Bone fragility in cerebral palsy (CP) is secondary to a complex interplay of functional, hormonal, and nutritional factors that affect bone remodelling. With increasing life expectancy, preserving bone and muscle health is key to maintaining independence. In young adults with CP, 40% have documented osteoporosis1, with prevalent fractures in up to 38%2. Hypogonadism is also common being present in 20% of young adults. Given that osteoporosis in CP begins in childhood but manifests throughout life as fractures, preventative and treatment strategies need to be tailored to an individual’s age and comorbidities3.
It is unclear whether low bone mass in adults with CP is predominantly due to less bone accrual during childhood, earlier onset of bone loss or accelerated bone loss in adulthood. Our recent longitudinal study of 45 subjects with CP aged >10 years assessed changes in areal bone mineral density (aBMD) during adolescence and young adulthood4. Mean age at first DXA was 19.4 years (range: 10 - 36 years), 57.8% were male and 80% were non-ambulatory. Mean Z-scores at baseline were <-2.0 at all sites but remained stable over time. The median change in aBMD was +1.2 to 1.9%/year in all subjects but in those <20 years of age, the median change was 4 to 8%/year. Peak bone mass was achieved late in the third decade of life.
Low baseline Z-scores remain stable over time suggesting bone mass deficits occur early in childhood. Bone accrual during puberty and subsequent maintenance occurs parallel to typically developing adolescents/adults, albeit at a lower set-point. This has important implications for timing of treatment, with early childhood intervention to optimise nutrition, mobility or use of pharmacological therapy likely key to adolescent and adult bone health. Puberty and its associated changes in bone mass should be monitored and timely pubertal induction given where necessary.