Interference in the endplate nutritional pathway causes intervertebral disc degeneration in an immature porcine model

Abstract

Purpose Previous studies have shown that blocking the endplate nutritional pathway with bone cement did not result in obvious intervertebral disc degeneration (IDD) in mature animal models. However, there are very few comparable studies in immature animal models. As vertebroplasty currently is beginning to be applied in young, even biologically immature patients, it is important to investigate the effect of cement blocking at the endplate in an immature animal model. Methods Two lumbar intervertebral discs in eight immature pigs were either blocked by cement in both endplate pathways or stabbed with a scalpel in the annulus fibrosus (AF) as a positive control, and with a third disc remaining intact as a normal control. Magnetic resonance imaging (MRI) and histology study were performed. Results After three months, the cement-blocked discs exhibited severe IDD, with the percentage of disc-height index (DHI), nucleus pulposus (NP) area, and NP T2 value significantly lower than the normal control. These IDD changes were histologically confirmed. Post-contrast MRI showed diseased nutritional diffusion patterns in the cement-blocked discs. Moreover, the degenerative changes of the cementblocked discs exceeded those of the injured AF positive controls.Conclusions The endplate nutritional pathway was interfered with and diseased after three months of bone cement intervention in an immature porcine model. Severe interference in the endplate nutritional pathway in an immature porcine model caused IDD. These findings also draw attention to the fact that interference in endplate nutritional pathways in immature or young patients may affect the vitality of adjacent discs.

Osteoporosis of the vertebra and osteochondral remodeling of the endplate causes intervertebral disc degeneration in ovariectomized mice

“…Because of the structural similarities between joint and intervertebral discs [ 13 , 14 ], it is well known that the intervertebral disc is a nonvascular structure and the exchange of substances between the intervertebral disc and the vertebra depends on the cranial and caudal endplates [ 15 – 17 ]. The endplate contains marrow contact channels which provide nutrients for the intervertebral disc and discharge metabolic waste through diffusion and liquid flow under cyclic loading [ 4 , 18 , 19 ].…”

High glucose‐induced excessive reactive oxygen species promote apoptosis through mitochondrial damage in rat cartilage endplate cells

“…Many studies have demonstrated that endplates have a certain number of capillaries, which are extremely important for nutritional supply to the intervertebral discs. Degeneration of the endplate is thought to be an initiating factor of IDD since it can hinder the transport of nutrients . A previous study by Fields reported that endplate degeneration such as endplate sclerosis, increased endplate thickness and decreased endplate porosity can be observed in type 2 diabetic rat .…”

Surgical repair of annulus defect with biomimetic multilamellar nano/microfibrous scaffold in a porcine model

“…Disc degeneration and regeneration are most frequently evaluated by MRI scan based on signal strength and the morphology in normal T1‐ and T2‐weighted images (Bölgen et al, ; Bouma et al, ; Chiang et al, ; Kang et al, ). Furthermore, quantitative MRI, such as T2‐ and T1‐ρ‐mapping can even detect pathological conditions of water and proteoglycan content in the disc (Bölgen et al, ).…”