Osteoporosis is a disease characterized by low bone mass and structural deterioration leading to increased fracture risk. While osteoporosis is considered a disease of the elderly, it is now well accepted that early-life experiences are important predictors of osteoporosis risk1,2. Many factors influence skeletal development during childhood and adolescence including genetics, sex, body composition, diet, and physical activity. Of the modifiable lifestyle factors that influence bone health, physical activity during childhood and adolescence may have the greatest impact on skeletal development, as research shows that the most active individuals accrue more bone mineral content (BMC) during the growing years3. Congenital heart disease (CHD) is the most common birth defect in the world with prevalence rates estimated to be between 8 to 10 per 1000 live births and as many as 1 in 45 children are currently living with CHD4,5. The American Heart Association guidelines recommend that children with CHD be physically active and follow the same physical activity guidelines as their typically developing peers (TDP)6. However, a study found that only 8% of children with CHD met the current physical activity guidelines7.

In addition to the reduced physical activity, children with CHD may be at increased risk of impaired bone accrual due to low birth weight, hypoxia, low nutrient intake, type of surgical correction, and medication intake among other factors8, 9, 10. The survival rates of children with CHD have been steadily increasing such that 1 in 150 young adults are expected to be living with CHD within the next decade11. Correspondingly, there is emerging evidence showing CHD is associated with disproportionately higher morbidity, mortality, and health care costs in the adult years12,13.

To address this high health care utilization in adulthood it is important to understand the development of chronic conditions such low bone mass in this population during the growing years. Currently, we have a poor understanding of the skeletal health of children with CHD and there is conflicting literature in the area. Rego and colleagues, found that adolescents with CHD had greater areal bone mineral density (aBMD) and aBMD z-scores at the lumbar spine compared to TDP14. However, the TDP had z-scores that were more than one standard deviation below the mean, and it is unclear what reference standard was used to create the z-scores14. In contrast, others have reported lower aBMD z-scores at the lumbar spine and total body15,16.

Using peripheral quantitative computed tomography (pQCT) to assess bone density and geometry at the forearm, Witzel and colleagues found most individuals with CHD had normal bone development in proportion to their reduced body height17. However, low trabecular volumetric BMD (vBMD) and cortical bone have been reported at the tibia in individuals with CHD18,19. Differences in findings may be related to the type of CHD lesion studied (simple vs complex CHD), the lack of adjustment for differences in body size, the inclusion of both young adults and children in many study populations, and the small sample sizes studied.

Therefore, the primary purpose of the current study was to examine the bone architecture of children with CHD compared to typically developing peers age- and sex-matched controls (TDP group) and secondarily to compare children with CHD based on a simple vs complex CHD lesion diagnosis. We hypothesized that children with CHD would have worse bone health compared to TDP and that children with complex CHD would have the poorest outcomes.