Abstract

Cigarette smoking and stress are considered risk factors that have been associated with periodontal disease progression. Conflicting results have been reported concerning the direct influence of smoking on the subgingival microbiota of periodontitis patients. Cytokine production may also be influenced by smoking and stress leading to an imbalance that disturbs the host-parasite relationship. The objective of the present study was to evaluate the influence of cigarette smoking on the gingival crevicular fluid (GCF) levels of interleukin (IL)-1beta, IL-4, IL-6 and IL-8 in aggressive or early onset periodontitis (EOP) patients and in healthy controls (H), psychosocial stress being considered as modifying factor. Sixty-five EOP and 35 periodontally healthy individuals participated in this cross-sectional study. All the participants were interviewed about their smoking habits and their stressful social events. Clinical examination included the assessment of plaque index (PI), bleeding on probing (BOP), clinical attachment level (CAL) and probing pocket depth (PPD). GCF was collected using durapore strips, from four sites per patient, randomly selected in each quadrant. The total amounts of IL-1beta, IL-4, IL-6 and IL-8 were measured in a total of 400 samples using commercially available enzyme-linked immunosorbent assays. All clinical parameters were significantly higher in the EOP group compared to the H group. There were no significant differences between EOP smokers and EOP non-smokers with regard to plaque accumulation, CAL and PPD of the sampling sites, whereas mean CAL and PPD of the diseased sites were greater in EOP smokers than in EOP non-smokers. In addition, EOP smokers seemed to have significantly less BOP and greater bone loss compared to EOP non-smokers. Significant interactions between "EOP" and "smoking" were present for total amounts of IL-1beta and IL-4. IL-1beta, IL-6 and IL-8 showed significant main effects with healthy smokers and healthy non-smokers, respectively. For IL-8, stress presented a statistically significant interaction with smoking status and EOP (F=4.742, p=0.030). More specifically EOP smokers were statistically affected by stress. Smoking influences host-related factors including cytokine network. The relative importance of smoking and stress-related alterations and their precise mode of action in increasing the risk of aggressive periodontitis remains to be elucidated.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.