Theoretical explorations generate new hypotheses about the role of the cartilage endplate in early intervertebral disk degeneration
Ruiz Wills, Carlos; Foata, Baptiste; González Ballester, Miguel Á.; Karppinen, Jaro; Noailly, Jérôme (2018-09-19)
Ruiz Wills C, Foata B, González Ballester MÁ, Karppinen J and Noailly J (2018) Theoretical Explorations Generate New Hypotheses About the Role of the Cartilage Endplate in Early Intervertebral Disk Degeneration. Front. Physiol. 9:1210. doi: 10.3389/fphys.2018.01210
© 2018 Ruiz Wills, Foata, González Ballester, Karppinen and Noailly. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Altered cell nutrition in the intervertebral disk (IVD) is considered a main cause for disk degeneration (DD). The cartilage endplate (CEP) provides a major path for the diffusion of nutrients from the peripheral vasculature to the IVD nucleus pulposus (NP). In DD, sclerosis of the adjacent bony endplate is suggested to be responsible for decreased diffusion and disk cell nutrition. Yet, experimental evidence does not support this hypothesis. Hence, we evaluated how moderate CEP composition changes related to tissue degeneration can affect disk nutrition and cell viability. A novel composition-based permeability formulation was developed for the CEP, calibrated, validated, and used in a mechano-transport finite element IVD model. Fixed solute concentrations were applied at the outer surface of the annulus and the CEP, and three cycles of daily mechanical load were simulated. The CEP model indicated that CEP permeability increases with the degeneration/aging of the tissue, in accordance with recent measurements reported in the literature. Additionally, our results showed that CEP degeneration might be responsible for mechanical load-induced NP dehydration, which locally affects oxygen and lactate levels, and reduced glucose concentration by 16% in the NP-annulus transition zone. Remarkably, CEP degeneration was a condition sine-qua-non to provoke cell starvation and death, while simulating the effect of extracellular matrix depletion in DD. This theoretical study cast doubts about the paradigm that CEP calcification is needed to provoke cell starvation, and suggests an alternative path for DD whereby the early degradation of the CEP plays a key role.
- Avoin saatavuus