ACCELERATION OF EXPERIMENTAL LAPINE OSTEOARTHRITIS BY CALCIUM PYROPHOSPHATE MICROCRYSTALLINE SYNOVITIS

被引:35
作者
FAM, AG
MORAVAPROTZNER, I
PURCELL, C
YOUNG, BD
BUNTING, PS
LEWIS, AJ
机构
[1] Sunnybrook Health Science Center, University of Toronto, Toronto, Ontario
来源
ARTHRITIS AND RHEUMATISM | 1995年 / 38卷 / 02期
关键词
D O I
10.1002/art.1780380208
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Objective. To investigate the effects of chronic calcium pyrophosphate dihydrate (CPPD) synovitis on the development of osteoarthritic (OA) lesions in an animal model. Methods. OA was induced in the right knees of 30 male New Zealand white rabbits by partial lateral meniscectomy and section of the fibular collateral and sesamoid ligaments (PLM/LS), followed by 8 weekly intraarticular (IA) injections of 1 mg (low-dose) or 10 mg (high-dose) of CPPD crystals in 3 sets of experiments (10 rabbits each). The contralateral left knees served as controls: experiment 1 PLM/LS alone, experiment 2 8 weekly IA injections of CPPD crystals alone, and experiment 3 sham surgery plus 8 weekly IA injections of CPPD crystals. Results. At 8 weeks, repeated IA injections of low-dose and high-dose CPPD crystals into meniscectomized right knees resulted in more severe OA than in meniscectomized but noninjected left knees (experiment 1) (P = 0.003 and P = 0.001, respectively). One-fourth of the meniscectomized knees (11 of 40), both CPPD-injected and noninjected, showed embedded synovial cartilage shards. Conclusion. The data demonstrate a worsening effect of chronic CPPD crystal-induced synovitis on experimental OA produced in the rabbit knees by PLM/LS, and support a possible role for CPPD microcrystalline inflammation in the progression of OA lesions in clinical CPPD crystal deposition disease.
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页码:201 / 210
页数:10
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