Differences in type II collagen degradation between peripheral and centralcartilage of rat stifle joints after cranial cruciate ligament transection

Citation
R. Stoop et al., Differences in type II collagen degradation between peripheral and centralcartilage of rat stifle joints after cranial cruciate ligament transection, ARTH RHEUM, 43(9), 2000, pp. 2121-2131
Citations number
42
Categorie Soggetti
Rheumatology,"da verificare
Journal title
ARTHRITIS AND RHEUMATISM
ISSN journal
00043591 → ACNP
Volume
43
Issue
9
Year of publication
2000
Pages
2121 - 2131
Database
ISI
SICI code
0004-3591(200009)43:9<2121:DITICD>2.0.ZU;2-I
Abstract
Objective. Type II collagen degradation is thought to be the key process in cartilage degradation during the development of osteoarthritis (OA). In th is study, we investigated the kinetics of type II collagen degradation duri ng surgically induced OA. Methods. Experimental OA was induced in male Wistar rats by transecting the cranial (anterior) cruciate ligament (CCL). Hematoxylin and eosin staining was used to study overall cartilage degradation, while immunostained secti ons were used to demonstrate denatured type II collagen (Co12-3/4m antibody ) and the collagenase cleavage site in type II collagen (Co12-3/ 4C(short) antibody). Results. During the first 3-4 weeks, cartilage destruction, associated with chondrocyte death, proteoglycan depletion, and a marked increase in the co llagenase cleavage neoepitope, was mainly located at the margins of the car tilage. From weeks 3-4, the central part of the cartilage showed increased surface fibrillation and apparent chondrocyte death. In these areas, increa sed denatured type II collagen staining but little cleavage-site staining w as present. Conclusion. These results indicate that cartilage degradation after CCL tra nsection in the rat consists of 2 phases. An early phase located at the car tilage margins and a late phase located at the central part of the cartilag e. In the early phase, collagenase-dependent cartilage damage occurred. Dur ing the late phase, the level of type II collagen denaturation increased.