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利用牛关节软骨稳态培养模型，我们研究了大骨节病患儿血清、病区正常儿童血清和非病区正常儿童血清对蛋白多糖合成代谢的影响。结果显示，与非病区儿童血清相比，大骨节病患儿血清显著抑制了培养软骨蛋白多糖的３５Ｓ掺入率及已糖醛酸含量。提示病区致病因子作用于血清中与软骨代谢有关的因子，导致了大骨节病软骨代谢的异常。
Using bovine articular cartilage steady-state culture model, we studied the effects of sera from children with Kashin-Beck disease, normal children’s sera and normal children’s sera on the synthesis and metabolism of proteoglycan. The results showed that compared with non-ward children’s sera serum in children with Kashin-Beck disease significantly inhibited the incorporation rate of 35S and the content of hexuronic acid in the culture cartilage proteoglycan. Tip ward pathogenic factor role in serum and cartilage metabolism-related factors, leading to Kashin-Beck disease cartilage metabolism.