Prevalence of osteoarthritis among adults with cerebral palsy
forms of CP. To support this notion, in a previous study
leveraging the same database and of the same year,
the prevalence of comorbid neurodevelopmental disa-
bilities (i.e. intellectual disabilities, autism spectrum
disorders) for adults with CP was lower than expected
(24). The presence of comorbid neurodevelopmental
disabilities increases the medical needs and complexity
of CP (25). Therefore, prevalence estimates are proba-
bly conservative, leading to more modest effect sizes
reported in this study. Nevertheless, the findings have
important implications for public health. The burden
of OA, represented as disability-adjusted life years,
has substantially increased over recent decades (4).
By 2032, predictions have estimated an additional
26,000 per million adults > 44 years of age will utilize
healthcare services for OA compared with 2012 (26).
The adult population with CP is projected to expand
over the coming decades (27, 28), and given their
early OA profile, this may lead to a disproportionate
increase in the disease and economic burden of OA
attributable to CP.
Many factors may contribute to the early develop-
ment of OA for adults with CP, some of which may
originate in childhood. The aetiology of CP leads to
altered neuromuscular control and gait mechanics (29),
low levels of physical activity (8), and a predisposition
for inadequate accrual of muscle and bone (8) throug-
hout growth and development. There are also a number
of skeletal deformities, malalignments, and problems
of the lower extremities present among individuals
with CP (30–32), such as greater femoral anteversion,
hip subluxation and joint dislocation. The motor fun-
ction and musculoskeletal pathological phenotype in
childhood is confounded by several CP-related factors
(33), including the type of CP (e.g. spastic, dyskinetic,
ataxic), the anatomical distribution of affected areas
(e.g. hemiplegia, diplegia, quadriplegia), and the level
of gross motor functional ability (e.g. independent
ambulation, use of assistive walking devices or wheel-
chair). Furthermore, the degree to which muscles are
affected (e.g. severity), how they are affected (e.g.
spasticity) and the number of affected muscles plays
a large, interactive role on joint health by altering
articular surface stresses incurred during movement;
all of which may lead to localized joint damage and
increased risk for OA.
The health and functional problems experienced
in childhood increase in severity as these individuals
age into their adult years (34, 35). In the first stage of
adulthood, 18–30-year-olds with CP have a similar
musculoskeletal disease prevalence as the general
population of adults ≥ 50 years of age (36), which be-
comes more prevalent throughout their lifespan (10).
Taken together, long-term altered mechanical loading
579
patterns and insufficient musculoskeletal integrity, fun-
ction, and structure, especially of regions surrounding
lower extremity joints, may impose additive risk for
early development of OA (11, 12).
It is also important to note that OA is implicated in
the pathogenesis of cardiometabolic diseases (37) and
mental health disorders (38) among adults without CP.
Adults with CP have elevated cardiometabolic disease
prevalence (9), higher incidence of depression and anx-
iety (39), and 2–3-fold increased risk of cardiovascular
mortality (40) compared with adults without CP. While
it is unknown how OA associates with non-commu-
nicable diseases and mortality among adults with CP,
OA has been shown to amplify daily pain levels and
negatively affect function and activities of daily living
for adults without CP (1). The association of OA with
mental health disorders may affect adults with CP to a
greater extent than adults without CP, possibly through
pathways of lower societal integration at earlier ages.
Studies are needed to determine if physical activity-
based interventions can slow the onset of OA or reduce
the worsening of OA progression for adults with CP,
which may also have a positive impact on reducing the
burden of other non-communicable diseases.
This study has several limitations. First, it was
not possible to determine the severity of CP using
administrative claims data. However, the overall CP
sample may reflect a healthier and higher functioning
segment of the CP population, thus biasing results to
be more conservative. Furthermore, the prevalence
of CP in this privately insured cohort of adults was
0.84 per 1,000, which is lower than the previously
reported 3.1 per 1,000 in children (41); however, no
adequately designed or powered epidemiological
studies have examined the prevalence of CP among
adults. Secondly, we used a single claim to define CP
and OA. Previous validation studies have shown that
using 2 or more claims for a medical condition tends
to improve the accurate identification of that medical
condition (17, 42). However, accurately identifying
medical conditions depends on the number of years for
the study period (43) and the medical condition exa-
mined (17, 43, 44). Given the short study period of 12
months, requiring 2 or more claims for OA may have
introduced disproportionate risk of biasing estimates
to be lower from patients without CP. Adults with CP
have complex healthcare needs and are more likely
to utilize healthcare resources, which would provide
more opportunities to be “flagged” for OA. Taken
together, the selected methodology to identify OA is
probably sufficient to reasonably detect that the cur-
rent data is evidence of differences in OA prevalence
across groups. Thirdly, administrative claims data are
subject to errors, such as inaccurate coding of medical
J Rehabil Med 51, 2019