Orthopaedic Department, West China Hospital, Sichuan University, Chengdu, China.
Osteoarthritis Cartilage. 2013 Aug;21(8):1108-15. doi: 10.1016/j.joca.2013.05.005. Epub 2013 May 21.
We investigated the combined roles of a low-nutrition diet (low levels of protein, iodine, and selenium) and T-2 toxin in bone development and to establish an experimental animal model of Kashin-Beck disease (KBD) that reliably mimics the disease's pathological changes for further study of the pathogenesis and prevention of the disease.
Sprague-Dawley rats were randomly divided among four groups: group A, normal diet; group B, normal diet plus T-2 toxin; group C, low-nutrition diet; and group D, low-nutrition diet plus T-2 toxin exposure. The radiographic and histopathological changes in the tibial growth zone, plate cartilage and metaphysis were examined.
In group D, all epiphyseal plates were blurred, thin, and irregular. Tibias were significantly shorter in group D than in groups A and B. After 4 weeks, epiphyseal plates showed chondrocyte necrosis, with the more obvious necrosis appearing in groups C and D. The positive rate of lamellar necrosis was significantly higher in group D than in groups B and A (P < 0.01). In group D, metaphyseal trabecular bone was sparse, disordered, and disrupted, and massive transverse trabecular bone appeared in the metaphysis at 12 weeks.
A rat model of KBD induced by a low-nutrition diet and T-2 toxin exposure demonstrated radiographic and histopathological abnormalities of the proximal epiphyseal plate and the tibial metaphysis that are very similar to the bone changes found in patients with KBD. This animal model will be helpful for further study of the pathogenesis and prevention of KBD.
本研究旨在探讨低营养饮食（蛋白质、碘和硒含量低）与 T-2 毒素在骨骼发育中的联合作用，并建立一种可靠模拟克山病（KBD）病理变化的实验动物模型，以进一步研究该病的发病机制和预防措施。
将 Sprague-Dawley 大鼠随机分为 4 组：A 组，正常饮食；B 组，正常饮食加 T-2 毒素；C 组，低营养饮食；D 组，低营养饮食加 T-2 毒素暴露。观察胫骨生长区、骺板软骨和干骺端的放射学和组织病理学变化。
D 组所有骺板均模糊、变薄、不规则。D 组大鼠胫骨明显短于 A 组和 B 组。4 周后，骺板软骨细胞出现坏死，C 组和 D 组坏死更为明显。D 组层状坏死阳性率明显高于 B 组和 A 组（P<0.01）。D 组干骺端骨小梁稀疏、紊乱、断裂，12 周时干骺端出现大量横向骨小梁。
低营养饮食和 T-2 毒素暴露诱导的 KBD 大鼠模型表现出与 KBD 患者相似的近侧骺板和胫骨干骺端的放射学和组织病理学异常。该动物模型将有助于进一步研究 KBD 的发病机制和预防措施。
