Some studies suggest that annulus fibrosus puncture injures the annulus, reduces intradiscal hydrostatic pressure, alters the intradiscal biomechanical environment, decreases nucleus pulposus pressure, and redistributes stress, thereby inducing intervertebral disc degeneration. Other scholars propose that nucleus pulposus tissue is not exposed to the immune system during individual growth and development. When the physiological barrier of the annulus fibrosus is disrupted, nucleus pulposus tissue contacts immune cells, triggering a series of autoimmune responses that lead to nucleus pulposus cell apoptosis. The extracellular matrix degenerates as it is no longer secreted and replenished by nucleus pulposus cells, ultimately resulting in intervertebral disc degeneration. Another view holds that annulus fibrosus puncture causes reduced blood supply, nutrient deficiency, and accumulation of metabolic products within the disc, leading to cellular metabolic dysfunction and eventual intervertebral disc degeneration.

New Zealand white rabbits (male, 2.5–3.0 kg)

Modeling method: The L4–5 and L5–6 lumbar intervertebral discs were punctured using a needle. The lumbar intervertebral disc degeneration model was successfully established after 4 weeks.

Evaluation indicators: MRI examination, HE staining, Masson staining

MRI

HE staining of lumbar intervertebral disc

Masson staining of lumbar intervertebral disc