Beil Frank Timo, Barvencik Florian, Gebauer Matthias, Seitz Sebastian, Rueger Johannes Maria, Ignatius Anita, Pogoda Pia, Schinke Thorsten, Amling Michael
Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
J Trauma. 2010 Nov;69(5):1259-65. doi: 10.1097/TA.0b013e3181c4544d.
Fracture healing is a complex and sequential process. One important step in fracture healing is callus remodeling. Estrogen deficiency is known to increase osteoclast bone resorption, whereas estrogen replacement can reverse this effect. Therefore, the aim of our study was to analyze whether estrogen deficiency and estrogen treatment, respectively, would affect callus remodeling in the fracture healing process.
Standardized femoral fractures were produced in 10 weeks old C57BL/6 mice using a guillotine-like fracture device. Mice were separated into three groups. The first group obtained a continuous administration of estrogen. Ovariectomy (OVX) was performed in the second group to generate an estrogen-deficiency model. The control group obtained no special treatment. At different stages of fracture healing, contact X-ray, micro-computed tomography, histologic, and biomechanical analyses were performed.
We observed that, in early stages of fracture healing, OVX leads to an impaired periosteal callus formation. When compared with the control group, chondrocytes area was decreased, and the subsequent mineralization was less distinctive. In the late stage of fracture healing, the OVX mice showed a thin and porous cortex. In sharp contrast, estrogen treatment led to an enhanced fracture healing. Chondrocyte areas were larger, callus mineralization was increased, and the neocortex was thicker. Biomechanical testing confirmed the beneficial effects of estrogen on restoration of biomechanical competence.
These results indicate that estrogen seems to be an important factor in all stages of fracture healing. The application of estrogens enhances fracture healing of long bones at least in mice.
骨折愈合是一个复杂且有序的过程。骨折愈合的一个重要步骤是骨痂重塑。已知雌激素缺乏会增加破骨细胞的骨吸收，而雌激素替代可以逆转这种作用。因此，我们研究的目的是分析雌激素缺乏和雌激素治疗分别是否会影响骨折愈合过程中的骨痂重塑。
使用类似断头台的骨折装置在10周龄的C57BL/6小鼠中制造标准化的股骨骨折。将小鼠分为三组。第一组持续给予雌激素。第二组进行卵巢切除术（OVX）以建立雌激素缺乏模型。对照组不进行特殊处理。在骨折愈合的不同阶段，进行接触X线、微计算机断层扫描、组织学和生物力学分析。
我们观察到，在骨折愈合的早期阶段，OVX导致骨膜骨痂形成受损。与对照组相比，软骨细胞面积减小，随后的矿化不那么明显。在骨折愈合的后期，OVX小鼠的皮质变薄且多孔。形成鲜明对比的是，雌激素治疗导致骨折愈合增强。软骨细胞面积更大，骨痂矿化增加，新皮质更厚。生物力学测试证实了雌激素对恢复生物力学能力的有益作用。
这些结果表明雌激素似乎是骨折愈合所有阶段的一个重要因素。至少在小鼠中，雌激素的应用可增强长骨的骨折愈合。
