Influence of smoking on gingival crevicular fluid cytokines in severe chronic periodontitis

Keelen D. Tymkiw, Daniel H. Thunell, Georgia K. Johnson, Sophie Joly, Kindra K. Burnell, Joseph E. Cavanaugh, Kim A. Brogden, Janet M. Guthmiller

Research output: Contribution to journalArticle

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Abstract

Aim: The aim of this study was to compare the expression of 22 chemokines and cytokines in gingival crevicular fluid (GCF) from smokers and non-smokers with periodontitis and periodontally healthy control subjects. Materials and Methods: Forty subjects with generalized severe chronic periodontitis (20 smokers and 20 non-smokers) and 12 periodontally healthy control subjects participated in this study. Four diseased and two healthy sites were selected from each of the periodontitis subjects. GCF samples were collected and cytokines analysed utilizing a multiplexed immunoassay (Luminex Â). Statistical analyses employed non-parametric tests including the Mann-Whitney and Wilcoxon matched-pairs signed-rank tests. Results: Compared with healthy control subjects, GCF in subjects with chronic periodontitis contained significantly higher amounts of interleukin (IL)-1α, IL-1β, IL-6, IL-12(p40) (pro-inflammatory cytokines); IL-8, macrophage chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, regulated on activation normal T-cell expressed and secreted (RANTES) (chemokines); IL-2, IFN-Î, IL-3, IL-4 (Th1/Th2 cytokines); IL-15 [regulator of T-cells and natural killer (NK) cells]. Smokers displayed decreased amounts of pro-inflammatory cytokines [IL-1α, IL-6, IL-12(p40)], chemokines (IL-8, MCP-1, MIP-1, RANTES), and regulators of T-cells and NK cells (IL-7, IL-15). Conclusions: Periodontitis subjects had significantly elevated cytokine and chemokine profiles. Smokers exhibited a decrease in several pro-inflammatory cytokines and chemokines and certain regulators of T-cells and NK-cells. This reflects the immunosuppressant effects of smoking which may contribute to an enhanced susceptibility to periodontitis.

Original languageEnglish (US)
Pages (from-to)219-228
Number of pages10
JournalJournal of Clinical Periodontology
Volume38
Issue number3
DOIs
StatePublished - Mar 1 2011

Fingerprint

Gingival Crevicular Fluid
Chronic Periodontitis
Smoking
Chemokines
Cytokines
Periodontitis
T-Lymphocytes
Interleukin-1
Natural Killer Cells
Macrophage Inflammatory Proteins
Interleukin-15
Healthy Volunteers
Interleukin-12
Interleukin-8
Interleukin-6
Macrophages
Interleukin-7
Interleukin-3
Immunosuppressive Agents
Immunoassay

Keywords

  • chronic periodontitis
  • gingival crevicular fluid
  • immune response
  • periodontal disease
  • periodontitis/aetiology
  • smoking

ASJC Scopus subject areas

  • Periodontics

Cite this

Influence of smoking on gingival crevicular fluid cytokines in severe chronic periodontitis. / Tymkiw, Keelen D.; Thunell, Daniel H.; Johnson, Georgia K.; Joly, Sophie; Burnell, Kindra K.; Cavanaugh, Joseph E.; Brogden, Kim A.; Guthmiller, Janet M.

In: Journal of Clinical Periodontology, Vol. 38, No. 3, 01.03.2011, p. 219-228.

