We report that a 5-unit increase in current BMI had a non-statistically significant 1.7-fold increased odds of MRI-based moderate and severe cartilage damage, although there was a trend towards statistical significance. A 5-unit increase in BMI is a clinically meaningful measure, since it means that a person would have changed into a higher BMI category, (e.g. going from normal to overweight or from overweight to obese). We also found a statistically significant 3-fold increased odds of cartilage damage in people with abnormal current BMI (BMI ≥25) compared to those with normal BMI, adding strength to the idea that increased weight is linked to cartilage damage, even in asymptomatic people. In symptomatic populations, the relationship between BMI and cartilage damage or OA has been elucidated to a much greater extent. Mezhov et al. (2014) [
9] reviewed 22 studies that examined the relationship between obesity and knee cartilage in patients with knee OA, concluding that there was a detrimental effect of BMI and fat mass on cartilage, though cohort studies were relatively lacking. In comparison, this is less clear in asymptomatic studies. Our finding of an increased odds of cartilage damage with BMI, although short of statistical significance, is in keeping with most [
3,
4,
7,
14‐
16], but not all studies [
2,
17]. Among the six studies reporting an association, only one included both tibiofemoral and patellar cartilage defects [
7], similar to ours. They studied 137 volunteers from the OAI without radiographic OA and reported cross-sectionally that cartilage damage was significantly more common in overweight and obese subjects compared to normal BMI subjects, and longitudinally, new or worsening cartilage lesions were significantly higher in obese subjects after 36 months [
7]. Their findings agree with our finding of an increased odds of threefold for patients with a BMI ≥ 25. However, in contrast to our study, they included a highly selected cohort of subjects at risk of OA. In addition, their definition of no knee pain included individuals with some knee symptoms who would have been excluded in our study. Other positive studies either examined only tibiofemoral cartilage [
3,
4] or only patellar cartilage [
14‐
16]. Brennan et al. (2010) [
3] reported an association between current BMI and prevalent tibiofemoral cartilage defects with an adjusted OR of 1.07 per one unit of BMI increase, which translates to an OR of 1.4 per 5 units of BMI increase. This finding is comparable to our study’s result of OR 1.65 per 5 units. Our study contributes to the literature in two ways. Firstly, our population-based study allows for more generalizability. Among these six positive studies, only two were population-based and they studied a younger (age 30-49) and only female population [
3,
14], whereas we included a wide age range (40-79 years) and both males and females. Secondly, our study is the first to examine and report on a trend to significance with a more severe grading of cartilage damage. In contrast, two studies did not find an association between BMI and prevalent cartilage damage [
2,
17]. Guermazi et al. (2012) [
2] stratified 710 participants into normal, overweight, and obese and found no differences in prevalence of tibiofemoral cartilage defects. In contrast to our study, they used a mixed population aged >50 years old with no radiographic evidence of knee OA with 29% experiencing some knee pain in the last month. While the other study by Berry et al. (2010) [
17] did not find an association between tibiofemoral cartilage defects and BMI, they did, however, establish an association with fat mass measured by dual X-ray absorptiometry. BMI is a crude, but clinically useful, measure of obesity. Although fat mass is a different marker of obesity, their finding parallels our study by suggesting an impact of obesity or adiposity on cartilage health in asymptomatic individuals.