In vitro Cellular Aging Stimulates Interleukin-1β Production in Stretched Human Periodontal-ligament-derived Cells

Although the severity of periodontal disease is known to be affected by host age, the pathological role of aging in periodontal disease, and especially that attributable to trauma from occlusion, has not been well-characterized. Interleukin (IL)-1β is a key mediator involved in periodontal diseases, a potent stimulator of bone resorption. Furthermore, it is produced by human periodontal ligament (PDL) cells in response to mechanical stress. To investigate the age-related changes in the biosynthetic capacity of IL-1β in PDL cells, we examined the effects of in vitro cellular aging with mechanical stress on IL-1β protein and gene expression by human PDL cells. Human PDL cells (young = 5th or 6th passage; old = 18-20th passage) were cultured on flexible-bottomed culture plates, and the cells were deformed at 6 cycles per min at 2 steps of tension force for 1 to 5 days. We found a two-fold increase in IL-lp production by old PDL cells subjected to mechanical tension compared with that by young PDL cells, although the constitutive levels of IL-1β were similar in both the young and old PDL cells. This increase was tension-dependent. IL-1β mRNA was also detected in both the cell types under basal conditions, and its expression was further enhanced by application of mechanical tension by use of reverse-transcription-polymerase chain-reaction (RT-PCR) and in situ hybridization methods. The increase in signal rate was higher in the old cells than in the young cells. IL-1β-converting enzyme mRNA remained unchanged. It is possible that a large amount of IL-1β produced by PDL cells from an aged host in response to mechanical force may be positively related to the accleration of alveolar bone resorption.