Establishment of a novel asymmetric force degenerative lumbar scoliosis aging bipedal rat model

The present study developed a long‑term asymmetric force (AF)‑induced degenerative lumbar scoliosis (DLS) model using bipedal upright rats and aimed to elucidate the role of AF in DLS pathogenesis. Sprague‑Dawley rats underwent humeral head resection and tail amputation, with elevated food placement to encourage bipedal standing and feeding. The present training protocol continued for 16 weeks to establish the bipedal rat model. Subsequently, an AF‑induced DLS rat model was established by implanting a nickel‑titanium spring with anchor screws for 24, 36 and 48 weeks, respectively. X‑ray imaging, micro‑computed tomography, transmission electron microscopy, hematoxylin and eosin staining and safranin‑O‑fast green staining were performed. AF was associated with structural lumbar scoliosis in bipedal rats. Prolonged AF exposure reduced bone volume fraction, trabecular number, trabecular thickness, bone mineral density and tissue mineral density in the L3 lower vertebral endplate, ultimately leading to bone loss, microarchitectural deterioration, diminished mechanical strength and DLS development, although structure model index and trabecular separation remained unaffected. Prolonged asymmetric stress also caused structural damage to the medullary nerve fibers, degeneration and necrosis of intervertebral disc cartilage endplate cells, disorder of annulus fibrosus and reduction of nucleus pulposus cells. Additionally, long‑term AF stimulation may have induced compensatory chondrocyte proliferation, contributing to early pathological repair processes, but appeared to reach a saturation point with extended exposure. The present study therefore successfully established a novel AF‑induced DLS aging bipedal rat model, providing a basis for exploring therapeutic strategies targeting mechanical stress intervention in DLS.