Effect of smoking on gingival crevicular fluid cytokine profile during experimental gingivitis.

摘要

BACKGROUND: Cigarette smoking is a significant risk factor in the pathogenesis of periodontal disease, able to influence both the subgingival microbiota and host responses. AIM: The aim of the present study was to determine the influence of smoking on the amount of IL-1beta, IL-4 and IL-8 in gingival crevicular fluid (GCF) during experimental gingivitis in humans. MATERIAL AND METHODS: Twenty-two healthy subjects, 10 smokers and 12 non-smokers, participated in the study. After professional cleaning, they performed optimal hygiene to reach perfect clinical gingival health. Oral hygiene measures were ceased for a period of 10 days. Clinical indices, including plaque index (PI), gingival index (GI), probing pocket depth (PPD) and bleeding on probing (BOP), were assessed 2 days before (day -2), at the beginning (day 0) and at the end of the experimental gingivitis period (day 10). At the same time, GCF was collected from 12 sites in each patient, by means of durapore filter membranes. Total amounts of IL-1beta, IL-4 and IL-8 were determined by enzyme-linked immunoadsorbent assay. RESULTS: Clinical data revealed that both smokers and non-smokers showed an increase in PI, GI and BOP scores during the experiment. Although no differences were noted with regard to PI at day 10, the GI and BOP were significantly less pronounced in smokers than non-smokers (p < 0.005). Non-smokers showed higher total amounts of IL-4 but lower amounts of IL-8 than smokers, throughout the experiment. Total amounts of IL-1beta and IL-8 increased significantly during plaque accumulation in both groups. IL-4 remained stable for the smoker group and decreased for the non-smoker group. CONCLUSIONS: The present results indicate that smoking interferes with cytokine production. When performing studies regarding the pathogenesis of periodontitis, the smoking status of the participants needs to be taken into consideration.