Modification of osteoarthritis by pulsed electromagnetic field - a morphological study

被引:118
作者
Ciombor, DM
Aaron, RK
Wang, S
Simon, B
机构
[1] Brown Med Sch, Dept Orthopaed, Providence, RI 02906 USA
[2] EBI, Parsippany, NJ 07054 USA
关键词
osteoarthritis; cartilage; morphology; pulsed electromagnetic fields;
D O I
10.1016/S1063-4584(03)00083-9
中图分类号
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学(修复外科学)];
学科分类号
摘要
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.
引用
收藏
页码:455 / 462
页数:8
相关论文
共 31 条
[1]
Acceleration of experimental endochondral ossification by biophysical stimulation of the progenitor cell pool [J].
Aaron, RK ;
Ciombor, DM .
JOURNAL OF ORTHOPAEDIC RESEARCH, 1996, 14 (04) :582-589
[2]
Aaron RK, 1999, BIOELECTROMAGNETICS, V20, P453, DOI 10.1002/(SICI)1521-186X(199910)20:7<453::AID-BEM7>3.0.CO
[3]
2-H
[4]
Upregulation of basal TGFβ1 levels by EMF coincident with chondrogenesis -: implications for skeletal repair and tissue engineering [J].
Aaron, RK ;
Wang, S ;
Ciombor, DM .
JOURNAL OF ORTHOPAEDIC RESEARCH, 2002, 20 (02) :233-240
[5]
EFFECTS OF BODY-WEIGHT RESTRICTION ON THE DEVELOPMENT AND PROGRESSION OF SPONTANEOUS OSTEOARTHRITIS IN GUINEA-PIGS [J].
BENDELE, AM ;
HULMAN, JF .
ARTHRITIS AND RHEUMATISM, 1991, 34 (09) :1180-1184
[6]
SPONTANEOUS CARTILAGE DEGENERATION IN GUINEA-PIGS [J].
BENDELE, AM ;
HULMAN, JF .
ARTHRITIS AND RHEUMATISM, 1988, 31 (04) :561-565
[7]
BENDELE AM, 1989, LAB ANIM SCI, V39, P115
[8]
CATERSON B, 1991, T ORTHOP RES SOC, V16, P251
[9]
TRANSFORMING GROWTH FACTOR-BETA IS A POTENT INHIBITOR OF IL-1 INDUCED PROTEASE ACTIVITY AND CARTILAGE PROTEOGLYCAN DEGRADATION [J].
CHANDRASEKHAR, S ;
HARVEY, AK .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1988, 157 (03) :1352-1359
[10]
Upregulation of enzymatic activity by interleukin-1 in osteoarthritis [J].
Chevalier, X .
BIOMEDICINE & PHARMACOTHERAPY, 1997, 51 (02) :58-62