There is evidence for synergy between tobacco and alcohol in the etiology of oral cancer but the reason for such an effect is unclear. One possible explanation is that alcohol enhances the penetration of carcinogens through the oral lining. We measured the permeability in vitro of three regions of porcine oral mucosa to the tobacco associated carcinogen, nitrosonornicotine (NNN) alone and in the presence of 5% or 50% ethanol. 50% ethanol did not significantly alter the permeability of oral mucosa to NNN except for buccal mucosa, where it was reduced. However, there was a significant increase in the permeability of gingiva and floor of mouth mucosa (but not buccal mucosa) in the presence of 5% ethanol; this increase occurred after far shorter exposures for floor of mouth than for gingiva. These results accord well with studies showing (a) that the Door of mouth is a “high risk area” for oral carcinoma and (b) that there is an increased relative risk of oral cancer for heavy smokers and drinkers and, in particular, for those individuals who consume beverages with a low alcohol content.
The permeability of porcine skin and keratinized and nonkeratinized oral mucosa to tritium-labeled water and horseradish peroxidase (HRPO) was determined using perfusion chambers. Small blocks from each tissue were also incubated with HRPO and the extent of penetration visualized microscopically; this enabled measurements to be made of the thickness of the permeability barrier to this water-soluble tracer. Results obtained after inverting the oral mucosa in the chambers or adding metabolic inhibitors indicated that both compounds diffuse across the tissue. The permeability constants derived directly in the study showed that skin was less permeable than oral mucosa and that the floor of the mouth was significantly more permeable than all other regions. When these constants were normalized in terms of a standard permeability barrier thickness and the different tissues compared, the values obtained for skin were again less than those of the oral regions but, of these, the buccal mucosa was significantly higher. The difference in permeability between epidermis and keratinized oral epithelium may be due to differences in the volume density of membrane-coating granules known to exist between the tissues; differences between the oral mucosal regions may reflect differences in the nature of the intercellular barrier material.
The gingival overgrowth obtained after maintaining ferrets on PHT appeared to be due entirely to the effect of the drug, for inflammation induced by banding had no influence on the action of PHT in eliciting the overgrowth. The significant change observed was an increase in relative volume of interstitial material (ground substance) in response to PHT. Although there was no appreciable alteration in numbers of cells present in the lesion, PHT had a significant effect on the ultrastructure of fibroblasts. These cells showed a decrease in the relative volume of phagosomes, although organelles concerned with synthesis (the rough endoplasmic reticulum and Golgi zones) were not affected. This suggests that the relative increase in ground substance may reflect decreased breakdown of extracellular material within fibroblasts, while synthetic activity is maintained at a constant level. As a consequence, there is an increase in connective tissue volume--an increase which is manifested as an overgrowth.
An epithelial hyperplasia is one of the reactions of skin and oral mucosa to chemical and mechanical insult. It is usually assumed that this reaction produces a more effective epithelial harrier, but there is no information as to whether a less permeable (issue results. To examine this question, hyperplasia was induced in the cheek pouches of hamsters by either chemical treatment with 0.0025% TPA in acetone or by mechanical abrasion with a rotating mop; untreated hamsters served as controls. The animals were killed and the cheek pouches were removed, mounted in diffusion chambers and the permeability to labelled water and horseradish peroxidase (IIRPO) determined. The results showed that higher values were obtained for the permeability constant of hyperplastic epithelia than for that of control tissue, suggesting that an increased epithelial thickness is not necessarily associated with an improved permeability barrier function. The presence of an inferior barrier layer in hyperplastic epithelia may be related to the increased rate of turnover of this tissue.
This study examined the effects of chlorhexidine (CHD) on the clinical appearance, morphology, and in vitro permeability of hamster cheek pouch mucosa. The cheek pouches were treated daily for 3 weeks with topical applications of saline, 0.2% CHD, or 2.0% CHD. Treatment with 2.0% CHD resulted in the formation of discrete white lesions in every animal in the group, whereas no changes were identified in any animal treated with 0.2% CHD or saline. Upon microscopic examination it was determined that treatment with 2.0% CHD resulted in a statistically significant (P less than 0.01) increase in epithelial thickness, when compared to the other groups, and the lesions were found to consist of hyperplastic areas of epithelium with associated inflammatory cell accumulations. Daily treatments with 2.0% CHD, 0.2% CHD or saline had no effect on the very low permeability of cheek pouch mucosa to 14C-CHD. However, treatment with 2.0% CHD resulted in decreased permeability to 3H2O (P less than 0.05) when compared to the other groups. Treatment with 2.0% CHD also resulted in a thickened permeability barrier (P less than 0.01), as determined using a tracer, horseradish peroxidase. It is concluded that topical applications of 0.2% T CHD have no detectable effect on cheek-pouch mucosa while applications of 2.0% CHD result in hyperplasia and a decrease in mucosal permeability. Our results suggest that CHD should be used with caution clinically and at a concentration of 0.2% or less.
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