Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2002
Expression of ICAM-1 and E-selectin in gingival tissues of smokers and non-smokers with periodontitis.
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Rezavandi K, Palmer R M, Odell E W, Scott D A, Wilson R F
Аннотация
BACKGROUND: Tobacco smoking affects systemic concentrations of soluble intercellular adhesion molecule (ICAM)-1, but its effect on local expression of adhesion molecules in gingival tissue has not been studied previously.
METHODS: E-selectin and ICAM-1 expression on small blood vessel endothelia in gingival biopsies obtained from smokers (n=17) and non-smokers (n=17) with periodontitis was examined with immunohistochemistry. Blood vessels were identified with monoclonal antibody for von Willebrand's factor.
RESULTS: A significantly larger number of vessels were observed in inflamed tissues of non-smokers than smokers (P<0.05). The number and proportion of vessels expressing both ICAM-1 and E-selectin was greater in sites with inflammation compared to non-inflamed sites in both smokers and non-smokers (P<0.05). The proportion of the total number of vessels expressing ICAM-1 in non-inflamed sites was greater in non-smokers compared with smokers (P<0.05).
CONCLUSIONS: These results suggest that the inflammatory response in smokers with periodontitis may not be accompanied by an equivalent increase in vascularity. Reduced ICAM-1 expression in non-inflamed areas of smokers could reflect a systemic effect of tobacco smoking on ICAM-1 independent of inflammation.
METHODS: E-selectin and ICAM-1 expression on small blood vessel endothelia in gingival biopsies obtained from smokers (n=17) and non-smokers (n=17) with periodontitis was examined with immunohistochemistry. Blood vessels were identified with monoclonal antibody for von Willebrand's factor.
RESULTS: A significantly larger number of vessels were observed in inflamed tissues of non-smokers than smokers (P<0.05). The number and proportion of vessels expressing both ICAM-1 and E-selectin was greater in sites with inflammation compared to non-inflamed sites in both smokers and non-smokers (P<0.05). The proportion of the total number of vessels expressing ICAM-1 in non-inflamed sites was greater in non-smokers compared with smokers (P<0.05).
CONCLUSIONS: These results suggest that the inflammatory response in smokers with periodontitis may not be accompanied by an equivalent increase in vascularity. Reduced ICAM-1 expression in non-inflamed areas of smokers could reflect a systemic effect of tobacco smoking on ICAM-1 independent of inflammation.