Effects of smoking on clinical parameters and the gingival crevicular fluid levels of il-6 and tnf-a in patients with chronic periodontitis

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J Clin Periodontol 2004; 31: 99–104 Printed in Denmark. All rights reserved

Copyright r Blackwell Munksgaard 2004

Effects of smoking on clinical parameters and the gingival crevicular fluid levels of IL-6 and TNF-a in patients with chronic periodontitis
Erdemir EO, Duran I, Haliloglu S: Effects of smoking on clinical parameters and the gingival crevicular fluid levels of IL-6 and TNF-a inpatients with chronic periodontitis. J Clin Periodontol 2004; 31: 99–104. r Blackwell Munksgaard, 2004. Abstract Objective: Smoking is an important environmental risk factor for the initiation and progression of periodontal diseases. The aim of this study was to evaluate the effects of smoking on clinical parameters and the gingival crevicular fluid (GCF) contents of the pro-inflammatory cytokinesinterleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a) levels in patients with chronic periodontitis. Material and Methods: The study base consisted of 41 patients including 22 volunteer current smokers with an age range of 32–59 (44.41 Æ 7.88) years and 19 volunteer non-smokers with an age range of 36–59 (46.94 Æ 6.07) years. The first month after non-surgical periodontal therapy was accepted asthe baseline of the study. The clinical parameters including plaque index (PI), gingival index (GI), bleeding on probing (BOP), probing depth (PD), clinical attachment loss (CAL) were recorded and GCF samples were collected for analysis of GCF contents of IL-6 and TNF-a levels. At the 3rd and 6th months, all of these procedures were repeated. Results: In smokers, only CAL was significantly higher atthe 3rd month compared with non-smokers (po0.05). GI and BOP were higher in non-smokers than smokers in both periods (po0.05). PI showed increases from the initial to the 6th month in smokers (po0.05). Although the differences between two groups with regard to IL-6 and TNF-a were not significant (p40.05), the total amount of TNF-a in GCF decreased from the initial to the 6th month in smokers(po0.05). There were no significant correlations between the mean total amount of IL-6 and TNF-a in GCF and clinical parameters in both evaluation periods in smokers (p40.05). Conclusion: The present study demonstrated that cigarette smoking increases the amount of dental plaque over time in smokers and does not influence GCF contents of IL-6 and TNF-a.

Ebru Olgun Erdemir1, Ismet Duran1 and SeyfullahHaliloglu2
1 Department of Periodontology, School of Dentistry, Selcuk University, Konya, Turkey; 2 Department of Biochemistry, Faculty of Veterinary Medicine, Selcuk University, Turkey

Key words: chronic periodontitis; GCF; IL-6; non-surgical therapy; smoking; TNF-a Accepted for publication 4 April 2003

Periodontitis is initiated by specific bacteria and the local host response to thesebacteria includes the recruitment of leukocytes and the subsequent release of inflammatory mediators and cytokines such as interleukin (IL)-1, IL-6, IL-8, IL-10, IL-12 and TNF-a, which are thought to play an important role in

the pathogenesis of the disease. These increased levels of several cytokines are involved in periodontal tissue destruction (Genco 1992). IL-6 is a multifunctional cytokine, ofwhich biological activities include B-lymphocyte differentiation, T-lymphocyte proliferation and stimulation of immunoglobulin

(Ig) secretion by B-lymphocytes, stimulation of acute-phase protein synthesis and complement cascade activation (Hirano et al. 1990). Of particular significance is the ability of IL-6 to induce bone resorption, both by itself and in conjunction with other boneresorbingagents (Ishimi et al. 1990).

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Erdemir et al.
Material and Methods
Selection of patients

TNF-a is also a monocyte-derived protein that has a wide range of proinflammatory and immunomodulatory effects on a number of different cell populations. TNF-a can stimulate fibroblasts, including gingival fibroblasts, to produce collagenase (Meikle et al. 1989), an enzyme implicated in the tissue...
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