Research output: Contribution to journalArticle

Tymkiw, KD, Thunell, DH, Johnson, GK, Joly, S, Burnell, KK, Cavanaugh, JE, Brogden, KA & Guthmiller, JM 2011, 'Influence of smoking on gingival crevicular fluid cytokines in severe chronic periodontitis', Journal of Clinical Periodontology, vol. 38, no. 3, pp. 219-228. https://doi.org/10.1111/j.1600-051X.2010.01684.x
Tymkiw, Keelen D. ; Thunell, Daniel H. ; Johnson, Georgia K. ; Joly, Sophie ; Burnell, Kindra K. ; Cavanaugh, Joseph E. ; Brogden, Kim A. ; Guthmiller, Janet M. / Influence of smoking on gingival crevicular fluid cytokines in severe chronic periodontitis. In: Journal of Clinical Periodontology. 2011 ; Vol. 38, No. 3. pp. 219-228.
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abstract = "Aim: The aim of this study was to compare the expression of 22 chemokines and cytokines in gingival crevicular fluid (GCF) from smokers and non-smokers with periodontitis and periodontally healthy control subjects. Materials and Methods: Forty subjects with generalized severe chronic periodontitis (20 smokers and 20 non-smokers) and 12 periodontally healthy control subjects participated in this study. Four diseased and two healthy sites were selected from each of the periodontitis subjects. GCF samples were collected and cytokines analysed utilizing a multiplexed immunoassay (Luminex {\^A}). Statistical analyses employed non-parametric tests including the Mann-Whitney and Wilcoxon matched-pairs signed-rank tests. Results: Compared with healthy control subjects, GCF in subjects with chronic periodontitis contained significantly higher amounts of interleukin (IL)-1α, IL-1β, IL-6, IL-12(p40) (pro-inflammatory cytokines); IL-8, macrophage chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, regulated on activation normal T-cell expressed and secreted (RANTES) (chemokines); IL-2, IFN-{\^I}, IL-3, IL-4 (Th1/Th2 cytokines); IL-15 [regulator of T-cells and natural killer (NK) cells]. Smokers displayed decreased amounts of pro-inflammatory cytokines [IL-1α, IL-6, IL-12(p40)], chemokines (IL-8, MCP-1, MIP-1, RANTES), and regulators of T-cells and NK cells (IL-7, IL-15). Conclusions: Periodontitis subjects had significantly elevated cytokine and chemokine profiles. Smokers exhibited a decrease in several pro-inflammatory cytokines and chemokines and certain regulators of T-cells and NK-cells. This reflects the immunosuppressant effects of smoking which may contribute to an enhanced susceptibility to periodontitis.",
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AU - Thunell, Daniel H.

AU - Johnson, Georgia K.

AU - Joly, Sophie

AU - Burnell, Kindra K.

AU - Cavanaugh, Joseph E.

AU - Brogden, Kim A.

AU - Guthmiller, Janet M.

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N2 - Aim: The aim of this study was to compare the expression of 22 chemokines and cytokines in gingival crevicular fluid (GCF) from smokers and non-smokers with periodontitis and periodontally healthy control subjects. Materials and Methods: Forty subjects with generalized severe chronic periodontitis (20 smokers and 20 non-smokers) and 12 periodontally healthy control subjects participated in this study. Four diseased and two healthy sites were selected from each of the periodontitis subjects. GCF samples were collected and cytokines analysed utilizing a multiplexed immunoassay (Luminex Â). Statistical analyses employed non-parametric tests including the Mann-Whitney and Wilcoxon matched-pairs signed-rank tests. Results: Compared with healthy control subjects, GCF in subjects with chronic periodontitis contained significantly higher amounts of interleukin (IL)-1α, IL-1β, IL-6, IL-12(p40) (pro-inflammatory cytokines); IL-8, macrophage chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, regulated on activation normal T-cell expressed and secreted (RANTES) (chemokines); IL-2, IFN-Î, IL-3, IL-4 (Th1/Th2 cytokines); IL-15 [regulator of T-cells and natural killer (NK) cells]. Smokers displayed decreased amounts of pro-inflammatory cytokines [IL-1α, IL-6, IL-12(p40)], chemokines (IL-8, MCP-1, MIP-1, RANTES), and regulators of T-cells and NK cells (IL-7, IL-15). Conclusions: Periodontitis subjects had significantly elevated cytokine and chemokine profiles. Smokers exhibited a decrease in several pro-inflammatory cytokines and chemokines and certain regulators of T-cells and NK-cells. This reflects the immunosuppressant effects of smoking which may contribute to an enhanced susceptibility to periodontitis.

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