Abstract
Introduction and Aims: Cartilage injury often leads to secondary osteoarthritis. However, the progression of cartilage lesions after injury has not been fully documented. Factors predictive of the rate and severity of progression are largely unknown. This study analysed the relationship between arthroscopic, histologic, and magnetic resonance imaging findings after acute joint trauma.
Method: Twenty patients were recruited into the study at a mean three months after acute knee injury. Each patient underwent cartilage-specific magnetic resonance imaging (MRI) sequences of the affected knee after injury and at six months, one year, and two years after arthroscopy. Cartilage lesions were graded on MRI and arthroscopy. Synovial fluid was sampled, and a 1.8 mm biopsy was obtained from the edge of cartilage lesion. Control biopsies were obtained from fresh cadaver donors. Cells undergoing DNA fragmentation in biopsies were counted.
Results: All cases of partial or full thickness cartilage loss were detected by MRI. Biopsies from cartilage lesions had significantly more cells undergoing DNA fragmentation (41%) than control biopsies (12%), suggesting apoptotic cell death. On MRI follow-up, cartilage lesion grade improved in five patients, worsened in two, and did not change in 13 patients. The percentage of cells undergoing DNA fragmentation correlated significantly with keratan sulfate levels in synovial fluid (R = 0.68). Keratan sulfate levels were markedly higher in knees with progressive lesions (72 vs. 31 microgm/ml).
Conclusion: Cartilage cell viability can directly impact the potential for repair. The development of accurate markers that may predict the eventual fate of the lesion is of tremendous clinical value. Elevated levels of matrix degradation products such as keratan sulfate can be predictive of a poorer prognosis.
These abstracts were prepared by Editorial Secretary, George Sikorski. Correspondence should be addressed to Australian Orthopaedic Association, Ground Floor, The William Bland Centre, 229 Macquarie Street, Sydney, NSW 2000, Australia.
At least one of the authors is receiving or has received material benefits or support from a commercial source.
