Influence of Defective Bone Marrow Osteogenesis on Fracture Repair in an Experimental Model of Senile Osteoporosis
Influence of Defective Bone Marrow Osteogenesis on Fracture Repair in an Experimental Model of Senile Osteoporosis
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DOI：
10.1002/jor.21041
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发表时间：
2010-06-01
影响因子：
2.8
通讯作者：
Richards, Peter J.
中科院分区：
文献类型：
--
作者：
Egermann, Marcus;Heil, Petra;Richards, Peter J.
老年骨质疏松骨的骨髓成骨功能受损，因此，可能对骨折修复的成功结果有重要意义。在这里，我们利用一个成熟的老年性骨质疏松症的小鼠模型，P6品系的衰老加速小鼠（SAMP 6），研究骨折愈合的老年骨质疏松症的骨。在SAMP 6和非骨质疏松年龄匹配的对照R1抗衰老小鼠（SAMR 1）中建立股骨截骨术。骨折愈合的过程进行了评估，在42天的时间内使用定量μ CT和组织学分析。对来自SAMP 6和SAMR 1小鼠的骨髓间充质祖细胞的分化能力进行了检查，并测定了它们的成骨潜能。虽然初步的体外分析证实，从SAMP 6小鼠分离的骨髓源性干细胞（BMSC）具有降低的成骨能力，但通过定量μ CT确定的骨折修复没有显著缺陷。这得到了组织学评估的支持，其中在SAMP 6和SAMR 1小鼠中，骨折间隙的完全桥接在第28天是明显的，并且在第42天完全愈合。进一步的体外研究表明，从SAMP 6小鼠中分离的骨膜衍生祖细胞（PDPC）具有与在SAMR 1小鼠中观察到的成骨潜力相当的成骨潜力。总之，SAMP 6小鼠的骨折愈合不受BMSC成骨损伤的影响，这表明骨髓介导的修复过程在这种老年性骨质疏松性骨折模型中对正常骨愈合是不利的。此外，PDPC在修复过程中的影响可能部分解释了SAMP 6小鼠骨折修复中没有任何可检测到的缺陷。(C)2009骨科研究学会。出版者：Wiley Periodicals，Inc，J Orthop Res 28：798-804，2010
Bone marrow osteogenesis in senile osteoporotic bone is impaired and, as such, may have significant implications on the successful outcome of fracture repair. Here we utilize a well-established murine model of senile osteoporosis, the P6 strain of senescence-accelerated mice (SAMP6), to investigate fracture healing in aged osteoporotic bone. A femoral osteotomy was created in SAMP6 and in non-osteoporotic age-matched control R1 senescence-resistant mice (SAMR1). The course of fracture healing was evaluated over a period of 42 days using quantitative mu CT and histological analysis. The differentiation capabilities of bone mesenchymal progenitor cells derived from SAMP6 and SAMR1 mice was examined, and their osteogenic potential determined. Although preliminary in vitro analysis confirmed that bone marrow-derived stem cells (BMSC) isolated from SAMP6 mice had a reduced osteogenic capacity, no significant deficit in fracture repair as determined by quantitative mu CT could be detected. This was supported by histology assessment, where complete bridging of the fracture gap was evident by day 28 and was fully healed day 42 in both SAMP6 and SAMR1 mice. Further in vitro studies revealed that periosteal-derived progenitor cells (PDPC) isolated from SAMP6 mice had an osteogenic potential comparable to that observed in SAMR1 mice. In conclusion, fracture healing in SAMP6 mice is not detrimentally affected by impairment of BMSC osteogenesis, suggesting that bone marrow-mediated repair processes are dispensable for normal bone healing in this senile osteoporotic fracture model. Furthermore, the influence of PDPC in the repair process may partly explain the absence of any detectable deficits in fracture repair in SAMP6 mice. (C) 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc, J Orthop Res 28:798-804, 2010