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The effect of volatile thiol compounds on permeability of oral mucosa Ng, William Man Fai
Abstract
Cumulative clinical and experimental evidence indicates that volatile sulphur compounds (VSC) the principal components of oral malodour, may play an important role in the pathogenesis of periodontal disease. As their (H₂S and CH₃SH) concentrations in gingival sulci increase with the severity of periodontal involvement, the objective of this investigation is to ascertain if they exert an effect on the permeability of oral mucosa. Permeability determinations were performed on excised porcine sublingual mucosal specimens which consisted of non-keratinized epithelium, basal membrane and connective tissue layers mounted in a two compartment perfusion apparatus. Using radioactive and fluorescent-labelled penetrants, it was found that exposure of the epithelial surface to an atmosphere containing physiological concentrations of both thiols (15 ng H₂S or CH₃SH / ml of 95% air - 5% C0₂) increased the permeability of the mucosa to (³⁵S)-S0₄⁻², (³H)-prostaglandin E₂ (PGE₂) and fluorescein isothiocyanate labelled E. coli lipopolysaccharide (F-LPS). A three hour exposure of the mucosa to H₂S and CH₃SH resulted in a 75% and 103% increase respectively in permeability to (³⁵S)-labelled sulphate ion. Similarly, the mercaptan induced up to a 70% increase in permeability of the mucosa to (³H)-prostaglandin E₂. The magnitude of changes in the permeability were found to depend on duration of exposure to the thiols and to their concentration. Studies using (³⁵S)-H₂S suggest that the observed changes in the tissue permeability are related to the reaction of the thiols with tissue components. In addition, the (³⁵S)-H₂S is capable of perfusing through all three layers of the mucosa at 12.3 ng / cm². In contrast to H₂S , the CH₃SH effect was irreversible in control air / C0₂ environment. This infers that CH₃SH is potentially a more deleterious agent to the tissue barrier. However, its effect can also be reversed by treatment of tissues with 0.22% ZnCl₂ either prior to or after exposure to mercaptan. This suggests that Zn⁺² ion may be useful in preventing the potentially harmful effects of VSC. Fluorescent studies with F-LPS indicate that thiols can also potentiate the penetration of endotoxin. Whereas the fluorescence of the F-LPS in control systems was confined to the superficial epithelial layer in contact with the endotoxin, the CH₃SH- exposed mucosa exhibited fluorescence throughout the epithelial and connective tissue layers. Fluorescent staining of the mucosal specimens with fluorescein diacetate followed by counter staining with ethidium bromide provides evidence of membrane impairment to some cells by CH₃SH. Collectively these observations provide strong experimental evidence that the VSC, products of putrefaction produced in the gingival sulcus by oral microflora, may adversely affect the integrity of the crevicular barrier to deleterious agents and thus contribute to the etiology of periodontal disease.
Item Metadata
Title |
The effect of volatile thiol compounds on permeability of oral mucosa
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
1986
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Description |
Cumulative clinical and experimental evidence indicates that volatile sulphur compounds (VSC) the principal components of oral malodour, may play an important role in the pathogenesis of periodontal disease. As their (H₂S and CH₃SH) concentrations in gingival sulci increase with the severity of periodontal involvement, the objective of this investigation is to ascertain if they exert an effect on the permeability of oral mucosa.
Permeability determinations were performed on excised porcine sublingual mucosal specimens which consisted of non-keratinized epithelium, basal membrane and connective tissue layers mounted in a two compartment perfusion apparatus. Using radioactive and fluorescent-labelled penetrants, it was found that exposure of the epithelial surface to an atmosphere containing physiological concentrations of both thiols (15 ng H₂S or CH₃SH / ml of 95% air - 5% C0₂) increased the permeability of the mucosa to (³⁵S)-S0₄⁻², (³H)-prostaglandin E₂ (PGE₂) and fluorescein isothiocyanate labelled E. coli lipopolysaccharide (F-LPS). A three hour exposure of the mucosa to H₂S and CH₃SH resulted in a 75% and 103% increase respectively in permeability to (³⁵S)-labelled sulphate ion. Similarly, the mercaptan induced up to a 70% increase in permeability of the mucosa to (³H)-prostaglandin E₂. The
magnitude of changes in the permeability were found to depend on duration of exposure to the thiols and to their concentration. Studies using (³⁵S)-H₂S suggest that the observed changes in the tissue permeability are related to the reaction of the thiols with tissue components. In addition, the (³⁵S)-H₂S is capable of perfusing through all three layers of the mucosa at 12.3 ng / cm². In contrast to H₂S , the CH₃SH effect was irreversible in
control air / C0₂ environment. This infers that CH₃SH is
potentially a more deleterious agent to the tissue barrier. However, its effect can also be reversed by treatment of tissues with 0.22% ZnCl₂ either prior to or after exposure to mercaptan.
This suggests that Zn⁺² ion may be useful in preventing the potentially harmful effects of VSC.
Fluorescent studies with F-LPS indicate that thiols can also potentiate the penetration of endotoxin. Whereas the fluorescence of the F-LPS in control systems was confined to the superficial
epithelial layer in contact with the endotoxin, the CH₃SH-
exposed mucosa exhibited fluorescence throughout the epithelial and connective tissue layers. Fluorescent staining of the mucosal specimens with fluorescein diacetate followed by counter staining with ethidium bromide provides evidence of membrane impairment to some cells by CH₃SH. Collectively these
observations provide strong experimental evidence that the VSC, products of putrefaction produced in the gingival sulcus by oral microflora, may adversely affect the integrity of the crevicular barrier to deleterious agents and thus contribute to the etiology of periodontal disease.
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Genre | |
Type | |
Language |
eng
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Date Available |
2010-07-16
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0097012
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.