Comparison of IL-1β, TNF-α, hBD-2, and hBD-3 Expression in the Dental Pulp of Smokers Versus Nonsmokers

J Endod. 2017 Dec;43(12):2009-2013. doi: 10.1016/j.joen.2017.08.017. Epub 2017 Oct 21.

Abstract

Introduction: To date, the endodontic literature lacks research on the effect of smoking on cytokine and defensin expression in the dental pulp. Therefore, the aim of this study was to investigate the expression of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, human beta defensin (hBD)-2 and hBD-3 in the dental pulp of smokers and compare them with nonsmokers. We hypothesized that cytokine and defensin expression would be reduced in smokers as compared with nonsmokers.

Methods: Thirty-two smokers and 37 nonsmokers with endodontic pulpal diagnoses of normal, symptomatic irreversible pulpitis and asymptomatic irreversible pulpitis were included in this cross-sectional study. Samples from pulp chambers were collected and stored in phosphate-buffered saline at -80°C. Luminex was used to measure IL-1β and TNF-α levels. The levels of hBD-2 and hBD-3 were measured using enzyme-linked immunosorbent assay. Marker levels were normalized to protein concentrations and data were analyzed using Kruskal-Wallis test, Mann-Whitney U test, and 2-way analysis of variance (α = 0.05).

Results: Pulpal concentrations of TNF-α and hBD-2 were significantly lower among smokers (P < .01), whereas no significant difference was observed for IL-1β, or hBD-3. Two-way analysis of covariance revealed that smoking status (P < .001), not endodontic diagnosis (pulpal status), significantly affected TNF-α and hBD-2 levels.

Conclusions: This study reported that smokers are immunologically deficient in TNF-α and hBD-2, suggesting that dental pulps of smokers possess limited defense mechanisms, affecting their endodontic prognosis and indicating a cause for their reported inferior outcome.

Keywords: Cytokines; dental pulp; endodontics; human beta defensins; immunology; inflammation; smokers.

Publication types

  • Comparative Study

MeSH terms

  • Adolescent
  • Adult
  • Cross-Sectional Studies
  • Dental Pulp / metabolism*
  • Female
  • Humans
  • Interleukin-1beta / biosynthesis*
  • Male
  • Middle Aged
  • Pulpitis / metabolism*
  • Smoking / metabolism*
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Young Adult
  • beta-Defensins / biosynthesis*

Substances

  • DEFB103A protein, human
  • DEFB4A protein, human
  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha
  • beta-Defensins