IADR Abstract Archives
Effect of Smoking on Immunological and Bacterial Parameters in Periodontitis
Objectives: Smoking was identified as major risk factor in the initiation and progression of periodontitis. However, there is only limited evidence on the effect of smoking on the activity of PMN released collagenase. Aim of this cross-sectional study was to investigate the influence of smoking on aMMP-8 concentration in gingival crevicular fluid and to correlate microbiological, immunological and clinical parameters in patients with periodontitis.
Methods: Thirty participants with no signs of gingival inflammation and no periodontal attachment loss served as controls (including n=15 smoker: >10 cigarettes/d; > 4 pack/years) and n=30 patients with generalized severe chronic periodontitis (incl. also n=15 smoker) formed the test group. From all individual were GCF samples collected either from (i) the mesio-buccal site of the first molar of each quadrant (controls) or from (ii) the deepest pocket of each quadrant (test). ELISA was used to measure immunological parameters (aMMP-8, IL-1ß, IL-4, IL-6, IL-8, IL-10, TNF-α/ß) and PCR was performed to analyse periodontopathogens, including Filifactor alocis. Statistical analysis included Kruskal-Wallis H-test, Mann-Whitney U-test, and regression analysis.
Results: The GCF concentration of aMMP-8 allows discrimination between periodontitis and periodontal health (35.73±25.31 ng/µl vs. 10.80±7.11 ng/µl, p<0.05). There were no statistical differences within the groups (smoking vs. non-smoking) regarding aMMP-8 level. While in periodontal health pro-and anti-inflammatory cytokines were depressed (significant lesser concentrations of IL-1ß, IL-6, IL-8, and IL-10 in periodontal healthy smoker than in non-smoker; p<0.05), this effect was not measurable in periodontitis patients. Filifactor alocis was more frequent measured in periodontitis patients who smoked, but it was never detected in periodontal healthy subjects.
Conclusions: Smoking has no effect on aMMP-8 concentration in GCF. In periodontal health, smoking may suppress host defence. Once a periodontitis occur, this effect may abrogate. Filificator alocis seems to be strongly associated with the aetiopathogenesis of periodontitis, especially in smoker.
Methods: Thirty participants with no signs of gingival inflammation and no periodontal attachment loss served as controls (including n=15 smoker: >10 cigarettes/d; > 4 pack/years) and n=30 patients with generalized severe chronic periodontitis (incl. also n=15 smoker) formed the test group. From all individual were GCF samples collected either from (i) the mesio-buccal site of the first molar of each quadrant (controls) or from (ii) the deepest pocket of each quadrant (test). ELISA was used to measure immunological parameters (aMMP-8, IL-1ß, IL-4, IL-6, IL-8, IL-10, TNF-α/ß) and PCR was performed to analyse periodontopathogens, including Filifactor alocis. Statistical analysis included Kruskal-Wallis H-test, Mann-Whitney U-test, and regression analysis.
Results: The GCF concentration of aMMP-8 allows discrimination between periodontitis and periodontal health (35.73±25.31 ng/µl vs. 10.80±7.11 ng/µl, p<0.05). There were no statistical differences within the groups (smoking vs. non-smoking) regarding aMMP-8 level. While in periodontal health pro-and anti-inflammatory cytokines were depressed (significant lesser concentrations of IL-1ß, IL-6, IL-8, and IL-10 in periodontal healthy smoker than in non-smoker; p<0.05), this effect was not measurable in periodontitis patients. Filifactor alocis was more frequent measured in periodontitis patients who smoked, but it was never detected in periodontal healthy subjects.
Conclusions: Smoking has no effect on aMMP-8 concentration in GCF. In periodontal health, smoking may suppress host defence. Once a periodontitis occur, this effect may abrogate. Filificator alocis seems to be strongly associated with the aetiopathogenesis of periodontitis, especially in smoker.