放射性骨丢失的多细胞调控机制

Multicellular regulation mechanism of radiation-induced bone loss

放射性骨丢失是临床放疗常见并发症之一,主要表现为骨密度降低,骨折及骨转移发生率增加,不仅降低患者生活质量,给社会也带来沉重经济负担,已成为重要的公共卫生问题。然而,目前对放射性骨丢失的机制研究仍停留在早期水平,普遍认为电离辐射干扰成骨细胞和破骨细胞正常功能后引起的骨重建失衡是放射性骨丢失的重要机制,较少涉及骨组织及骨髓中的其他细胞群,包括骨细胞、血管内皮细胞及免疫细胞,这些细胞群的相互作用决定了骨重建失衡的发生发展。本文在前人研究的基础上重点从骨组织的多细胞水平阐述放射性骨丢失的机制,为临床放射性骨丢失防治提供重要理论依据。

Radiation-induced bone loss,presented with reduced bone mineral density and increased incidence of fractures and bone metastases, is one of common complications in patients received radiotherapy. The complication not only decreases the quality of life of patients, but also brings heavy financial burden to the society, becoming an important public health problem. However, the research on the mechanism of radiation-induced bone loss remains in an immature level. Although it has been generally accepted that bone remodeling imbalance caused by dysfunction of bone formation and osteoclastogenesis suppression after irradiation is the critical mechanism of radiation-induced bone loss, less attention has been acquired in other cells of bone tissue and bone marrow, including osteocytes,endothelial cells and immune cells, which play important roles in the development of bone remodeling imbalance. Therefore, on the basis of previous studies, this article is aiming to elucidate the multicellular regulation mechanism of radiation-induced bone loss and provide an important evidence for the prevention and treatment of radiation-induced bone loss.