The cartilaginous endplates (CEP) are key components of the intervertebral disc (IVD) necessary for sustaining the nutrition of the disc while distributing mechanical loads and preventing the disc from bulging into the adjacent vertebral body. The size, shape, and composition of the CEP are essential in maintaining its function, and degeneration of the CEP is considered a contributor to early IVD degeneration. In addition, the CEP is implicated in Modic changes, which are often associated with low back pain. This review aims to tackle the current knowledge of the CEP regarding its structure, composition, permeability, and mechanical role in a healthy disc, how they change with degeneration, and how they connect to IVD degeneration and low back pain. Additionally, the authors suggest a standardized naming convention regarding the CEP and bony endplate and suggest avoiding the term vertebral endplate. Currently, there is limited data on the CEP itself as reported data is often a combination of CEP and bony endplate, or the CEP is considered as articular cartilage. However, it is clear the CEP is a unique tissue type that differs from articular cartilage, bony endplate, and other IVD tissues. Thus, future research should investigate the CEP separately to fully understand its role in healthy and degenerated IVDs. Further, most IVD regeneration therapies in development failed to address, or even considered the CEP, despite its key role in nutrition and mechanical stability within the IVD. Thus, the CEP should be considered and potentially targeted for future sustainable treatments.

Intervertebral disc (IVD) degeneration is the leading cause of low back pain in young adults, and the cartilaginous endplate (CEP) is likely to play a key role in early IVD degeneration. To elucidate the effects of pro-inflammatory cytokines on the mechanobiology of the CEP, human CEP cells were seeded into 2% agarose, dynamically compressed up to 7%, and stimulated with tumor necrosis factor (TNF). It was hypothesized that dynamic compression would be sufficient to induce anabolism, while stimulation with TNF would induce catabolism. TNF was sufficient to induce a catabolic, time-dependent response in human CEP cells through downregulation of anabolic gene expression and increased secretion of pro-inflammatory proteins associated with herniated discs, bacteria inhibition, and pain. However, 7% strain or scaffold material, agarose, may not lead to full activation of integrins and downregulation of pro-inflammatory pathways, demonstrated in part through the unchanged gene expression of integrin subunits α₅ and β₁.

Little is known about cartilaginous endplate (CEP) mechanobiology or how it changes in a catabolic microenvironment, partly due to difficulties in conducting mechanotransduction in vitro. Recent studies have found blended collagen–agarose hydrogels to offer improved mechanotransduction in chondrocytes compared to agarose alone. It was hypothesized that blended collagen–agarose hydrogels would be sufficient to improve the mechanobiological response in CEP cells relative to that in agarose alone, while maintaining the chondrocyte phenotype and ability to respond to pro-inflammatory stimulation. Thus, human CEP cells were seeded into blended 2% agarose and 2 mg/mL type I collagen hydrogels, followed by culture with dynamic compression up to 7% and stimulation with TNF. Results confirmed CEP cells retained a rounded phenotype and high cell viability during culture in blended collagen–agarose hydrogels. Additionally, TNF induced a catabolic response through downregulation of pericellular marker COL6A1 and anabolic markers ACAN and COL2A1. No significant changes were seen due to dynamic compression, suggesting addition of collagen to agarose was not sufficient to induce mechanotransduction in human CEP cells in this study. However, blended collagen–agarose hydrogels increased stiffness by 4× and gene expression of key cartilage marker SOX9 and physioosmotic mechanosensor TRPV4, offering an improvement on agarose alone.

Background: The vertebral bony endplate (BEP) plays a role in regulating both mechanical load transfer and nutrient transport to the intervertebral disc, functions strongly influenced by its microstructural porosity. Variations in porosity impact bone strength, elasticity, and solute diffusion, affecting its overall mechanical competence. Methods: A semi‐automated modeling workflow was established to quantify pore geometry and connectivity of the BEP and relate them to zone‐specific mechanical and transport properties using relationships previously established in the literature. Six to eight BEPs from four bovine subjects were imaged using micro‐computed tomography. The central zone and two peripheral zones of each BEP were segmented, and their microstructural properties, including tortuosity, porosity, and pore radii, were quantified using the pipeline to assess BEP heterogeneity. These metrics were then used to infer the BEP's zone‐dependent density, Young's modulus, compressive strength, and shear modulus. Results: The BEPs showed spatial, intra‐subject, and inter‐subject morphological variability, which affected their predicted mechanical and transport properties. These findings highlight the limitations of purely idealized BEP representations in silico simulations and support the incorporation of uncertainty modeling strategies that account for physiologically relevant variations in the BEP. Conclusion: This semi‐automated modeling approach represents a tangible step toward more realistic in silico simulations of vertebral endplate function.