Signaling pathways of pro-IL-1β production induced by mechanical stress in gingival epithelial cells

Mechanical stress on the teeth and alveolar bone caused by bruxism, orthodontics, and implants affects the periodontal tissues, causing gingival recession and alveolar bone resorption, and entire body, including the heart and vascular system. Although the same forces exerted on the alveolar bone and teeth are exerted on gingival epithelial cells, little is known about the effects of mechanical stress on these cells. This study investigated the effects of mechanical stress on gingival epithelial cells.

Ca9-22 cells (human gingival epithelial cells) were used. They were seeded onto the silicone and stretched cyclically. Mechanical stress-stimulated Ca9-22 cells were evaluated for pro-inflammatory interleukin (pro-IL)-1β production using Western blotting and analyzed to assess the phosphorylation level of intracellular signaling molecules.

Mechanical stress induced pro-IL-1β upregulation in Ca9-22 cells, which was significantly inhibited by ruthenium red. Ruthenium red significantly inhibited mechanical stress-induced phosphorylation of focal adhesion kinase (FAK), P130cas, and extracellular signal-regulated kinase 1 and 2 (ERK1/2) induced by mechanical stress. Additionally, Y15 significantly inhibited the upregulation of pro-IL-1β expression and phosphorylation of FAK, P130cas, and ERK1/2 stimulated by mechanical stress.

In Ca9-22 cells, mechanical stress may increase pro-IL-1β production via mechanosensitive ion channels and FAK. These findings revealed the mechanisms of inflammation in mechanically-stressed Ca9-22 cells and may aid in the development of therapeutic approaches to prevent bone resorption.