or ‘Blount’s disease’ is a disorder characterized by abnormal growth of the
proximal tibial physis, which results in progressive varus angulation below
the knee [16, 17]. The disease can be classified into three age-onset groups:
infantile (less than 3 years), juvenile (4–10 years) and adolescent (11 years and
older). All three forms of tibia vara have similar clinical, roentgenographic and
histopathologic characteristics, but differ in the amount of remaining growth,
the magnitude of medial compression forces across the knee and recurrence
rates after surgical correction [18]. Similar histopathologic findings with injury
to the growth plate as demonstrated by fissuring and clefts in the physis as
well as fibrovascular and cartilaginous repair tissue at the physeal-metaphyseal
junction indicate a common etiology of all three groups [19]. The observations
are also similar to histopathologic findings in slipped capital femoral epiphysis
(SCFE), suggesting a common etiology [18].
The clinical characteristics of most study groups with tibia vara are very
similar and often focus on marked obesity besides normal height, black race
and slowly progressive genu varum [Thompson et al., 1984]. In a very well
documented series of 8 patients with juvenile-onset as well as 9 patients with
adolescent-onset disease, Thompson and Carter [18] found marked obesity in
all children. While the mean height of the children was in the 75th percentile
(range 50th to 95th percentile) the weight exceeded the 95th percentile in every
case by a mean of 20kg (range 10–61 kg).
Dietz et al. [20] reported a series of 18 patients with infantile- and juvenileonset
disease. Twelve children (67%) had weights for height greater than 120%
ideal body weight (mean 156% ideal body weight). An interesting finding in
this study group is a highly significant correlation between the body weight and
the femoro-tibial shaft angle. From this result, the authors conclude that the
degree of obesity might be a primary determinant of the tibial deformity. Due
to a greater risk of recurrence the obese patients had also more osteotomies than
the non-obese children in this population.
In a recently presented group of 19 patients with late-onset tibia vara, the
average weight was 258 lb and all adolescents weighed 95th percentile [21].
Wenger et al. [19] found that most children with adolescent tibia vara
maintain a mild degree of infantile physiologic genu varum. In these cases
predisposing factors, such as obesity, extreme activity, or rapid growth, injure
the posteromedial physis continuously. The result of repetitive trauma in a limb
already in mild varus is growth suppression and further varus. Another interesting
hypothesis for the etiology of adolescent tibia vara was presented by
Davids et al. [22]: In a biomechanical investigation the hypothesis was examined
that dynamic gait deviations to compensate for increased thigh girth due
to obesity (‘fat-thigh gait’) could result in increased loading of the medial
compartment of the knee during the gait cycle. With three-dimensional motion
analysis certain gait deviations like dynamic stance-limb knee varus, increased
stance-limb knee rotation, and swing-limb circumduction could be identified.
These loading conditions, in conjunction with excessive body weight, can obviously
generate compressive forces of sufficient magnitude to alter physeal
growth.
Although in most investigations the relationship between the onset of
obesity and the onset of Blount’s disease could not be determined due to a
retrospective study design, there is enough evidence to conclude a causal effect
of elevated body weight in the pathogenesis of the disease. The natural history
is somewhat unclear, but a majority of patients seems to develop knee
osteoarthritis [21]. Therefore, it is justified to suggest that the development of
obesity in a child with physiologic bowing should be viewed with concern and
efforts should be directed at weight reduction.
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