In this population of healthy community‐based adults with no clinical knee OA, baseline (1990–4) and current (2003–4) FFM were both positively associated with tibial cartilage volume, independent of FM. Increase in FFM over the time period was associated with an increase in tibial cartilage volume. In contrast, FM was associated with an adverse effect on knee cartilage. Current FM was associated with reduced tibial cartilage volume, and both baseline and current FM were associated with an increase in tibiofemoral cartilage defects, independent of FFM. Taken together, these findings suggest a beneficial effect of FFM, but a negative effect of FM, on knee cartilage in healthy people.
In this study, we found compelling evidence for a beneficial effect of FFM on cartilage. Both current FFM and FFM measured 10 years earlier were associated with an increased tibial cartilage volume in healthy people independent of FM. It has been shown that increased muscle size and mass is related to increased knee cartilage volume.6,21
We have also recently shown that lower muscle mass is associated with an increased loss of medial and lateral tibial cartilage over 2 years in people without knee OA.6
In the present study, we also showed an additional beneficial effect of increase in FFM over time that was associated with increased cartilage volume. These data suggest that increased muscle mass, including gains later in life, may be protective against the loss of cartilage volume. The mechanism by which this occurs is not known but may be due to greater stabilisation at the knee joint during dynamic tasks. The effect of FFM on cartilage volume cannot simply be explained by physical activity, because adjustment for physical activity in the analyses did not change our findings (results not shown). Although it may be that muscle mass and cartilage volume are co‐inherited, our finding that an increase in FFM over the time period was associated with increased tibial cartilage suggests that muscle mass is an important determinant of cartilage volume. These data suggest that a change in muscle mass has the capacity to affect changes in cartilage volume.
Obesity is an established risk factor for cardiovascular disease as well as knee OA.1,2
However, unlike for cardiovascular disease,8
the distribution of body fat has been inconsistently associated with the risk of knee OA.2,9,10
A recent cross‐sectional study showed that BMI, FM, percentage FM and waist circumference were higher in women with OA than in those without, but that there were no differences in WHR between the two groups.22
We found that BMI was associated with an increased presence of cartilage defects, which is consistent with a previous study showing a correlation between BMI and an increased prevalence and severity of cartilage defects.23
Although BMI is a good measure of body weight, independent of height, it fails to distinguish between adipose and non‐adipose body mass.5
Our data suggest a negative effect of FM on knee cartilage, with a reduction in volume and an increase in cartilage defects. Moreover, the positive association between FFM and WHR and knee cartilage defects found in this study could be explained by the effect of FM. Cartilage defects have previously been shown to be predictive of cartilage loss, independent of cartilage volume, suggesting a continuum from normal to abnormal cartilage even in healthy people, and that the defects may represent early cartilage abnormalities.15,24
It is therefore possible that FM may be an important factor in the development and progression of cartilage defects, ultimately leading to longitudinal cartilage loss and knee OA. This may be important in helping to understand the association between obesity and the onset and/or progression of OA.
A potential limitation of this study was the method used to assess body composition. Body composition can be estimated by several different techniques. For instance, lean body mass can be considered a surrogate measure of muscle mass.25
In this study, we used FFM, which is the total weight of the body without any fat, referring to all skeletal bones and muscles and other body tissues not containing fat, as a surrogate measure of muscle mass. However, FFM may not always accurately reflect specific changes in muscle mass or differences in muscle mass between individuals.26
Nevertheless, our findings persisted after adjustment for age, gender and bone size (tibial plateau bone area), confirming that FFM was a more accurate measure of muscle mass.
A potential strength of our study is that we examined both current body composition as well as data objectively collected about 10 years earlier. This has been recently raised in the context of examining risk factors for OA, particularly in relation to obesity, as any development of symptomatic disease may be associated with a reduction in physical activity and obesity.27
In this study we examined asymptomatic people and used a novel methodology that allowed us to examine knee cartilage in a sensitive, validated way. This allowed us, for the first time, to examine cartilage in a continuum from the healthy through to the diseased state so that we can examine the effect of body composition on knee joint morphology in asymptomatic people with no disease or early subclinical disease.
How FFM confers a beneficial effect on knee cartilage whereas FM is associated with a reduction in cartilage and an increase in defects is unclear. The emerging data suggest that beneficial effects of FFM on the joint may be related to biomechanical stabilisation of the joint.6,7
Obesity increases joint loading, which may predate cartilage degeneration at weight‐bearing sites such as the knee. However, if this were the only explanation, we would expect a similar effect of FFM, which was not the case. Furthermore, our findings that WHR was not associated with an increased presence of tibiofemoral cartilage defects, independent of FM, suggest that this pattern of fat distribution may not be important in OA. However, it has long been recognised that the effect of obesity cannot simply be explained by the biomechanical effect of weight. For example, it has previously been suggested that OA at non‐weight‐bearing sites such as the carpometacarpal joints and the proximal interphalangeal joints of the hands may be due to metabolic factors related to adiposity.28
It may be that hormones such as leptin that indirectly reflect body fat stores and have a role in immunomodulation29
may be important in OA.30
Chondrocytes from joint cartilage have been shown to express leptin receptors,30,31
which, when stimulated, produce nitrous oxide, leading to inflammatory alterations in cartilage including phenotype loss of chondrocytes, apoptosis and metalloproteases activation.32,33
In this population of healthy adults, our results suggest a beneficial effect of baseline FFM, current FFM and increase in FFM on tibial cartilage volume over the time period of the study. In contrast, FM was deleterious, being associated with a reduction in tibial cartilage volume and an increase in tibiofemoral cartilage defects independent of FFM. The relative importance of these factors differed according to structure, possibly suggesting different mechanisms of effect. These data suggest that weight‐loss programmes aimed at reducing FM but preserving/increasing FFM may be important in maintaining cartilage health, thus preventing the onset and/or progression of knee OA.