Degeneration of normal articular cartilage induced by late phase osteoarthritic synovial fluid in beagle dogs.
OBJECTIVE
To investigate the pathogenesis of late phase osteoarthritic (OA) synovial fluid (SF) on normal articular cartilage in vivo and provide an understanding of degenerative cartilage extending in OA joint.


METHODS
A random knee, each of 8 beagle dogs, received anterior cruciate ligament transection (ACLT) and was confirmed to have late phase OA degenerative changes at 24 weeks after operation. Thereafter, one random elbow of each canine was injected with autologous late phase OA knee SF. The contralateral elbow was injected with normal saline (NS) of the same volume as SF aspirated from ACLT knee. These two groups of elbows were labeled "SF" and "NS". 8 other beagle dogs were left intact and placed in Group Control. After aseptic arthrocentesis was performed weekly on both elbows for 24 weeks, morphological changes were observed in the cartilage of the elbows, and expressions of 7 biological etiological factors of chondrocytes of the elbows were determined in Group SF, Group NS and Group Control, respectively.


RESULTS
Morphological changes were observed in articular cartilage of the elbows in Group SF. Levels of unit area of collagen type I in the noncalcified, calcified and full zones of articular cartilage of the elbows in Group SF increased significantly. Level of unit area of collagen type III in the calcified zone of articular cartilage of the elbows in Group SF remained unchanged. Meanwhile, expressions of MMP-1 and MMP-3 of chondrocytes of the elbows in Group SF increased significantly. There was almost no difference between articular cartilage in Group NS and Group Control.


CONCLUSIONS
Based on these results, we conclude that OA degeneration of normal articular cartilage can be independently induced by late phase OA SF. Endogenous OA biological etiological factor may be one of the reasons causing degenerative cartilage extending in OA joint.
Xu
Qing Rong
QR
Department of Orthopaedics, Renji Hospital, Medical School of Shanghai Jiaotong University, Shanghai 200127, China.
Dong
Ying Hai
YH
Chen
Shun Le
SL
Bao
Chun De
CD
Du
Hui
H
D000818:Animals; D001798:Blood Proteins / Q000378:metabolism; D002358:Cartilage, Articular / Q000473:pathology*; D019902:Chondrocytes / Q000473:pathology / Q000648:ultrastructure; D004285:Dogs; D015870:Gene Expression; D020781:Matrix Metalloproteinase 1 / Q000235:genetics / Q000378:metabolism; D053509:Matrix Metalloproteinase 13 / Q000235:genetics / Q000378:metabolism; D019278:Matrix Metalloproteinase 3 / Q000235:genetics / Q000378:metabolism; D008855:Microscopy, Electron, Scanning; D046529:Microscopy, Electron, Transmission; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics; D020370:Osteoarthritis, Knee / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D013582:Synovial Fluid / Q000378:metabolism; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000235:genetics / Q000378:metabolism; D016211:Transforming Growth Factor alpha / Q000235:genetics / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism
D001798:Blood Proteins; D019715:Tissue Inhibitor of Metalloproteinase-1; D016211:Transforming Growth Factor alpha; D053773:Transforming Growth Factor beta1; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D053509:Matrix Metalloproteinase 13; D019278:Matrix Metalloproteinase 3; D020781:Matrix Metalloproteinase 1