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Gingival crevicular fluid levels of human beta‐defensin‐2 and cathelicidin in smoker and non‐smoker patients: a cross‐sectional study
Author(s) -
Ertugrul A. S.,
Sahin H.,
Dikilitas A.,
Alpaslan N. Z.,
Bozoğlan A.,
Tekin Y.
Publication year - 2014
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12105
Subject(s) - gingivitis , cathelicidin , medicine , periodontitis , beta defensin , gastroenterology , chronic periodontitis , dentistry , aggressive periodontitis , bleeding on probing , clinical attachment loss , immunology , innate immune system , receptor
Background and Objective Cathelicidin ( LL ‐37) and human β‐defensin‐2 (h BD ‐2) are antimicrobial peptides that have additional functions in innate immunity. The purpose of this study was to evaluate LL ‐37 and h BD ‐2 levels in the following patient groups: non‐smoker patients with gingivitis ( G ), smoker patients with gingivitis ( SG ), non‐smoker patients with generalized aggressive periodontitis (AgP) and smoker patients with generalized aggressive periodontitis ( SA g P ). Material and Methods A total of 80 patients, including 20 G, 20 SG , 20 A g P and 20 SA g P were enrolled in the study. Clinical periodontal parameters, including periodontal status were assessed by measuring bleeding on probing, plaque index, gingival index, probing depth and clinical attachment loss. Enzyme‐linked immunosorbent assays were done to quantify LL ‐37 and h BD ‐2 levels in gingival crevicular fluid. Results Clinical periodontal parameters were found to have no statistically significant differences between the SAgP and AgP groups or between the SG and G groups. LL‐37 and h BD ‐2 levels were significantly lower in G patients than in other groups. LL‐37 and h BD ‐2 levels in the gingival crevicular fluid of SAgP patients were significantly higher than in other groups. LL‐37 and h BD ‐2 levels in SG patients were also significantly higher than in G patients. Conclusions Epithelial cells in contact with microorganisms release LL‐37 and h BD ‐2 to eliminate them. The release response of LL‐37 and h BD ‐2 formed against microorganisms can change depending on factors such as smoking, which activates the nicotinic receptors present on epithelial surfaces. This interaction can increase the release of LL‐37 and h BD ‐2. Smoking may also affect the capillary tissues and reduce leukocytic chemotaxis. The increased number of colonized microorganisms may lead to higher levels of LL‐37 and h BD ‐2 release in the tissues of smokers than in non‐smokers.