A histological analysis of the early effects of alcohol and tobacco usage on human lingual epithelium

Abstract

Macroscopically normal tongues were examined from 161 necropsies. Two types of lingual epithelium were investigated by morphometry and the results were statistically analysed in relation to known levels of alcohol and tobacco usage in each case. Alcohol and tobacco were each associated with a reduction in epithelial thickness brought about by a reduction in the maturation layer due mainly to cell shrinkage By contrast, the progenitor layer increased in size, due to hypertrophy rather than hyperplasia Changes occurred in each type of epithelium and were more severe with alcohol. There was no significant interaction between alcohol and tobacco. The structural changes appeared to be non‐specific reactions to local toxic effects of alcohol and tobacco. They could, if accompanied by equivalent functional decrements, indicate an increased vulnerability to carcinogens, whether or not these derive from alcoholic drinks or tobacco smoke.

Exploring the mechanisms of alcohol-related damage in oral mucosa – is oxidative stress associated with the increase in cell proliferation in rat tongue epithelium?

“…This finding differs from those reported in previous studies, which found higher proliferative activity in the suprabasal layer cells of dorsal tongue epithelium (Valentine et al, 1985;Maier et al, 1994;Maito et al, 2003;Carrard et al, 2004). This difference could be explained by the models used (rats instead of mice), since different animal models appear to have differential sensitivity to alcohol (Tabakoff & Hoffman, 2000).…”

“…This finding corroborates the results of studies that found an increased cell proliferation in the tongue epithelium of mice after longer intake periods (Maito et al, 2003;Carrard et al, 2004). Valentine et al (1985) found an increase in the thickness of the proliferative compartment of the tongue epithelium in humans that usually consume alcohol.…”

“…Several studies support evidence that cell proliferation increases in oral epithelium after chronic alcohol intake (Valentine et al, 1985;Maier et al, 1994;Maito et al, 2003;Carrard et al, 2004). However, the exact mechanism implicated in such an increase is yet to be investigated (Wight & Ogden, 1998;Carrard et al, 2004;Goldstein et al, 2010).…”

“…Clearly, alcohol consumption results in lower Nrf2 immunocontent, which is potentially noxious to cell function. Considering these findings, decrease in epithelial keratinization and/ or differentiation observed by Valentine et al (1985) due to alcohol consumption could probably be explained by Nrf2 decrease.…”

“…In these situations, ROS can react with and damage complex cellular molecules such as lipids, proteins, and DNA (Wu et al, 2006). This phenomenon could be one of the mechanisms associated with the alcohol-mediated increase in cell proliferation rates (Valentine et al, 1985;Maito et al, 2003;Carrard et al, 2004) as well as the risk of oral cancer attributed to alcohol (Guyton & Kensler, 1993;Klaunig & Kamendulis, 2004). A previous study (Carrard et al, 2009) suggested that even a short term exposure to alcohol induced biochemical disturbances in oral mucosa of rats.…”