Methods: PDL cells harvested from caries-free and periodontally healthy teeth were exposed to hypoxia (3% O2), inflammatory or biomechanical stress for 24 h. Interleukin-1 beta (IL-1β), which has been shown to be increased at inflamed periodontal sites, was used to simulate an inflammatory environment in vitro. In order to mimic functional loading of the periodontium, dynamic tensile strain (DTS, 3%, 1 Hz) was applied to cells. Unstimulated cells served as controls. Analysis of cell proliferation was performed by bromodeoxyuridine (BrdU) assay. Apoptosis was analyzed by a cell death detection ELISA. One-Way ANOVA and the post-hoc multiple comparison Tukey test were applied.
Results: All stressors had a remarkable influence on PDL homeostasis. Proliferation was altered significantly by hypoxia. In addition, apoptosis was regulated significantly by DTS and hypoxia. Hypoxia, DTS and the combined effect of IL-1β and DTS significantly changed gene expression of some members of the IGF system, e.g. IGF-1, IGFBP1 and IGFBP3.
Conclusions: The findings of our in-vitro study suggest that inflammatory, hypoxic and biomechanical stress can regulate proliferation and apoptosis of human PDL cells and thereby the homeostasis of PDL tissue. Our study suggests that the IGF system is part of that regulation in PDL cells.