Volume 6 Supplement 3

Global Arthritis Research Network (GARN): 4th World Congress on Arthritis in Montreal

Open Access

Imaging and osteoarthritis

  • F Cicuttini1 and
  • A Wluka1
Arthritis Res Ther20046(Suppl 3):26

https://doi.org/10.1186/ar1361

Published: 13 September 2004

Understanding of joint cartilage development and the pathophysiology of osteoarthritis (OA) has previously been limited by the lack of a noninvasive method for assessing joint cartilage in vivo. There has been increasing interest in the use of magnetic resonance imaging (MRI) in the measurement of articular cartilage volume as a possible outcome measure in arthritis. Recent work has shown that the cartilage volume, as measured by MRI, can be measured in a valid and reproducible way, with a coefficient of variation of ~2%. The knee cartilage volume correlates inversely with the radiographic grade of OA. Studies have shown that significant loss in knee cartilage has already occurred by the time radiographic change occurs at the knee. Subjects with OA lose approximately 5% of their knee cartilage per annum, while normal, healthy males and females lose between 1% and 3% per annum. There is evidence from longitudinal data that loss of knee cartilage volume is associated with a worsening of knee symptoms and that those in the top tertile of rate of cartilage loss have a sevenfold increased risk of progressing to a knee replacement within 4 years. Other joint structures can be measured using MRI. Interesting data have emerged from examining knee bone marrow oedema and cartilage defects: bone marrow oedema has been shown to be associated with pain and progression of knee OA in the adjacent tibiofemoral compartment. Recent data suggest that knee cartilage defects predict healthy subjects at risk of losing knee cartilage and increase the risk of progressing to a knee replacement in those with knee OA. The emerging data suggest that MRI assessment of joints in normal subjects and those with OA has the potential to significantly increase our understanding of the pathogenetic mechanisms involved in the development of OA, and thus to identify strategies to prevent and treat this disease.

Authors’ Affiliations

(1)
Department of Epidemiology and Preventive Medicine, Monash University Medical School, Central and Eastern Clinical School, Alfred Hospital

Copyright

© The Author(s) 2004

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