IADR Abstract Archives
Gingival Fluid Volume and Inflammatory Markers in Cigarette Smokers
Objectives: Gingival crevicular fluid (GCF) is a measurable indicator of gingival tissue inflammation. Our objective was to compare the relation of GCF volume with its content of four selected inflammatory markers between cigarette smokers and non-smokers.
Methods: A total of 41 periodontitis affected individuals (attachment loss =>4 mm on >4 teeth) were selected from a previously evaluated cohort of subjects, 24 current cigarette smokers and 17 non-smokers, all systemically healthy. Plaque index (PI), gingival index (GI), probing depth (PD) and attachment levels (AL) were recorded. GCF was collected for 30 seconds on paper strips from 3 randomly selected sites (PD >4mm) per subject. The levels of interleukin-1b (IL-1b), tumor necrosis factor-alpha (TNFa) and interleukin-8 (IL-8) were determined with Luminex assay. Matrix Metalloproteinase 8 (MMP-8) was determined with standard ELISA assay.
Results: Average (SD) age 55.24 (13.83) years, males 43.90%, Whites 56.10%. GCF volume, PI, GI, PD, AL and levels of all four inflammatory markers were comparable between smokers and non-smokers. Multiple regression analysis was performed to identify markers that associated with GCF volume by smoking status. In non-smokers: prediction of GCF volume in the first regression equation indicated only TNFa (std. beta =0.60, p=0.06). At the next step, the remaining variables were entered as predictors of TNFa. Only one variable, IL-8, emerged as a predictor of TNFa (std. beta =0.79, p=0.04). At the next step the remaining variables were entered as predictors of IL-8. Here, MMP-8 emerged as a reliable predictor (std. beta =0.90, p=0.0008). In the final regression, IL-1b predicted MMP-8 (std. beta =0.56, p=0.02). In smokers: none of the markers showed any association with GCF volume. IL-1b predicted MMP-8 (std. beta =0.86, p=0.0005).
Conclusions: Cigarette smoking does not impact GCF volume and GCF levels of inflammatory markers, however it obscures the relation between GCF volume and its content of inflammatory markers.
Methods: A total of 41 periodontitis affected individuals (attachment loss =>4 mm on >4 teeth) were selected from a previously evaluated cohort of subjects, 24 current cigarette smokers and 17 non-smokers, all systemically healthy. Plaque index (PI), gingival index (GI), probing depth (PD) and attachment levels (AL) were recorded. GCF was collected for 30 seconds on paper strips from 3 randomly selected sites (PD >4mm) per subject. The levels of interleukin-1b (IL-1b), tumor necrosis factor-alpha (TNFa) and interleukin-8 (IL-8) were determined with Luminex assay. Matrix Metalloproteinase 8 (MMP-8) was determined with standard ELISA assay.
Results: Average (SD) age 55.24 (13.83) years, males 43.90%, Whites 56.10%. GCF volume, PI, GI, PD, AL and levels of all four inflammatory markers were comparable between smokers and non-smokers. Multiple regression analysis was performed to identify markers that associated with GCF volume by smoking status. In non-smokers: prediction of GCF volume in the first regression equation indicated only TNFa (std. beta =0.60, p=0.06). At the next step, the remaining variables were entered as predictors of TNFa. Only one variable, IL-8, emerged as a predictor of TNFa (std. beta =0.79, p=0.04). At the next step the remaining variables were entered as predictors of IL-8. Here, MMP-8 emerged as a reliable predictor (std. beta =0.90, p=0.0008). In the final regression, IL-1b predicted MMP-8 (std. beta =0.56, p=0.02). In smokers: none of the markers showed any association with GCF volume. IL-1b predicted MMP-8 (std. beta =0.86, p=0.0005).
Conclusions: Cigarette smoking does not impact GCF volume and GCF levels of inflammatory markers, however it obscures the relation between GCF volume and its content of inflammatory markers.