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目的本研究旨在了解大骨节病(KBD,在中国发生的一种地方性骨关节病)患者软骨CD44和蛋白聚糖的代谢及相关影响。方法用免疫组织化学方法分析分化抗原-44(CD44)、BC-13以及3-B-3(-)在所采集KBD患者和正常人软骨切片中的表达;采用夹心酶联免疫吸附测定法检测血清中可溶性CD44(sCD44)、白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)以及基质金属蛋白酶-1的水平。结果苏木素&伊红(HE)染色以及甲苯胺兰染色显示,在KBD病患儿以及成人软骨中有细胞坏死和蛋白聚糖的缺失;免疫组织化学染色发现,KBD成人和儿童患者软骨组织中CD44、BC-13和3-B-3(-)具很强的阳性表达;sCD44I、L-1β和TNF-α在KBD成人和儿童血清的水平明显高于正常成人及儿童对照组,经统计学分析具显著性差异。有意思的现象是,KBD病区正常儿童血清中IL-1β和TNF-α的水平亦明显高于非KBD病区正常儿童的水平,这些都提示可能还有一些未被确定的因素(例如遗传因素)或许对KBD发病具有一定的影响。结论大骨节病患者CD44I、L-1β和TNF-α代谢发生的改变,以及KBD成人和儿童软骨由于聚集蛋白聚糖酶活性增强所产生的蛋白聚糖的丢失,可能是KBD发病机理中起关键作用的重要因素,可以引起病态的关节形成和关节的不稳定,这些都可以导致在KBD患者中发生继发性的骨性关节炎。
Objectives This study was designed to understand the metabolism and related effects of cartilage CD44 and proteoglycan in patients with Kashin-Beck disease (KBD), a endemic osteoarthrosis that occurs in China. Methods The expressions of CD44, BC-13 and 3-B-3 (-) were detected by immunohistochemistry in the cartilage sections of KBD patients and normal people. The levels of CD44, CD44, Serum levels of soluble CD44 (sCD44), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and matrix metalloproteinase-1. Results Hematoxylin & Eosin (HE) staining and toluidine blue staining showed that there were cell necrosis and proteoglycan loss in children with KBD and in adult cartilage. Immunohistochemical staining revealed that CD44 in cartilage of KBD adults and children , BC-13 and 3-B-3 (-). The serum levels of sCD44I, L-1β and TNF-α in KBD adults and children were significantly higher than those in normal adults and children, Analysis of significant differences. Interestingly, serum levels of IL-1β and TNF-α in normal children with KBD were also significantly higher than those of non-KBD patients, suggesting that there may be some undefined factors (such as genetic factors ) May have a certain impact on the pathogenesis of KBD. Conclusions The changes of the metabolism of CD44I, L-1β and TNF-α in patients with KBD and the loss of proteoglycan produced by the enhancement of aggrecanase activity in KBD adults and children’s cartilage may play a key role in the pathogenesis of KBD An important factor in the effects that can cause morbid joint formation and joint instability can all contribute to secondary osteoarthritis in KBD patients.