We have no detailed information from large and well-documented cohorts
about the natural history of obesity-induced foot, knee and hip deformities
discussed above. There is enough evidence, however, that at least major
disturbances of joint anatomy in advanced tibia vara as well as SCFE can
lead to early and severe cartilage degradation with clinical and radiographic
signs of OA. In these cases cartilage surfaces cannot tolerate daily mechanical
loading over time, as the transmission of forces is altered due to joint
Another interesting question is, however, if even anatomically normal
joints – without evidence of axial deformation or epiphyseal tilt – tolerate
high mechanical loads over time in obese patients or if they also develop
osteoarthritic changes. A positive association between obesity and OA of the
knee has been observed in several large studies [35–39] and weight loss has
been shown to reduce the incidence of knee OA in women . Recent studies
also report an association between high BMI and OA of the hip, but results are
less compelling [39, 41–44]. In all these series no special emphasis was given
to specific deformities of hip or knee joints.
In the Ulm Osteoarthritis Study , we tried to assess independent
associations of obesity (30 or more kg/m2) and overweight (25 or more but less
than 30kg/m 2) with radiographically defined OA patterns in men and women
with advanced knee and hip OA. As we looked for specific anatomic changes
of the investigated joints (tilt deformity, axial malalignment of the legs) as
well, an analysis with and without these confounding risk factors for OA was
possible. We observed a positive association between obesity, overweight and
BMI and a pattern of bilateral radiographic knee osteoarthritis and the association
was even more pronounced after controlling for potential confounders.
No association, however, between relative weight and bilateral OA was observed
in participants with hip OA.
There is still an ongoing discussion about the contribution of local biomechanical
factors and systemic or metabolic factors to explain the higher risk
of OA in obese populations. In our study, a metabolic link between obesity
and OA is not very likely, as we found an association in knee disease but not
The time sequence between obesity and OA pattern can not be addressed
in a cross-sectional study. Theoretically, OA could lead to higher body weight
through a sedentary life style. Neither the results of our study with different
associations in knee and hip disease (in contrast to similar functional impairment
in both study groups) nor data from other case-control or even cohort
studies support this theory. Mechanical rather than systemic effects of obesity
appear to be a reason for the causal relationship with OA.
In conclusion, we can find associations between obesity in children and
specific deformities of feet, knee and hip joints. Although the natural course of
these deformations is not very well documented, it can be assumed that at least
tibia vara and slipped capital femoral epiphysis lead to clinically relevant knee
and hip OA. Even without manifest deformation of a single joint through high
body weight the continuous mechanical overload seems to result in cartilage
degradation as well. Strong associations between obesity and knee OA (and
also weaker associations between obesity and hip OA) support this theory.
Meanwhile there is enough evidence that obesity and OA are linked together in
a causal relationship.
Considering the adverse effects of elevated body weight on the musculoskeletal
system, we must increase our efforts to lower the incidence and
prevalence rates of overweight and obesity in children, adolescents and adults.