Interleukin 1 and receptor antagonist levels in gingival crevicular fluid in heavy smokers versus non‐smokers
Authors: Rawlinson Andrew , Grummitt John M. , Walsh Trevor F. , Ian Douglas C. W. 
Published: March 2003

Background/aims:  This study aimed to investigate the concentration of the cytokine interleukin (IL)‐1β and its receptor antagonist IL‐1ra in gingival crevicular fluid (GCF) in patients with adult periodontitis who were heavy smokers compared with non‐smokers.

Method:  GCF samples were collected from two groups of subjects: smokers and non‐smokers. Thirty‐nine GCF samples were harvested from 13 subjects with moderate to severe adult periodontitis who were heavy smokers. A further 30 GCF samples were harvested from 10 subjects with moderate to severe adult periodontitis who were non‐smokers. Subjects were selected from both genders and none had any relevant systemic illness, were pregnant, had recent medication or had received any periodontal therapy in the preceding 3 months. One deep bleeding site, one deep non‐bleeding site and one healthy site were investigated in each subject. Clinical measurements were recorded for each site, after obtaining a GCF sample using a Periopaper® strip. IL‐1β and IL‐1ra were quantified using new commercially available ELISA kits (Quantikine™), and could be detected in all samples.

Results:  For smokers, the mean concentrations for IL‐1β were 2714.5 (SD 4416.2) pg/µL for healthy sites, 37.0 (SD 57.2) pg/µL for non‐bleeding periodontitis sites and 24.5 (SD 29.2) pg/µL for bleeding periodontitis sites. The concentrations of IL‐1β for non‐smokers for the same category of sites were 393.8 (SD 867.1), 74.2 (SD 107.0) and 73.1 (SD 61.0) pg/µL, respectively. The mean concentrations of IL‐1ra for smokers were 5.8 × 105 (SD 9.7) pg/µL for healthy sites, 2.2 × 105 (SD 0.15) pg/µL for deep non‐bleeding sites and 0.19 × 105 (SD 0.07) pg/µL for deep bleeding sites. The concentrations for non‐smokers were: 4.1 × 1010 (SD 3.8), 18.1 × 105 (SD 20.4) and 3.2 × 105 (SD 2.3) pg/µL, respectively. Significance levels of P < 0.05 were found for comparisons of healthy vs. deep bleeding and deep non‐bleeding sites for IL‐1β and IL‐1ra in smokers, before adjustments for multiple testing. However, none of these comparisons reached statistical significance following adjustments for multiple testing. P < 0.05 for the correlation between IL‐1β and IL‐1ra at healthy sites in smokers only. Differences in GCF concentrations for IL‐1β in smokers vs. non‐smokers were significant for deep bleeding sites only (P < 0.05), the mean concentration of IL‐1β being lower in GCF from smokers vs. non‐smokers. All differences in GCF concentrations of IL‐1ra reached statistical significance for smokers vs. non‐smokers. The mean concentrations of IL‐1ra in GCF were lower in smokers compared with non‐smokers for all categories of sites.

Conclusions:  A decreased concentration of IL‐1β and also IL‐1ra was found in GCF from periodontitis sites compared to healthy sites in smokers and in non‐smokers, although this did not reach statistical significance following adjustments for multiple testing. For comparisons between heavy smokers and non‐smokers, statistically significant differences were found in the GCF concentrations of IL‐1β from deep bleeding sites only. Statistically significant differences were found in the IL‐1ra concentrations for smokers vs. non‐smokers for all categories of sites.