Li G P, Zhang S D, Chen G, Chen H, Wang A M
Am J Sports Med. 1985 Sep-Oct;13(5):285-94. doi: 10.1177/036354658501300501.
Sequential changes in remodeling of the internal structure of the tibia caused by controlled, excessive jumping and running were studied in 20 rabbits. Vascular changes and circulatory disturbances within the cortical bone occurred before osteoclastic resorption. Degeneration and necrosis of osteocytes due to circulatory disturbances also occurred. Periosteal new bone formation, found at and after 12 days of the experiment, was a compensatory reaction to support the tibia weakened by accelerated osteoclastic resorption. Small cracks appeared at the cement line and developed through the neighboring cement line of the haversian systems. At 21 days, incomplete fracture of the tibial cortex was found in two rabbits. Complete fracture through one side of the cortex was seen in one animal at the 50th day of the experiment. In this study, however, most of the tibias did not have visible fracture lines after a period of stressful exercise. This result suggests that most tibias adapt to changes in stress requirements through proper internal remodeling so that a complete fracture does not occur.
在20只兔子身上研究了由可控的过度跳跃和奔跑引起的胫骨内部结构重塑的连续变化。皮质骨内的血管变化和循环紊乱发生在破骨细胞吸收之前。由于循环紊乱导致的骨细胞变性和坏死也会发生。在实验第12天及之后发现的骨膜新骨形成是一种代偿反应，以支撑因加速破骨细胞吸收而变弱的胫骨。在黏合线处出现小裂缝，并通过哈弗斯系统相邻的黏合线扩展。在第21天，两只兔子的胫骨皮质出现不完全骨折。在实验第50天，一只动物的皮质一侧出现完全骨折。然而，在本研究中，经过一段时间的应激运动后，大多数胫骨没有可见的骨折线。这一结果表明，大多数胫骨通过适当的内部重塑适应应力需求的变化，从而不会发生完全骨折。
