The lack of a statistically significant association between either body shape or thigh girth and EKAM, after controlling for the effect of weight suggests that excess weight is the main factor responsible for the more extreme medial compartment loading during obese gait. Thus, rather than thigh or abdominal fat distribution, it seems to be the presence of obesity that increases medial compartment loading. The increased medial loading with obesity found in this study may help to explain why obese subjects have been noted to have enlarged medial tibial bone area.50
The lack of a difference between lower-body and central obesity on estimates of medial knee joint loading is consistent with the findings of epidemiologic studies of obesity and knee OA.19,20,51,52
After adjusting for age, race, and BMI, the NHANES-I did not demonstrate an association between body fat distribution (central or peripheral fat distribution) and knee OA.51
Data from the Baltimore Longitudinal Study of Aging, also after adjusting for BMI, did not reveal a significant association between percent body fat (measured by skin folds) or WHR and knee OA.20
The NHANES-III also demonstrated that continuous waist circumference did not contribute to predicting risk for knee OA once BMI was in the model.53
Our study was designed to address a limitation of these studies, the lack of assessment of thigh circumference in obese adults. The combined results of these studies, therefore, suggest that neither increased central nor thigh fat distribution seems to be the mechanism by which obesity increases risk for knee OA.
It is interesting that when treated as categorical variables, the higher tertiles of waist circumference within each tertile of BMI increased risk for knee OA in NHANES-III although not when BMI and waist circumference were treated as continuous variables.53
Our finding that centrally obese subjects had a more extreme EKAM than lower-body obese subjects, although not significantly so, may be consistent with this increased risk for knee OA in subjects categorized as the highest tertile of central obesity in NHANES-III. However, the consistency among the results of NHANES-I, Baltimore Longitudinal Study of Aging, NHANES-III continuous analyses, and the results of the current study suggest that obesity is a much stronger risk factor for knee OA than the pattern of obesity.
Although not independent of weight, the presence of a more extreme absolute first peak EKAM and impulse in those with a central obesity pattern is indicative of the moment that is actually experienced by the knee joint. Considering that an increased first peak EKAM has been associated with risk for knee OA and angular impulse is related to severity of knee OA,32,54,55
this increased absolute load may have consequences. In addition, considering that 4 of the 20 subjects with a central obesity pattern had first peak EKAM values considerably more extreme than others (outliers) and not all obese people develop knee OA, it may be this subset that is at increased risk for knee OA. This supposition is supported by the fact that normalizing the first peak EKAM to body mass for the whole central group did not bring first peak EKAM values to comparable levels with the control group (as was seen when the outliers were removed).
There was a proportional decrease in second peak EKAM for both obese groups that is reflected in significantly lower, normalized values for the lower-body obesity group. This relative decrease in the second peak points to a somewhat modified walking strategy seen in the obese groups (and evident in ). Although all three groups showed a relative decrease in the second peak EKAM, the lower-body obesity group demonstrated the greatest reduction in magnitude, such that the bimodal characteristics were minimized and the amplitude was not different from the control group. Previous research has associated changes in the second peak EKAM with the amount of toe-out, gait speed, or sex.55,56
Such associations were not demonstrated in the current study. Given that a symmetrical bimodal ground reaction force was seen in all groups, the changes observed for the lower-body obesity group point toward dynamic alignment changes that may be positively influenced by body mass distribution. These changes are also represented in the impulse data where trends point to greater loading in the central obesity group.
Although our results regarding estimated knee joint loading in subjects without OA were consistent with results reported in epidemiologic studies including subjects with knee OA, there were several potential limitations. First, the EKAM is an estimate of knee joint forces rather than a direct measure. However, this estimate is highly correlated with risk for progressive knee OA and therefore merited assessment.32,33
Second, there was a relative lack of male subjects in this study despite efforts to recruit both men and women. Although this limited ability to compare results by sex, the availability of female subjects was informative, considering both the prevalence of knee OA and the association between obesity and knee OA is higher in women. Importantly, results for the overall study and for women only did not differ. When restricted to the 50 female subjects, nonnormalized EKAM significantly differed between control (−21.2 N m) and lower (−33.6 N m) by 12.4 N m (95% confidence interval, 1.3–23.5; P
< 0.0001), and between control and central (−44.0 N m) by 22.8 N m (95% confidence interval, 10.8 –34.9; P
< 0.0001). Even after controlling for weight, body shape was a significant predictor of EKAM (P
= 0.0001). In addition, toe rotation did not differ between central and lower-body obese groups in women.
This study found that estimates of medial knee joint loading are more dependent on weight than on fat distribution or thigh girth in obese subjects. This study did not assess the effects on knee joint loading in people with high BMI or high thigh girth because of excess muscle. Although this could be studied separately in subjects with excess muscle, we are not aware of an increased risk for knee degeneration in such individuals, and excess fat tissue is by far, the most common reason for a high BMI.
This study was designed to assess the effect of fat distribution on medial knee joint loading in an effort to address a portion of the larger question, “why does obesity increase risk for knee OA?” Although the mechanism is unclear, it does seem that excess weight plays an important role. With obesity, that excess weight is mostly fat, a noncontractile tissue that may load the knee without providing joint protection. In other words, whereas lean mass may aid in controlling knee joint movement or providing active stabilization of the joint, excess fat would not provide such control. These circumstances may lead to exceeding a threshold of EKAM that either damages cartilage or prevents it from healing and therefore contributes to medial knee OA.
There are likely numerous factors, outside the focus of this study, that may better characterize why obesity predisposes to knee OA and which adults are at increased risk. Longitudinal epidemiologic studies have suggested that factors in the local joint environment, such as strength, laxity, malalignment,57,58
and history of an injury59
may interact with obesity to contribute to risk for knee OA.57,58,60–62
Because this study was intended to assess for differences in the dynamic frontal plane moment at the knee in people without knee OA, who had lower-body and central obesity, other risk factors associated with knee OA were not assessed. For example, radiographic lower-limb alignment was not measured because the focus of this study was on the EKAM. Although lower-limb mechanical axis is recognized as a predictor of knee peak adduction moments,63
the correlation between radiographic lower-limb alignment and the EKAM has not been consistently reported to be high. Although lower-limb mechanical axis is recognized as a predictor of knee peak adduction moments,63
it explains <50% of the variability in the dynamic frontal plane moment.64
reported that the inclination of the tibia in the coronal plane rather than angulation at the knee predicts the adduction moment because of the ground reaction force. From this, he concluded that there is no correlation between knee angular deformities on radiographs and joint forces. Others have also reported that static alignment does not predict the location or magnitude of knee joint forces.29,30
In contrast, studies of patients after unicompartmental arthroplasty have revealed a relationship between knee coronal radiographic alignment and the knee adduction moment.66,67
Although reasons for the differences in correlations have not been fully elucidated, preliminary evidence suggests that the relationship may be stronger in subjects after mechanical realignment of the knee.68
The discrepancy between static alignment and dynamic moments also may be as a result of antalgic or proprioceptive compensations, such as increased toe-out, widened base, or alteration of gait velocity.65
Therefore, for studies of the development of knee OA or surgical realignment, radiographic mechanical alignment may be of value.