Articular collagen degradation in the Hulth-Telhag model of osteoarthritis.
OBJECTIVE
This study employed immunohistochemistry to investigate the pattern of type II collagen (CII) degradation in an acute injury model of osteoarthritis. It was hypothesized, based on previous studies of primary osteoarthritis (OA), that the worst areas of CII degradation would be located in the superficial and upper middle zones of the articular cartilage, with staining extending into the deep zone as the OA became more severe.


METHODS
In this model of secondary OA, rabbits were made osteoarthritic by transecting the anterior and posterior cruciate ligaments and removing the meniscus. At various times post surgery, articular cartilage was examined for CII degradation using monoclonal antibody 18:6:D6. This antibody reacts to an epitope that is exposed when CII is degraded as the result of protease cleavage. Proteoglycans (PG) were localized using Safranin-O/Fast Green. Staining intensities were quantitated using image analysis software.


RESULTS
In the joints with surgically induced OA, degradation of CII was seen as early as 3 weeks with the majority of the degradation localized in zones I and III. At 14 weeks the destruction of CII was more pronounced, but there was a surprising lack of degradation in zone II. There were also several other unexpected findings. The sham-operated joints, for example, were intended to serve as controls yet CII degradation was observed in rabbits killed 3 weeks after surgery. It was also expected that greater CII degradation would occur in cartilage from medial condyles, but after 14 weeks there was no significant difference between medial and lateral condyles. Finally, the loss of staining for PG correlated with the degradation of CII except in zone III where limited PG loss was observed.


CONCLUSIONS
Differences were observed between the pattern of articular cartilage destruction in this model of secondary OA and that of primary OA. Further investigation of the mechanical and biochemical processes underlying the development of both types of OA needs to be conducted.
Rogart
J N
JN
Department of Orthopaedics, Brown University School of Medicine, Providence, RI 02903, USA.
Barrach
H J
HJ
Chichester
C O
CO
D000818:Animals; D002358:Cartilage, Articular / Q000378:metabolism* / Q000473:pathology; D003094:Collagen / Q000378:metabolism*; D004195:Disease Models, Animal; D007124:Immunoenzyme Techniques; D007718:Knee Injuries / Q000150:complications; D010003:Osteoarthritis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D011489:Protein Denaturation; D011509:Proteoglycans / Q000378:metabolism; D011817:Rabbits
D011509:Proteoglycans; D003094:Collagen