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Effects of mechanical stress on human oral mucosa‐derived cells
Author(s) -
Nakamura Koya,
Yamamoto Toshiro,
Ema Ryo,
Nakai Kei,
Sato Yoshiki,
Yamamoto Kenta,
Adachi Keiji,
Oseko Fumishige,
Yamamoto Yoshiaki,
Kanamura Narisato
Publication year - 2021
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.13638
Subject(s) - inflammation , p38 mitogen activated protein kinases , oral mucosa , proinflammatory cytokine , kinase , cytokine , mapk/erk pathway , dentures , hydrostatic pressure , chemistry , medicine , immunology , microbiology and biotechnology , pathology , biology , dentistry , physics , thermodynamics
Objectives Placement of a denture results in the application of mechanical stress (MS), such as occlusal force, onto the oral mucosa beneath the denture. To better understand the molecular mechanism underlying MS‐induced inflammation in the oral mucosa, we examined the impact of MS on human oral epithelial cells (HO‐1‐N‐1) and human fibroblasts (HGFs) in this study. Materials and Methods MS was applied on HO‐1‐N‐1 and HGFs using a hydrostatic pressure apparatus. The expression and production of inflammatory cytokines and growth factors were examined by real‐time RT‐PCR and ELISA. MS‐induced intracellular signal transduction via MAP kinase (MAPK) was also examined. Results 1 MPa MS resulted in a significant increase in inflammatory cytokines, and 3 MPa MS resulted in a significant increase in FGF‐2. MS also increased p‐38 phosphorylation and the addition of a p‐38 inhibitor significantly suppressed the production of inflammatory cytokines. Discussion Our study suggested that MS applied through a denture increases the production of inflammatory cytokines from oral mucosal epithelial cells and fibroblasts via the p38 MAPK cascade. These responses to MS likely lead to inflammation of the mucosal tissue beneath dentures. On other hand, up‐regulation of growth factors is likely a manifestation of the biological defense mechanism against excessive MS.