小鼠基因型对骨创伤愈合及辐射诱导的愈合延迟的影响。
Effects of mouse genotype on bone wound healing and irradiation-induced delay of healing.
作者信息
Glowacki Julie, Mizuno Shuichi, Kung Jason, Goff Julie, Epperly Michael, Dixon Tracy, Wang Hong, Greenberger Joel S
机构信息
Orthopedic Research, Brigham and Women's Hospital, 75 Frances Street, Boston, MA 02115, U.S.A.
出版信息
In Vivo. 2014 Mar-Apr;28(2):189-96.
We tested the effects of mouse genotype (C57BL/6NHsd, NOD/SCID, SAMR1, and SAMP6) and ionizing irradiation on bone wound healing. Unicortical wounds were made in the proximal tibiae, and the time course of spontaneous healing and effects of irradiation were monitored radiographically and histologically. There was reproducible healing beginning with intramedullary osteogenesis, subsequent bone resorption by osteoclasts, gradual bridging of the cortical wound, and re-population of medullary hematopoietic cells. The most rapid wound closure was noted in SAMR1 mice, followed by SAMP6, C57BL/6NHsd, and NOD/SCID. Ionizing irradiation (20 Gy) to the leg significantly delayed bone wound healing in mice of all four genotypes. Mice with genetically-determined predisposition to early osteopenia (SAMP6) or with immune deficiency (NOD/SCID) had impairments in bone wound healing. These mouse models should be valuable for determining the effects of irradiation on bone healing and also for the design and testing of novel bone growth-enhancing drugs and mitigators of ionizing irradiation.
我们测试了小鼠基因型（C57BL/6NHsd、NOD/SCID、SAMR1和SAMP6）以及电离辐射对骨创伤愈合的影响。在胫骨近端制造单皮质伤口，并通过影像学和组织学方法监测自发愈合的时间进程以及辐射的影响。愈合过程可重复，始于骨髓内成骨，随后破骨细胞进行骨吸收，皮质伤口逐渐桥接，骨髓造血细胞重新填充。在SAMR1小鼠中观察到伤口闭合最快，其次是SAMP6、C57BL/6NHsd和NOD/SCID。对腿部进行20 Gy的电离辐射显著延迟了所有四种基因型小鼠的骨创伤愈合。具有遗传易感性的早期骨质减少（SAMP6）或免疫缺陷（NOD/SCID）的小鼠在骨创伤愈合方面存在障碍。这些小鼠模型对于确定辐射对骨愈合的影响以及新型骨生长增强药物和电离辐射减轻剂的设计和测试应具有重要价值。
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