Effect of tobacco and alcohol consumption on the Langerhans cell population of human lingual epithelium determined using a monoclonal antibody against HLADR.

Tobacco and alcohol consumption are known predisposing factors to the development of oral cancer, though the mechanism by which they act is unclear. The density of Langerhans cells (LC) has been shown to decrease in the uterine cervix of smokers, possibly indicating reduced immune surveillance and increased risk of malignant change. This study examined biopsies of normal human lateral border of tongue taken from 41 necropsies whose histories of tobacco and alcohol consumption were known. LC were identified in fixed, wax-embedded sections using a monoclonal antibody to HLADR and an immunoperoxidase technique. The mean density of LC in smokers of the equivalent of 11 or more cigarettes daily was significantly higher than moderate and non-smokers when counts were expressed per mm epithelial surface and basement membrane length. There were no significant differences in LC numbers in relation to alcohol consumption, age or sex, but there was a significant interaction between tobacco and alcohol. The results suggest that either human oral LC respond to external toxins, or that physical changes in the epithelial barrier induced by such toxins necessitate the presence of more LC to maintain the integrity of the epithelium.