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Nicotine inhibits osteogenic differentiation of human periodontal ligament cells under cyclic tensile stress through canonical Wnt pathway and α7 nicotinic acetylcholine receptor
Author(s) -
Yu W.,
Hu B.,
Shi X.,
Cao Z.,
Ren M.,
He Z.,
Lin J.,
Deng H.,
Hu R.
Publication year - 2018
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.12545
Subject(s) - nicotine , wnt signaling pathway , chemistry , alkaline phosphatase , periodontal fiber , nicotinic acetylcholine receptor , microbiology and biotechnology , cellular differentiation , runx2 , acetylcholine receptor , signal transduction , receptor , medicine , biochemistry , dentistry , biology , enzyme , gene
Background and Objectives Nicotine, the main psychoactive component of tobacco, affects cell metabolism, proliferation, adhesion and, importantly, the osteogenic differentiation of fibroblasts. Approximately 15% of all orthodontic patients are adults among who one‐fifth are smokers. Hence, it is necessary to have insight into the effects of nicotine on the osteogenic differentiation of hPDLC s during orthodontic tooth movement. This study aimed to investigate the effects and mechanisms of nicotine on the osteogenic differentiation of human periodontal ligament cells (hPDLCs) under the application of cyclic tensile stress. Material and Methods hPDLC s were obtained from donor third molars. The hPDLC s were treated with nicotine and/or cyclic tensile stress that was applied with a cell stress plus unit. The effect of nicotine on cell viability was analyzed using the MTT assay. The osteogenic differentiation of hPDLC s was detected by alkaline phosphatase staining, Alizarin Red S staining, quantitative real‐time polymerase chain reaction and western blotting. Results In combination with cyclic tensile stress, nicotine prevented the tensile stress‐induced increase in alkaline phosphatase activity, formation of mineralization nodules and the upregulation of mRNA and protein expression of Runt‐related transcription factor 2, transcription factor Sp7 and collagen type I; however, canonical Wnt pathway was activated. Furthermore, the addition of Dickkopf‐related protein 1 and α‐bungarotoxin counteracted the negative effect of nicotine and rescued the osteogenic differentiation of hPDLC s, respectively. Conclusion These results indicate that nicotine prevents the increased osteogenic potential of hPDLC s induced by cyclic tensile stress by binding to an α7 nicotinic acetylcholine receptor and activating the canonical Wnt pathway.