Establishment and evaluation of a rat model of lumbar intervertebral disc degeneration secondary to posterior...

Intervertebral disc degeneration (IDD) is linked to abnormal mechanical loading. This study investigated early pathological changes in the subchondral bone microenvironment following mechanical destabilization and explored underlying mechanisms. Thirty-six Sprague-Dawley (SD) rats were divided into Control, Sham-operated, and Model groups. The Model group underwent resection of posterior spinal structures (L1-L6) to induce lumbar instability. Multimodal analyses were performed at 4, 8, and 12 weeks postoperatively, including micro-computed tomography (micro-CT) imaging, histopathological staining, serum enzyme-linked immunosorbent assay (ELISA) for inflammatory cytokines, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and reverse transcription-polymerase chain reaction (RT-PCR) for apoptosis-related genes. The Model group demonstrated significant disc height loss, deterioration of subchondral bone microstructure characterized by reduced bone volume fraction, trabecular thickness, trabecular number, and bone mineral density, along with altered trabecular separation. Progressive degradation of the disc matrix was also observed. Concurrently, elevated systemic levels of IL‑6, TNF‑α, and IL‑1β, increased apoptotic cells in subchondral bone, and dysregulated expression of Bax, Caspase‑3, and Bcl‑2 were observed in the Model group. Posterior lumbar instability successfully induced IDD accompanied by significant subchondral bone impairment. Microstructural decay and apoptosis in the subchondral bone were closely associated with disc degeneration, suggesting its potential involvement in mechanically induced IDD and highlighting the bone‑disc interface as a promising therapeutic target.