How nutrient transport affect disk degeneration?

Spinal disease, disk degeneration, and herniated disk are leading causes of pain radiation affecting movement and decreasing the patient’s quality of life. Nevertheless, technology in the biomechanical realm has provided multiple treatments, such as axial decompression, to ease the pain and slow the process of these degenerative conditions. However, biological factors may contribute to the healing process; it is well-known that diseases continuously deplete our nutrients pool. Therefore, proper nutrition and spinal decompression are crucial for spinal disease prevention and reversal.

Disk nutrients:

The intervertebral spinal disk (IVD) is a highly specialized tissue with complex conformation and, therefore, nutrient-specific necessities. Indeed, nutrients and metabolism play a pivotal role in IVD’s constitution. For instance, glucosaminoglycans (GAGs) are critical for IVDs’ mechanical strength and integrity of the disk’s extracellular matrix. These GAGs are a metabolic product of glucose metabolism in combination with oxygen and lactate. 

A wide array of nutrients are critical for ECM integrity and renewal, such as collagen, vitamin C, curcumin, glucose, proline, and lysine, among many others. Furthermore, proper supplementation is needed and recommended to maintain appropriate levels in our nutrient pool; promoting good nutrient delivery routes is crucial to preventing spinal degeneration.

Nutrient route: how to enter a disk?

The IVD is a highly specialized tissue, and part of its uncommon features is being avascular. This particular characteristic leads us to the following question: how do nutrients enter a disk?

There are two blood delivery routes:

1. Capillary beds route: These locate on the cartilaginous endplate, and it is the main route that supplies the IVD with
2. Peripheral annulus: This surrounds the nucleus pulposus (NP) and anchors the intervertebral disc to the vertebra.

Furthermore, their transport will differ depending on each nutrient’s molecular size. For instance, larger molecules such as glucosaminoglycans, enzymes, proteins, and hormones will use a gradient mechanism powered by the concentration of nutrients on any given side of the membrane. On the other hand, smaller molecules (glucose, lactate, oxygen) will use diffusion as their primary transportation mechanism. 

Disk degeneration: risky environment and nutrition.

The interplay of decreased nutrition pools and structural failure creates an environment where disk degeneration is present. Indeed, nutrient metabolism is the main character in this play called disk renewal. The stage in which this story evolves becomes the main factor determining if this becomes a tragedy or a light-hearted play.

• Acidic environment: Glycolysis is the metabolic route that uses glucose to create ATP (energy) and lactate. Lactate production promotes an increased pH (between 7.0-7.3) in the center of the disk, and this is critical to fostering protein and proteoglycan synthesis. Nevertheless, low pH slows glycolysis, therefore less lactate production, contributing to a possible matrix breakdown.
• Proteoglycan loss: The loss of proteoglycans can be related to aging, as it increases with age. Furthermore, this decrease in proteoglycan synthesis can increase cytokine and enzymes in the disk, promoting a degeneration loop. Glycosaminoglycan’s function is to maintain hydration in the disk. Without them, the mechanical load can increase tissue stress and surface damage.
• Hydration and porosity: Diffusion relies on the membrane’s levels of porosity. A higher amount of water will require a bigger pore size to go through the membrane and present the glucose molecule. Therefore, a lower degree of hydration may compromise the number of small molecules that enter the disk.
• Density: Some authors report that 11% of cell density is lost when disk degeneration occurs. In this case, disk degeneration is due to a chronic shortage of nutrients. Furthermore, when low cellular density in a disk is present, intracellular signaling is limited, and since they locate near the endplates, nutrients cannot be transported.
• Metabolic demand: A disk packed with cells will need a greater nutrient demand, as well as a disk that is constantly stressed by mechanical load. Nevertheless, higher-density nutrients rely on their concentration and their transport mechanism. Therefore, some of these nutrients may not reach the disk’s center when cellular demand increases.
• Endplate permeability: The nucleus pulpous receives nutrients through the endplate and excretes toxic metabolites. Nevertheless, the endplates depend on their contact with the blood vessels and nutrient concentration. However, fractures may block the endplate compromising the nutrient delivery and toxin deposition. Furthermore, other factors contribute to this process: sclerosis and age-related mineralization may compromise the central endplate’s portion, blocking the most critical route of nutrient delivery.

Disk health is a multifactorial entity that relies on the interplay between what we do to maintain our disks, what we eat, and how these nutrients reach this tissue. A patient with nutritional deficiencies that comes into a chiropractic practice should not be unnoticed. Indeed, it is critical to assess the patient with disk degeneration from a holistic point of view. Supplying the proper amount of nutrients, enhancing or enabling the correct delivery pathway, and supporting metabolic pathways also decrease disk degeneration. – Ana Paola Rodriguez Arciniega, MS

Bibliography:

De Geer C. M. (2018). Intervertebral Disk Nutrients and Transport Mechanisms in Relation to Disk Degeneration: A Narrative Literature Review. Journal of chiropractic medicine, 17(2), 97–105. https://doi.org/10.1016/j.jcm.2017.11.006

Illien-Jünger, S., Gantenbein-Ritter, B., Grad, S., Lezuo, P., Ferguson, S. J., Alini, M., & Ito, K. (2010). The combined effects of limited nutrition and high-frequency loading on intervertebral discs with endplates. Spine, 35(19), 1744–1752. https://doi.org/10.1097/BRS.0b013e3181c48019