ACCELERATION OF EXPERIMENTAL LAPINE OSTEOARTHRITIS BY CALCIUM PYROPHOSPHATE MICROCRYSTALLINE SYNOVITIS

Citation
Ag. Fam et al., ACCELERATION OF EXPERIMENTAL LAPINE OSTEOARTHRITIS BY CALCIUM PYROPHOSPHATE MICROCRYSTALLINE SYNOVITIS, Arthritis and rheumatism, 38(2), 1995, pp. 201-210
Citations number
58
Categorie Soggetti
Rheumatology
Journal title
ISSN journal
00043591
Volume
38
Issue
2
Year of publication
1995
Pages
201 - 210
Database
ISI
SICI code
0004-3591(1995)38:2<201:AOELOB>2.0.ZU;2-H
Abstract
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 r abbits each). The contralateral left knees served as controls: experim ent 1 PLM/LS alone, experiment 2 8 weekly IA injections of CPPD crysta ls alone, and experiment 3 sham surgery plus 8 weekly IA injections of CPPD crystals. Results. At 8 weeks, repeated IA injections of low-dos e and high-dose CPPD crystals into meniscectomized right knees resulte d 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 noninjec ted, showed embedded synovial cartilage shards. Conclusion. The data d emonstrate a worsening effect of chronic CPPD crystal-induced synoviti s on experimental OA produced in the rabbit knees by PLM/LS, and suppo rt a possible role for CPPD microcrystalline inflammation in the progr ession of OA lesions in clinical CPPD crystal deposition disease.