Green Danielle E, Rubin Clinton T
Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY 11794-5281, USA.
Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY 11794-5281, USA.
Bone. 2014 Jun;63:87-94. doi: 10.1016/j.bone.2014.02.018. Epub 2014 Mar 5.
The rising levels of radiation exposure, specifically for medical treatments and accidental exposures, have added great concern for the long term risks of bone fractures. Both the bone marrow and bone architecture are devastated following radiation exposure. Even sub-lethal doses cause a deficit to the bone marrow microenvironment, including a decline in hematopoietic cells, and this deficit occurs in a dose dependent fashion. Certain cell phenotypes though are more susceptible to radiation damage, with mesenchymal stem cells being more resilient than the hematopoietic stem cells. The decline in total bone marrow hematopoietic cells is accompanied with elevated adipocytes into the marrow cavity, thereby inhibiting hematopoiesis and recovery of the bone marrow microenvironment. Poor bone marrow is also associated with a decline in bone architectural quality. Therefore, the ability to maintain the bone marrow microenvironment would hinder much of the trabecular bone loss caused by radiation exposure, ultimately decreasing some comorbidities in patients exposed to radiation.
辐射暴露水平的不断上升，特别是在医疗治疗和意外暴露方面，引发了人们对骨折长期风险的极大关注。辐射暴露后，骨髓和骨骼结构都会遭到破坏。即使是亚致死剂量也会导致骨髓微环境受损，包括造血细胞数量减少，而且这种损害呈剂量依赖性。不过，某些细胞表型对辐射损伤更敏感，间充质干细胞比造血干细胞更具抗辐射能力。骨髓造血细胞总数的减少伴随着骨髓腔内脂肪细胞的增多，从而抑制造血和骨髓微环境的恢复。骨髓功能不佳还与骨骼结构质量下降有关。因此，维持骨髓微环境的能力将有助于减少辐射暴露导致的大部分小梁骨丢失，最终降低辐射暴露患者的一些合并症。
