BACKGROUND: The association between smoking and periodontal disease is well established; however, the mechanism by which smoking augments the destruction of periodontal tissue is not clear. We hypothesize that smoking is related to an increased expression of receptor of advanced glycation end products (RAGE) in gingival tissues of smokers. METHODS: Gingival biopsies from five smokers and five age- and gender-matched non-smokers were examined. In addition, gingival epithelial cells (GECs) were reacted with 1 muM nornicotine for 4, 16, 24, and 48 hours for mRNA for RAGE and an additional 72 hours for protein expression. RAGE mRNA was amplified by reverse transcriptase-polymerase chain reaction (RT-PCR), and expression of RAGE at the protein level in GECs was studied with Western blots. RESULTS: In the gingival biopsies from all 10 subjects, RT-PCR with RAGE-specific primers produced a band of the predicted size. For all pairs, the smoker biopsies expressed a greater level of RAGE compared to the matched non-smokers. When viewed as groups, analysis of the band intensity indicated that RAGE mRNA in smokers was approximately 1.4-fold of the expression in non-smokers (Wilcoxon test; P = 0.031). In GECs treated with nornicotine, there was a time-dependent increase in RAGE expression up to two-fold at 48 hours. RAGE protein levels initially were reduced but increased to 1.4-fold after 48 hours. CONCLUSION: The ability of nornicotine to elevate RAGE expression in GECs, along with increased RAGE expression in inflamed gingival tissue from smokers, indicates that RAGE may be associated with periodontal disease linked to smoking.
BACKGROUND: The association between smoking and periodontal disease is well established; however, the mechanism by which smoking augments the destruction of periodontal tissue is not clear. We hypothesize that smoking is related to an increased expression of receptor of advanced glycation end products (RAGE) in gingival tissues of smokers. METHODS: Gingival biopsies from five smokers and five age- and gender-matched non-smokers were examined. In addition, gingival epithelial cells (GECs) were reacted with 1 muMnornicotine for 4, 16, 24, and 48 hours for mRNA for RAGE and an additional 72 hours for protein expression. RAGE mRNA was amplified by reverse transcriptase-polymerase chain reaction (RT-PCR), and expression of RAGE at the protein level in GECs was studied with Western blots. RESULTS: In the gingival biopsies from all 10 subjects, RT-PCR with RAGE-specific primers produced a band of the predicted size. For all pairs, the smoker biopsies expressed a greater level of RAGE compared to the matched non-smokers. When viewed as groups, analysis of the band intensity indicated that RAGE mRNA in smokers was approximately 1.4-fold of the expression in non-smokers (Wilcoxon test; P = 0.031). In GECs treated with nornicotine, there was a time-dependent increase in RAGE expression up to two-fold at 48 hours. RAGE protein levels initially were reduced but increased to 1.4-fold after 48 hours. CONCLUSION: The ability of nornicotine to elevate RAGE expression in GECs, along with increased RAGE expression in inflamed gingival tissue from smokers, indicates that RAGE may be associated with periodontal disease linked to smoking.