Structural and mechanical repair of diffuse damage in cortical bone in vivo.

Structural and mechanical repair of diffuse damage in cortical bone in vivo.
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DOI:
10.1002/jbmr.2309
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发表时间:
2014-12
影响因子:
6.2
通讯作者:
Schaffler, Mitchell B.
Schaffler, Mitchell B.
中科院分区:
医学1区
文献类型:
--
作者:
Seref-Ferlengez, Zeynep;Basta-Pljakic, Jelena;Kennedy, Oran D.;Philemon, Claudy J.;Schaffler, Mitchell B.

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生理性磨损和撕裂在几个层次上引起骨微损伤,并且这些具有不同的生物学后果。骨重建被广泛认为是骨微损伤修复的机制。然而,最近的研究表明,与典型的线性微裂纹不同,小裂纹损伤,亚微米尺寸的基质裂纹簇也称为扩散损伤(Dif.Dx),不会激活重塑。因此,弥漫性损伤在体内的命运是未知的。为了验证这一点,我们通过使用末端负荷尺骨弯曲蠕变模型在体内选择性地诱导大鼠尺骨中的Dif.Dx。在加载后立即通过组织形态测定法和机械测试评估损伤含量的变化(即,急性负荷)或损伤诱导后14天(即,生存溃疡)。在负荷后14天的存活期内,Dif.Dx面积显著减少(p<0.02)。我们没有观察到任何皮质内吸收,并且在存活的溃疡中皮质骨面积没有增加。急性负荷性骨折的全骨刚度降低在存活性骨折中恢复到基线水平(p>0.6)。显微压痕研究表明,Dif.Dx引起尺骨皮质弥漫性损伤区域弹性模量的高度局部化降低。加载后14天,这些先前受损骨骼区域的模量恢复到对照值。我们目前的研究结果表明,骨中的小裂纹损伤可以在没有骨重建的情况下修复,并表明骨中存在替代修复机制来处理亚微米尺寸的基质裂纹。这些机制目前尚不清楚,需要进一步的研究来阐明这种直接修复发生的机制。
Physiological wear and tear causes bone microdamage at several hierarchical levels, and these have different biological consequences. Bone remodeling is widely held to be the mechanism by which bone microdamage is repaired. However, recent studies showed that unlike typical linear microcracks, small crack damage, the clusters of submicron-sized matrix cracks also known as diffuse damage (Dif.Dx), does not activate remodeling. Thus, the fate of diffuse damage in vivo is not known. To examine this, we induced selectively Dif.Dx in rat ulnae in vivo by using end-load ulnar bending creep model. Changes in damage content were assessed by histomorphometry and mechanical testing immediately after loading (i.e., acute loaded) or at 14 days after damage induction (i.e., survival ulnae). Dif.Dx area was markedly reduced over the 14-day survival period after loading (p<0.02). We did not observe any intracortical resorption and there was no increase in cortical bone area in survival ulnae. The reduction in whole bone stiffness in acute loaded ulnae was restored to baseline levels in survival ulnae (p>0.6). Microindentation studies showed that Dif.Dx caused a highly localized reduction in elastic modulus in diffuse damage regions of the ulnar cortex. Moduli in these previously damaged bone areas were restored to control values by 14 days after loading. Our current findings indicate that small crack damage in bone can be repaired without bone remodeling, and suggest that alternative repair mechanisms exist in bone to deal with submicron-sized matrix cracks. Those mechanisms are currently unknown and further investigations are needed to elucidate the mechanisms by which this direct repair occurs.
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