Influence of smoking on gingival crevicular fluid interleukin 1β and interleukin-8 in patients with severe chronic periodontitis among a Rural Population in India

Abstract

Background and Objective: Smoking is widely prevalent among rural Indian populations. Smoking is considered a significant risk factor for periodontal diseases. The aim of the present study was to evaluate the influence of smoking on the inflammatory cytokines interleukin (IL) IL-1β and IL-8 in gingival crevicular fluid (GCF) and compare these between smokers and nonsmokers with periodontitis in diseased and healthy sites. Materials and Methods: A total of thirty patients with severe chronic periodontitis (15 smokers and 15 nonsmokers) participated in this study. Clinical parameters assessed were gingival index, bleeding on probing, probing depth (PD), and clinical attachment level. One diseased and one healthy site from each of the periodontitis patients were selected for GCF collection and assigned to the following four groups: healthy sites in smoker (SH), diseased sites in smoker (SD), healthy sites in nonsmoker (NH), and diseased sites in nonsmoker (ND) and were analyzed by enzyme-linked immunosorbent assay test (Quantikine ® ). Results: Intragroup comparisons revealed statistically significant levels of IL-1β in ND sites compared to NH sites ( P < 0.005) and SD sites showed statistically significantly higher levels of IL-1β compared to SH sites ( P < 0.0001). However, there was no significant difference in IL-8 levels between NH and ND sites as well as between SH and SD sites. Intergroup comparisons revealed that SH sites exhibited significantly lower amounts of IL-8 ( P < 0.01) compared to NH sites and SD sites showed significantly lower levels of IL-8 compared to ND sites ( P < 0.001). However, the comparison of NH and SH sites as well as ND and SD sites showed no significant difference in the levels of IL-1β. Conclusions: Cytokine levels were significantly elevated in periodontitis patients. Smokers exhibited a decrease in IL-8 and increase in IL-1β levels. Hence, this reflects the influence of smoking on immunosuppression and its role in the pathogenesis of periodontal disease.

A double‐blind randomized clinical trial of inflammatory cytokine and pepsin levels in the saliva of patients with voice prostheses

“…28 IL-1β is considered a biomarker of periodontitis. 29,30 Research also show an increase in level of this cytokine in saliva of smokers comparing to non-smokers. 31,32 Studies indicate also that salivary IL-1β levels increase in oral Streptococcus mutans colonization, 33 which are also likely to colonize the VPs.…”

A scope systematic review to clarify immune response to tobacco in Buerger

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Fenotipo periodontal en pacientes tabáquicos. Revisión de la literatura

“…Desde un punto de vista anatómico, la encía interproximal es más gruesa que la encía vestibular; en un estudio cuyo objetivo fue evaluar el grosor gingival mediante sondaje transgingival en fumadores y no fumadores, se observó que las áreas vestibulares como las interproximales eran más gruesas entre los fumadores en comparación con los no fumadores 14 . Varios factores han sido atribuidos al aumento del espesor gingival en fumadores; los estudios han sugerido que la nicotina aumenta la tasa de proliferación del epitelio gingival, aumentando así el espesor del epitelio entre los fumadores; esto podría explicarse por el hecho de que el tabaquismo conduce a una disminución de la densidad vascular y reduce por consiguiente, el área de la luz de los vasos gingivales provocando vasoconstricción en los vasos sanguíneos periféricos aumentando así en el espesor del epitelio gingival [14][15][16][17][18] . Fumar por un tiempo menor a 5 años es asociado con grosor gingival delgado (1.5 y 2 mm), mientras que pasado los 5 años se puede observar más asociación con un grosor gingival mayor a 2 mm 19, 20 .…”