Articular cartilage metabolism in patients with Kashin-Beck Disease: an endemic osteoarthropathy in China
Articular cartilage metabolism in patients with Kashin-Beck Disease: an endemic osteoarthropathy in China
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DOI：
10.1016/j.joca.2007.09.002
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发表时间：
2008-06-01
影响因子：
7
通讯作者：
Caterson, B.
中科院分区：
文献类型：
--
作者：
Cao, J.;Li, S.;Caterson, B.
目的：本研究的目的是研究大骨节病（KBD）患者的CD44和蛋白多糖代谢，大骨节病是一种地方性骨关节病，影响着中国3000万大骨节病患者中的250万人。方法：采用免疫组化方法对大骨节病患者和正常患者软骨组织进行CD44、BC-13和3-B-3表达分析。此外，采用三明治酶联免疫吸附法测定血清可溶性CD44 （sCD44）、白细胞介素-1 β (IL-1 β)、肿瘤坏死因子- α (tnf - α)和基质金属糖蛋白酶-1的水平。结果：苏木精伊红和甲苯胺蓝染色显示，大骨节病儿童和成人软骨均有细胞坏死和蛋白聚糖丢失。CD44、BC-13和3-6-3（-）的免疫组化染色出现在大多数成人大肠癌患者和大多数儿童大肠癌患者中。此外，与正常成人和儿童对照组相比，成人和儿童KBD患者血清中sCD44、IL-1 β和tnf - α水平均有统计学意义的升高。有趣的是，与来自非大骨病地区的正常儿童相比，来自大骨病地区的正常儿童的IL-1 β和tnf - α血清水平都很高，这表明未知因素（例如遗传易感性）可能保护一些人免受大骨病病理的影响。结论：我们的研究结果表明，CD44、IL-1 β和tnf - α代谢的改变在大骨节病的发病过程中发生，并且大骨节病成人和儿童软骨中聚集酶基因评价的蛋白聚糖损失增加。这些原发性代谢变化可能是导致骨关节病患者继发性骨关节炎的病理性关节形成和不稳定的重要因素。(C) 2007国际骨关节炎研究学会。Elsevier Ltd.出版。版权所有。
Objective: The objective of this study was to investigate CD44 and proteoglycan metabolism in patients suffering from Kashin-Beck Disease (KBD), an endemic osteoarthropathy that affects 2.5 million of 30 million people living in the KBD regions of China.Methods: Immunohistochemical analyses of cluster of differentiation-44 (CD44), BC-13 and 3-B-3(-) expression were performed in cartilage sections harvested from KBD and normal patients. In addition, the serum levels of soluble CD44 (sCD44), interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha) and matrix metal lop roteinase-1 were determined using a sandwich enzyme linked immunosorbent assay.Results: Hematoxylin & eosin and toluidine blue staining indicated that there was cell necrosis and proteoglycan loss in cartilage from both KBD children and adult cartilage. Strong immunohistochemical staining for CD44, BC-13 and 3-6-3(-) occurred in the majority of adult KBD patients and most KBD children. Furthermore, statistically significant elevated levels of sCD44, IL-1 beta and TNF-alpha were found in the sera of both adult and child KBD patients when compared to the levels of normal adult and child controls. Interestingly, IL-1 beta and TNF-alpha serum levels were all high in normal children from KBD regions when compared to normal children from non-KBD regions suggesting that unidentified factors (e.g., a genetic predisposition) may protect some people from KBD pathology.Conclusion: Our results demonstrate that altered CD44, IL-1 beta and TNF-alpha metabolism occurs in the pathogenesis of KBD and there is an increased aggrecanase-gene rated proteoglycan loss from KBD adult and child cartilage. These primary metabolic changes are likely to be significant contributing factor causing pathological joint formation and instability that leads to secondary osteoarthritis in KBD patients. (C) 2007 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.