Women have an increased risk of knee osteoarthritis (OA). However, little is known about gender differences in cartilage health before the onset of clinical knee OA. The aim of this study was to examine whether there are longitudinal gender differences in knee cartilage in a cohort of healthy, asymptomatic adults with no clinical knee disease.
Two hundred seventy-one participants (169 women) aged between 50 and 79 years with no clinical history of knee pain or pathology were examined using magnetic resonance imaging at baseline and 2.3 years later. From these images, changes in tibial and patella cartilage volume and progression of cartilage defects were determined.
In multivariate analyses, after adjustment for potential confounders, the average annual percentage loss of total tibial cartilage volume was significantly greater in women (1.6% [95% CI, 1.1-2.2]) than in men (0.4% [95% CI, −0.4 to 1.2]) (P = 0.05 for difference). Likewise, the female gender was also associated with an increased risk for the progression of tibiofemoral cartilage defects (odds ratio, 3.0; 95% CI, 1.1-8.1; P = 0.03). At the patella, the average annual percentage loss of cartilage volume was significantly greater in women (2.3% [95% CI, 1.7-2.8]) than in men (0.8% [95% CI, 0.1-1.6]) (P = 0.02 for difference).
The female predisposition toward knee OA may, at least in part, be due to gender differences in cartilage health, even before the onset of clinical knee disease. Understanding the mechanism for these gender differences may provide a means to reduce the risk of knee OA in women.
Women, in comparison to men, tend to lose more tibial and patellar cartilage volume and are more likely to show increased severity of cartilage defects. This may in part explain the increased risk of knee osteoarthritis in women compared with men. The mechanism for this gender difference remains unknown.
From the 1Department of Epidemiology and Preventive Medicine, Monash University, Central and Eastern Clinical School, Alfred Hospital, Melbourne, Victoria, Australia; 2Baker Heart Research Institute, Commercial Rd, Melbourne, Victoria, Australia; 3Cancer Epidemiology Centre, The Cancer Council of Victoria, Carlton, Victoria, Australia; and 4Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, The University of Melbourne, Victoria, Australia.
Received November 4, 2008; revised and accepted December 11, 2008.
Dr. Hanna and Mr. Teichtahl are joint first authors.
Funding/support: This study was funded by a program grant from the National Health and Medical Research Council (NHMRC; 209057) and was further supported by infrastructure provided by The Cancer Council of Victoria. This study was also supported by NHMRC (project grant 334150), Colonial Foundation and Shepherd Foundation. Dr. Hanna is the recipient of an NHMRC public health (Australia) Fellowship (NHMRC 418916). Dr. Wang is the recipient of an NHMRC Public Health (Australia) Fellowship (NHMRC 465142); Dr. Wluka is the recipient of an NHMRC Public Health (Australia) Fellowship (NHMRC 317840) and corecipient of the Cottrell Fellowship, Royal Australasian College of Physicians; and Dr. Urquhart is the recipient of an NHMRC Clinical Research Fellowship (NHMRC 284402).
Financial disclosure/conflicts of interest: None reported.
Address reprint requests to: Flavia Cicuttini, MBBS, FRACP, PhD, Department of Epidemiology and Preventive Medicine, Monash University, Alfred Hospital, Melbourne, Victoria 3004, Australia. E-mail: email@example.com