Impact of Smoking on the IL-1Β, IL-8, IL-10, IL-17 and TNF-α Production in Chronic Periodontitis Patients

Background: Cigarette smoking is a significant risk factor in the pathogenesis and progression of periodontal disease, leading to an increase in periodontal tissue destruction as a consequence of altered production of cytokines, inflammatory markers and host-cell function. Objectives: The purpose of the present investigation is to study the serum cytokine profile in chronic periodontitis subjects and the influence of cigarette smoking on the serum levels of cytokines. Subjects and Methods: Sixty subjects with chronic periodontitis (30 smokers and 30 non-smokers) and 30 healthy control individuals participated in this study. Serum samples separated from the whole blood of patients and healthy individuals. The levels of cytokines were determined by an enzyme-linked immunosorbent assay. Results: The study showed statistically significant elevation in levels of IL-1β, IL-8 and IL-17 in chronic periodontitis patients compared to healthy control (p<0.001). Moreover, the IL-1β, IL-8 and IL-17 levels were also significantly higher in smokers than non-smokers patients (p<0.05). On the other hand, there are no significant differences in levels of IL-10 and TNF-α between patients and healthy controls and nor between smokers and non-smokers (p>0.05). Concussion: The present findings suggest that serum levels of IL-1β, IL-8 and IL-17 reflect the activity of periodontal destruction, as well as the enhanced production of these inflammatory cytokines (IL-1β and IL-17) and chemokin (IL-8) in the presence of smoking may have clinical consequences. Thus these results could be one of several explanations why smoking aggravates periodontitis.