Development of a novel rabbit model of angular kyphosis and characterization of its neuropathological features.

Abstract

Background: Angular kyphosis, often resulting from congenital anomalies, trauma, infections, or tumors, can cause severe spinal cord compression, ischemia, and neurological dysfunction. Due to its sharp curvature and complexity, angular kyphosis remains challenging to treat surgically. This study aimed to establish a rabbit model to mimic the progression of angular kyphosis and its neurological consequences.

Methods: Fifty-six New Zealand white rabbits were divided into four groups: Group A (sham), and Groups B-D (2, 4, and 8 weeks postoperative, respectively). Angular kyphosis was induced via a V-shaped osteotomy between the L2 and L3 vertebrae. Motor function was assessed using Basso-Beattie-Bresnahan Locomotor Rating Scale(BBB scores). Radiological evaluations included Cobb angle and spinal canal occupancy. Histological and apoptosis analyses were conducted to evaluate spinal cord damage.

Results: The induced model reliably produced progressive kyphosis with worsening neurological function. BBB scores declined over time, while Cobb angles and canal occupancy rates increased significantly. Histological examination revealed spinal cord ischemia and increased neuronal apoptosis, aligning with observed motor deficits.

Conclusion: This rabbit model effectively replicates the clinical features of angular kyphosis, including progressive spinal cord compression and neurological impairment. It provides a reliable platform for investigating the pathophysiology of spinal deformities and evaluating therapeutic interventions.