The study shows gingival crevicular fluid's different marker levels among smokers and non-smokers following periodontal therapy

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The study shows gingival crevicular fluid's different marker levels among smokers and non-smokers following periodontal therapy

A recent study has shown the immunosuppressant effect of smoking in regulating the inflammatory and bone remodeling markers captured in gingival crevicular fluid following periodontal therapy. Bunaes D F and colleagues conducted a study to compare gingival crevicular fluid levels of inflammatory and bone remodeling markers in smokers and non-smokers following periodontal therapy in patients with chronic periodontitis.

Smoking is one of the most vulnerable causes of morbidity and premature death worldwide. One of the major problem due to smoking is the periodontal (gum) diseases. As the periodontal health is mediated by abolishing microorganisms activating a local inflammatory host response, smoking may impair this process.

In the present study, a total 50 patients were included. Out of them, 25 were smokers, and other 25 were non-smokers. The Gingival crevicular fluid and subgingival plaque were collected from patient's deep periodontal pockets. The fluid and plaque were collected in three phases, at baseline (T0), following active (T1) and 12 months of supportive periodontal therapy (T2). Smoking status among smokers was evaluated by serum cotinine levels. The multiplex and singleplex micro-bed immunoassays were used to measure marker levels of gingival crevicular fluid. To evaluate subgingival plaque samples, checkerboard DNA-DNA hybridization technique was used. Further, the comparison of marker levels among smokers and non-smokers was done by calculating the effect size. 

The results showed an overall reduced effect size at T0 and T2 in smokers. These are mainly, chemokines, growth factors and proinflammatory markers at T0, osteoprotegerin at T1, chemokines and proinflammatory markers at T2. Among smokers, the levels of interleukin-8 (IL-8) were highly detectable at the T2 stage.  Ten different markers responded to periodontal therapy among non-smokers, which was nil in other cases. From the overall study, it was found that smoking is negatively related with subgroups of markers at sites presenting ≥ 105 red complex periodontal microbial species.

Hence, besides for an up-regulation of IL-8, smokers don't exhibit increased levels of markers at T0, T1, and T2. Further, among non-smokers, only inflammatory responses adapted to periodontal therapy. Probably, smoking shows an immunosuppressant effect in regulating the inflammatory and bone remodeling markers captured in gingival crevicular fluid following periodontal therapy.

Source:

Journal of Periodontal Research

Link to the source:

http://onlinelibrary.wiley.com/doi/10.1111/jre.12438/abstract;jsessionid=93ACE1243AB382CBDF0A5C3211BE57E1.f04t01

The original title of the article:

The effect of smoking on inflammatory and bone remodeling markers in gingival crevicular fluid and subgingival microbiota following periodontal therapy

Authors:

D.F.Bunaes; M.mustafa; et al.

SearchTags: 
Smoking, Inflammatory, Bone remodeling markers, Gingival crevicular fluid, Subgingival, Periodontal
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