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Comparison of relative TLR ‐2 and TLR ‐4 expression level of disease and healthy gingival tissue of smoking and non‐smoking patients and periodontally healthy control patients
Author(s) -
Fatemi K,
Radvar M,
Rezaee A,
Rafatpanah H,
Azangoo khiavi H,
Dadpour Y,
Radvar N
Publication year - 2013
Publication title -
australian dental journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 71
eISSN - 1834-7819
pISSN - 0045-0421
DOI - 10.1111/adj.12089
Subject(s) - periodontitis , medicine , receptor , chronic periodontitis , context (archaeology) , immunology , bleeding on probing , biology , paleontology
Background Toll‐like receptors are a family of sensor proteins that induce the inflammatory diseases in context of microbial infection. The role of these proteins in periodontal disease and their interaction with smoking status are yet to be investigated. The aim of the present study was to evaluate the effect of smoking on gene expression of toll like receptor 2 ( TLR ‐2) and toll‐like receptor 4 ( TLR ‐4) in patients with periodontitis. Methods RNAs were extracted from gingival biopsies of healthy sites (no bleeding on probing and pocket depth ≤3 mm) as well as diseased sites (with bleeding on probing and pocket depth ≥5 mm) of 20 smoker and 17 non‐smoker subjects with chronic periodontitis. Gingival biopsies from eight periodontally healthy, never‐smoker subjects served as control. Real‐time PCR was carried out to evaluate the relative quantities of TLR‐2 and TLR‐4 mRNA concentrations. Results Regardless of smoking status, the relative expression levels of TLR‐2 and TLR‐4 were significantly greater (about 3 fold) at diseased sites compared to healthy sites of patients with periodontitis and healthy controls (p < 0.05). In sites with periodontitis, smoking caused an increase of about 6.5 fold in mRNA levels of TLR‐4 in gingival tissue (p < 0.05). Conclusions Although periodontitis might significantly increase TLR ‐2 and TLR ‐4 gene expression in gingival tissues, smoking habit in periodontitis subjects could selectively potentiate TLR ‐4 gene expression.