anatomic sites within the oral cavity and oropharynx, but most commonly from the oral, mobile tongue.1 In the 1980s, 2 cancer centers in the United States (U.S.) reported an increase in the proportion of incident oral tongue cancers diagnosed in men younger 40 years.2,3 Although absolute numbers had increased, these reports provided no real evidence of rising incidence. Shortly thereafter, however, a significant 2-fold increase in oral tongue cancer mortality rates between 1950 and 1982 was reported in the U.S. for men younger than 30 years. 4 This finding was corroborated by a study in Scotland. 5 Further analysis of the Scottish data revealed that the increase in incidence was not restricted to those younger than 40 but extended to all age groups less than 65 years of age born after 1920-a strong ''cohort effect.'' The cohort effect was indicated by a strong effect of year of birth on oral cancer incidence rates. A flurry of research on global changes in oral cancer incidence was stimulated by these reports.

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“…Antioxidants have induced regression of precancerous oral lesions including leukoplakia (Enwonwu & Meeks, 1995), suggesting that ROS are involved in the pathogenesis of precancerous lesions. ROS are considered to participate in carcinogenesis by forming oxidative DNA lesions, such as 8-oxodG (Kawanishi et al, 2001;Kawanishi et al, 2002).…”

Section: Leukoplakia Oral Lichen Planus and Oral Cancermentioning

confidence: 99%