Specimens from four regions of oral mucosa (palate, buccal mucosa, lateral border of the tongue, and the floor of the mouth) and of abdominal skin were taken from 58 individuals at autopsy, for determination of permeability constants (Kp) to tritium-labeled water. Comparisons between fresh specimens and those stored at -80 degrees C revealed no significant effect on Kp as a result of freezing; similar results were found with use of specimens from corresponding regions of the pig. Values for Kp were significantly different for all of the tissue regions examined and ranged from 44 +/- 4 x 10(-7) cm/min for skin to 973 +/- 33 x 10(-7) cm/min for the floor of the mouth, which was the most permeable region. Similar differences were evident among corresponding regions of porcine oral mucosa and skin. Moreover, the Kp values obtained for human tissues were not significantly different from those of the pig, except for the floor of the mouth, which was more permeable in human than in pig tissue. The results reveal interesting differences in the permeability of human oral mucosa that might be related to susceptibility to mucosal disease in those conditions where local extrinsic etiological agents are implicated.

These results suggest that short-term exposure to ethanol may act as a permeability enhancer, possibly by causing molecular rearrangement of the permeability barrier, not as a result of lipid extraction.

ABSTRACT:In discussing permeability, we are describing one of the fundamental barrier functions of oral mucosa. Despite assumptions to the contrary, the oral mucosa is not a uniformly, highly permeable tissue like gut, but shows regional variation. The keratinized areas, such as gingiva and hard palate, are least permeable and nonkeratinized lining areas are most permeable. This variation appears to reflect differences in the types of lipid making up the intercellular permeability barrier in the superficial layers of the epithelium. Differences in permeability may be related to regional differences in the prevalence of certain mucosal diseases and can be utilized to advantage for local and systemic drug delivery.

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Nineteen pieces of muco‐gingival tissue from man and monkey were examined by histological and histochemical methods. Neither a surface groove nor a change from keratinisation to non‐keratinisation were consistently seen in all specimens; the differing elastic tissue content of the gingiva and alveolar mucosa was therefore used to define the muco‐gingival junction. The surface groove, the keratinisation pattern, the distribution of hydrolytic enzymes and the glycogen content have been related to this junction. The gingiva and alveolar mucosa meet without a gradual transition zone suggesting that an intrinsic difference exists between them. This junction provides a useful model system for the examination of epithelial‐connective tissue interrelationships.

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This study examined the reaction of the local vasculature of the oral mucosa in 16 Sprague Dawley rats receiving systemic nicotine delivered (1.5 mg/kg/day) via subcutaneous minipumps for 24 h or 2wk. Control animals received saline. After treatment animals were killed and biopsies taken from palate, maxillary gingiva and buccal mucosa, frozen and cryostat sections incubated to demonstrate alkaline phosphatase, which is a capillary marker. The total length of the capillary fragments in the nicotine treated groups was significantly less than of the control group. There was also a decrease in capillary height in both of the nicotine groups when compared to the control animals. This study indicates that morphologic alterations occur in the microvasculature of the oral mucosa following systemic nicotine administration. This may have implications for the role of chronic tobacco use in the etiology of oral mucosal disease, including periodontal disease.