Modification of osteoarthritis by pulsed electromagnetic field - a morphological study
Modification of osteoarthritis by pulsed electromagnetic field - a morphological study
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DOI：
10.1016/s1063-4584(03)00083-9
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发表时间：
2003-06-01
影响因子：
7
通讯作者：
Simon, B
中科院分区：
文献类型：
--
作者：
Ciombor, DM;Aaron, RK;Simon, B
目的：Hartley豚鼠自发发展关节炎，其形态、生化和免疫组织化学与人类骨关节炎相似。其特征是12个月大时出现浅表纤维性颤动，18个月大时出现严重的软骨病变和灼烧。本研究探讨了脉冲电磁场（PEMF）治疗对动物模型骨关节炎形态学进展的影响。设计：Hartley豚鼠从12个月开始，每天暴露于特定的PEMF 1小时，持续6个月。对照动物同样接受治疗，但没有接触电磁场。通过对软骨新表位、3B3（-）和BC-13的免疫组织化学检查，以及对胶原酶（MMP-13）和基质溶解素（MMP-3）的免疫反应，对胫骨关节软骨进行关节炎严重程度的组织学/组织化学分级。检测了对tgf - β、白细胞介素(IL)-1 β和IL受体拮抗剂蛋白（IRAP）抗体的免疫反应性，以提示PEMF活性的可能机制。结果：PEMF治疗保留了关节软骨形态，延缓了骨关节炎病变的发展。软骨新表位3B3（-）和BC-13的减少以及基质降解酶、胶原酶和基质溶解素的抑制支持了这一观察结果。对IL-1免疫阳性的细胞数量减少，而irap阳性的细胞数量增加。PEMF治疗显著增加了tgf - β免疫阳性细胞的数量。结论：在这种骨关节炎模型中，PEMF治疗似乎可以改善疾病。由于tgf β被认为上调聚集蛋白的基因表达，下调基质金属蛋白酶和IL-1活性，上调基质金属蛋白酶抑制剂，因此刺激tgf β可能是PEMF有利影响软骨稳态的机制。(C) 2003年由Elsevier Science Ltd代表国际骨关节炎研究学会出版。
Objective: Hartley guinea pigs spontaneously develop arthritis that bears morphological, biochemical, and immunohistochemical similarities to human osteoarthritis. It is characterized by the appearance of superficial fibrillation by 12 months of age and severe cartilage lesions and eburnation by 18 months of age. This study examines the effect of treatment with a pulsed electromagnetic field (PEMF) upon the morphological progression of osteoarthritis in this animal model.Design: Hartley guinea pigs were exposed to a specific PEMF for 1 h/day for 6 months, beginning at 12 months of age. Control animals were treated identically, but without PEMF exposure. Tibial articular cartilage was examined with histological/histochemical grading of the severity of arthritis, by immunohistochemistry for cartilage neoepitopes, 3B3(-) and BC-13, reflecting enzymatic cleavage of aggrecan, and by immunoreactivity to collagenase (MMP-13) and stromelysin (MMP-3). Immunoreactivity to TGFbeta, interleukin (IL)-1beta, and IL receptor antagonist protein (IRAP) antibodies was examined to suggest possible mechanisms of PEMF activity.Results: PEMF treatment preserves the morphology of articular cartilage and retards the development of osteoarthritic lesions. This observation is supported by a reduction in the cartilage neoepitopes, 3B3(-) and BC-13, and suppression of the matrix-degrading enzymes, collagenase and stromelysin. Cells immunopositive to IL-1 are decreased in number, while IRAP-positive cells are increased in response to treatment. PEMF treatment markedly increases the number of cells immunopositive to TGFbeta.Conclusions: Treatment with PEMF appears to be disease-modifying in this model of osteoarthritis. Since TGFbeta is believed to upregulate gene expression for aggrecan, downregulate matrix metalloprotease and IL-1 activity, and upregulate inhibitors of matrix metalloprotease, the stimulation of TGFbeta may be a mechanism through which PEMF favorably affects cartilage homeostasis. (C) 2003 Published by Elsevier Science Ltd on behalf of OsteoArthritis Research Society International.