In this large population‐based prospective cohort study with a long‐term follow‐up, we found that BMI is a strong independent determinant of incident knee ROA, but not of incident hip ROA. It seems that BMI is also a moderate determinant of progression of knee ROA but not of progression of hip ROA.
This study confirmed that obesity is an important risk factor for the onset of ROA of the knee. The results of this study indicate that overweight is not related to the onset of ROA of the hip. Two case–control studies investigated the relationship between BMI and an incident total hip replacement during the follow‐up period and reported conflicting results.17,18
So far, no studies have been published that investigated the relationship between BMI and incident ROA of the hip in a longitudinal study.
The strength of this study is that the relationship between BMI and incidence and progression of ROA has been investigated in a single study with a similar population and a similar design. Therefore, the reported association between BMI and progression of knee ROA was independent of the definition used for progression. We used two definitions of progression of ROA—namely a JSN and an increase in the Kellgren and Lawrence index. For both definitions, we found a moderate association between BMI and progression of knee ROA. So far, studies that have investigated this topic have reported inconsistent results.4,19,20,21,22,23,24
We confirmed in this large study that BMI is not related to the progression of hip ROA, as suggested earlier by Lievense et al
The fact that participants had to be mobile enough to visit the research centre at baseline and at follow‐up, and survive the follow‐up period (mean 6.6 years), led to the selection of a younger and healthier population. Compared with the total Rotterdam Study population, our study population was younger, had a lower prevalence of lower limb disability, and a lower prevalence of knee and hip pain. Therefore, in this younger and (possibly) healthier population, the number of cases with incident and progression of osteoarthritis at follow‐up may have been underestimated. This could have resulted in an underestimation of the reported associations.
We argued whether the reported estimates could be flawed by limited contrast between those people with a BMI >27.5 kg/m2
compared with those with a BMI
. In our study population, only a few people had a BMI >30 kg/m2
. Additionally, we assessed the association of a BMI >30 kg/m2
with the incidence and progression of osteoarthritis, compared with those with a BMI
. We found similar estimates for the hip and knee; however, for JSN, it just failed to reach significance (95% CI 0.8 to 9.9). Besides, it is plausible that if we had used a population with a higher BMI, the mean BMI of the highest group (>27.5 kg/m2
) would have been much higher. Consequently, the contrast between the reference group and this group would have been greater, with probably a higher risk estimate. We assume that the reported risk estimate in this study would have been even stronger in a population with a higher BMI.
A possible explanation for the difference between the knee and hip might be that the relationship between BMI and osteoarthritis is mediated by another local factor, such as changed mechanical loading of the joint by—for example, malalignment. Sharma et al33
and Felson et al34
reported that the relationship between obesity and osteoarthritis is modified by the presence of malalignment of the knee. In an earlier study, we did not find that a changed mechanical loading (acetabular dysplasia) of the hip distinctively modified the association between BMI and the onset of hip osteoarthritis.35
These results suggest that changed mechanical loading of the joint is an effect‐modifier for the relationship between BMI and osteoarthritis for the knee but not for the hip. This difference might be explained by the difference in anatomy; the knee joint is a hinge joint, whereas the hip is a ball‐and‐socket joint. Although malalignment is per definition not a problem in a ball‐and‐socket joint (eg, the hip joint), it might be a problem in a hinge joint (eg, the knee joint). If the forces on the joint are higher because of higher stresses (eg, obesity, heavy lifting), forces in a malaligned hinge joint might even double or triple as compared with a normal aligned joint, owing to the smaller area that the forces act on.
The relationship between BMI and osteoarthritis could also be modified by trauma of the joint, particularly the knee joint. Englund and Lohmander36
reported that patients who had undergone total meniscectomy with obesity (BMI
) had a greater likelihood of knee ROA than those with a BMI <25 kg/m2
Besides the biomechanical effects, there also seems to be a systemic metabolic effect of obesity that influences the onset or progression of osteoarthritis. Leptin, a small polypeptide that regulates food intake and energy expenditure at the hypothalamic level, may provide the metabolic link between obesity and osteoarthritis. Plasma levels of leptin strongly correlate with fat mass, and levels fall after weight loss.37
Recent studies detected functional leptin receptors on human adult articular chondrocytes.38,39
Leptin may also play a part in the development of osteoarthritis through changes in the bony matrix.40,41
As obesity and osteoarthritis are both associated with genetic predispositions, these two dispositions may be linked. However, Manek et al42
could not detect a shared genetic pathway between BMI and knee osteoarthritis.
However, this possible systemic effect of obesity does not explain why obesity is related to knee osteoarthritis and hardly at all to hip osteoarthritis.
The distinction between the incidence and progression of already existing osteoarthritis is arbitrary. This distinction depends on the point during the ongoing process of degenerative changes in the joint at which the cut‐off point of the present osteoarthritis is defined.43
If osteoarthritis is diagnosed earlier in the future, because of more sensitive diagnostic tools, cases formerly considered to be “incident cases” will then be considered as “progressive cases”. In the case of the Kellgren and Lawrence index, incident ROA is usually defined as minimally grade 2 at follow‐up and grade 0 or 1 at baseline. However, one can question whether the cut‐off point of
grade 2 is valid and whether it is correct to classify people with grade 1 as “normal”. Recently Hart and Spector44
investigated whether the Kellgren and Lawrence grade 1 of the knee was a reliable indicator of knee osteoarthritis in a longitudinal population‐based study. After 10 years of follow‐up, >60% of the participants with grade 1 at baseline had developed grade
2, whereas 20% of those with a Kellgren and Lawrence grade 0 at baseline had developed a grade
2. For the hip, we found that after 6 years of follow‐up, 7.6% of participants with a Kellgren and Lawrence hip grade 1 v
1.4% with grade 0 at baseline developed a grade
2. These results suggest that the cut‐off point of
grade 2 for the hip seems to be valid, whereas a cut‐off point of
grade 1 for the knee seems more appropriate. Overall, the distinction between incident ROA and progression of ROA seems arbitrary. Owing to the absence of consensus on how to define progression, we used two definitions in this study—namely JSN
1.5 mm, and also an increase of minimally 1 grade in the Kellgren and Lawrence index. We believe that a better insight into the consistency of reported results is possible with the use of several cut‐off points.
In this study, we included those knees and hips with a presence of radiographic osteoarthritic signs at baseline defined by a Kellgren and Lawrence score at baseline of grade 1, 2 or 3 for the progression analyses. Additionally, we repeated these analyses for those knee and hips with a Kellgren and Lawrence score of grade 2 or 3 at baseline. All assessed ORs remain similar to those reported in tables 3 and 4; however, owing to lower numbers, the risk estimates failed to reach significance.
On the basis of the results of this study, we conclude that BMI is associated with the incidence and progression of knee ROA, and that these associations are independent of age and sex. Furthermore, it seems that BMI is not associated with the incidence and progression of hip ROA.