K Rezavandi1, R M Palmer, E W Odell, D A Scott, R F Wilson. 1. Department of Periodontology and Preventive Dentistry, Guy's, King's and St. Thomas' Schools of Medicine, Dentistry, King's College London, London, UK.
Abstract
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.
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.
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