Assessment of Vertebral Body Bone Quality in Adolescent Idiopathic Scoliosis (AIS) Using Micro-CT, qBEI, and...

Adolescent idiopathic scoliosis (AIS) is the most common three-dimensional spinal deformity, predominantly affecting females aged 10-16 years. Although no single etiological factor has been definitively identified, alterations in bone quality and biomechanical properties have been proposed as contributing factors to AIS development.

We developed a surgical protocol to obtain trabecular bone biopsies from the apex vertebra during anterior corrective surgery for AIS. Multimodal analysis was performed on samples from eight AIS participants (14.8 ± 1.5 years), including microstructural assessment via micro-computed tomography (micro-CT), bone mineral density distribution (BMDD) via quantitative backscattered electron imaging (qBEI), and mechanical characterization via nanoindentation. Correlations with major curve angle, apical wedge angle, and Risser grade were investigated.

Mean trabecular bone volume fraction (BV/TV) was 0.146 ± 0.029, comparable to values reported in healthy populations. Mean trabecular thickness (Tb.Th) was 0.146 ± 0.011 mm, suggesting slightly thicker trabeculae than typically reported in healthy young cohorts. BMDD analysis revealed CaPeak values of 23.34 ± 1.02 wt% Ca, and greater CaWidth values (4.26 ± 0.33 wt% Ca) compared to healthy adolescent and adult reference data. CaPeak was significantly negatively correlated with apical wedge angle, indicating lower mineralization with increasing vertebral wedging. Nanoindentation showed a negative association between reduced modulus (13.37 ± 2.5 GPa) and apical wedge angle, with hardness values of 0.412 ± 0.079 GPa.

These findings provide novel insights into vertebral trabecular bone alterations in AIS and their association with deformity severity. To our knowledge, this is the first study to integrate micro-CT, qBEI, and nanoindentation analyses in AIS vertebral biopsies, revealing structural, compositional, and mechanical differences that may contribute to the pathogenesis and progression of AIS.