Purpose: Previous studies using mouse osteoblast derived MC3T3-E1 and mouse myoblast derived C2C12 cells have not completely explained the mechanisms responsible for osteoradionecrosis. Thus, the aim of this study was to advance the in vitro experimental approaches for investigations of osteoradionecrosis.
Materials and methods: The pluripotent stem cell line, mouse embryo derived C3H10T1/2, was treated with all-trans-retinoic acid after irradiation (1, 3 and 6 Gy), and cell growth, cell cycle distribution, apoptosis, and alkaline phosphatase (ALP) activity were assessed.
Results: We demonstrated that ionising radiation inhibited the growth and decreased ALP activity in C3H10T1/2 cells. The decrease in cell growth was not due to apoptosis but was due to cell cycle delay. The decrease in ALP activity persisted in cells that were induced to an osteoblastic lineage 24 h after irradiation.
Conclusions: Our results suggested that C3H10T1/2 cells are suitable for investigating the effects of ionising irradiation on osteoblast precursor cells.