Etiology of Kaschin-Beck Disease

大骨节病（KBD）是中国东北地区儿童最常见的风湿病。虽然它是在环境中获得的，并经常导致终身致残，但病因尚不清楚。岩田教授访问了长春、北京和天津，对大骨节病和其他相关关节炎患者进行了检查。随后铃木教授访问了长春和成都，就软骨研究的现状进行了讲座。最后，杨教授来到大阪和东京，结束了这次合作项目。在18个月的时间里，研究人员分别给4只年轻的猕猴喂食来自河南大裂谷病疫区或非疫区的粮食和水。来自大骨节病流行地区的粮食和水均可引起猴子生长板和关节软骨的一系列病理变化以及血清和尿液的生化变化。这些变化与人类大骨节病相似。从大腿骨、股骨髁、胫骨平台和肋骨处去除软骨。食粮区和水区猕猴各软骨中糖胺聚糖的含量和合成速率均低于对照。结果表明，大骨节病的发病因素与病区饮食中的粮食和水分有关。另一组猴子以当地特有的谷物和水中添加硒为食。富硒组的软骨水平明显高于其他组。然而，补充硒不能刺激人类婴儿软骨细胞的生长。因此，数据几乎没有证据支持硒缺乏是人类大骨节病的主要病因的假设。因此，病因尚不清楚，我们需要在进一步的联合研究项目中继续研究大骨节病中软骨的代谢和分子生物学。

Kaschin-Beck disease (KBD) is the most frequent rheumatologic problem of children in norheastern China. Although it is acquired environmentally and frequently leads to life-long crippling, the etiology is still unknown. Professor Iwata visited changchun, Beijing, and Tianjin to examine KBD and other related arthritis patients. Then Professor Suzuki visited Changchun and Chengdu to give lectures on the current status of cartilage research. Finally, Professor Yang came to Osaka and Tokyo to conclude this joint project.Four young macaque monkeys each were fed with grain and water from areas actively endemic or non-endemic for KBD in Henan for 18 months. Both dietary grain and water from geographical areas endemic for KBD induced a sequence of pathological changes in the growth plates and articular cartilage and biochemical changes in the serum and urine of monkeys. These changes are similar to those in human KBD.Cartilage was removed from head of femurs, condyle of femurs, tibia plateaus, and ribs. The content and the rate of synthesis of glycosaminoglycans in various cartilages of monkeys fed grain and water endemic area were lower than those of the coontrol monkeys. The results suggest that the pathological factors of KBD relate both to grain and water in the diet in endemic areas. Another group of monkeys were fed diets of endemic grain and water from that were supplemented with selenium. Cartilages of the selenium-generous group showed significantly higher levels than those in the other groups. However, Selenium supplementation failed to stimulate growth of human infant chondrocytes. Therefore, the data provided little evidence to support the hypothesis that Selenium deficiency is a major etiologic factor in human KBD.Thus, the etiology remains unclear and we need continuing studies of the metabolism and molecular biology of cartilage in KBD in further joint research program.