Performed showed that X-ray irradiation decreased oxidative stress in osteoblasts and did not alter cell viability, cellular proliferation or cellular apoptosis. A previous study demonstrated that 2 Gy X-ray ionizing radiation induced time-dependent cell cycle arrest and had no significant effects on osteoblast proliferation and differentiation in an osteoblastic cell line. However, Park et al. reported that 2 Gy X-ray irradiation not only increased differentiation and mineralization of the cells but also upregulated the expression of ALP, Col1, OPN and OCN in the early stage of differentiation. It is generally considered that sequential proliferation and differentiation of osteoblasts is indispensable for bone remodeling and healing. Our preliminary studies surprisingly demonstrated that 1 Gy X-ray irradiation promoted callus formation and mineralization in a rat model, and this type of radiation was also shown to have different effects on the proliferation and differentiation of osteoblasts in vitro. However, the underlying mechanism has not been evaluated in osteoblasts exposed to Dasatinib low-dose irradiation. In this study, we investigated the mechanism by which low-dose X-ray irradiation influences the proliferation and differentiation of osteoblasts and promotes fracture healing. Osteogenic gene expression patterns were evaluated to explore the possible mechanisms involved in irradiation-stimulated osteoblast differentiation in vivo and in vitro. Our findings provide a greater understanding of the biological responses of osteoblasts exposed to low-dose X-ray irradiation and highlight the potential positive effects of this treatment. In this study, we observed increased proliferation and differentiation among osteoblasts in cell culture and fracture healing models stimulated by low-dose irradiation. Given that osteoblasts exhibit a developmental sequence of events, including distinct proliferative, differentiating and mineralizing stages, we selected different time points for the proliferation and differentiation analyses in our study. After single-dose 0.5 Gy X-ray irradiation, osteoblastic cell activity was enhanced, consistent with increased osteoblast proliferation. Similarly, increased numbers of PCNApositive cells were detected in calluses early during the fracturehealing process. In addition, low-dose X-ray irradiation promoted osteoblastic cell survival and reduced apoptotic cell death based on the sub-G1 cell cycle analysis of cultured cells.