The disk
The disk is located between the vertebrae and is part of the “joint mechanism” between the vertebrae. Key features of the disk:

Shock absorbers that absorb power / load from body weight and muscles
The disk distributes the load evenly to adjacent vertebrae
Enables movement between the vertebrae
Disk structure / physiology
Nucleus pulposus
Is the gelatinous pulp located in the center of the counter. It is made up of hydrophilic tissue (water-loving), contains water and sparsely with cells.

A network of randomly distributed collagen fibers and a smaller amount of elastin fibers.


The elastin fibers are embedded in a gel consisting of proteoglycans, which are coupled to hyaluron molecules.


The collagen is, just like joint fracture, primarily collagen type 2. About 20% of the nucleus weight (dry weight). There are also collagen types 6, 9 and 11 but in very small amounts.


About 50% of the nucleus consists of proteoglycans (dry weight). They are divided into two classes:

Large aggregate proteoglycans (aggregate and versican)
Minor proteoglycans (biglycan, decorin, fibromodulin & lumican)

The significance of the small and large proteoglycans is not fully understood. It is believed that the smaller ones have a more restorative function while the larger ones have a more structural significance.

The ancestor is the most dominant and most important macromolecule in the nucleus. It is characterized by highly negatively charged glycosaminoglycans (GAG). The aggregate is also highly hydrophilic (water-loving) which allows them to bind water molecules to the disk matrix. This allows the disk to retain its viscosity (thickness) and thus the tension and elasticity of the disk.

Metalloproteinases are enzymes that break down collagen and aggregate. They participate in the remodeling of matrix, ie a natural process that breaks down and regenerates the tissue. It has been seen that an imbalance of metalloproteinases and the inhibitor itself can be an important factor for disk degeneration.

Anulus fibrosus
Anulus fibrosus encloses the nucleus and consists of about 15-20 concentric rings. The collagen that the rings consist of is mainly type 1 (70% dry weight). There is also collagen type 2 but sparingly.

Between the collagen fibers are elastin fibers that bind the collagen together and allow the anulus to regain its shape after loading. Anulus fibrosus is usually described as “the monk sitting around the core”.

Cartilaginous end plate
The cartilaginous end plate serves as a growth zone for the vertebral body in children. It looks microscopically just like the epiphyses in the long tubular bones. With increasing age, the function disappears.

The end plate extends / covers the mineralized cartilage and the subcondral bone. It covers the end plate to about 90% with hyaline cartilage and is then the vertebral body’s contact surface against the counter. The mineralized part of the end plate is pierced and this is where the capillary ends end.

The end plate is about 0.6 mm thick hyaline cartilage
Capillary ends disappear after age 10
Disk nutrition
The disk is the body’s largest avascular tissue and has only blood vessels in the outer layers of the anulus. This means that the nutritional supply and transport of slag products is entirely dependent on the permeability of the cartilaginous end plates.

Depending on the weight, size and shape of the molecule, it will be transported differently quickly across the end plate into the nucleus. The one we mentioned earlier is a negatively charged ion and therefore positively charged ions are easier to pass into the counter. Negatively charged ions are thus more difficult to pass over the end plate into the nucleus.

It is believed that a naturally aging disk retains the diffusion capacity while the degenerate disk has a decreased diffusion capacity.

Positively charged ions are easier to enter via the end plate to the nucleus
Depending on the weight, size and shape of the molecule, it is rapidly transported into the nucleus

Natural aging has retained diffusion capacity
Degenerated disks have impaired diffusion capacity
Disc Degeneration
The dishes age just like everything else in the body. It can be very difficult to distinguish between the natural aging of the disk and the pathological aging. It has been seen that x-ray, structural and biochemical you have the same changes in a naturally aged disk as in the degenerate.

You can see disk degeneration / age changes as early as childhood. Age changes have been seen as early as 10 years and then you can also see that the notochordal cells disappear and the blood supply to the end plates ceases.

As age increases, the disc gradually hardens and the end plate is calcified. In the long term, this will reduce the diffusion capacity. These changes reach a maximum between 50 and 70 years of age, after which the diffusion capacity is basically constant.

The structural, mechanical, and molecular changes that occur result in a shift from collagen types 1 and 2 toward a more connective tissue-like composition. The biggest change that occurs is that the content of proteoglycan itself decreases, which leads to a completely changed structure. Reduced fluid content and thus also reduced capacity to handle load.

Reduced circulation and degeneration
Today, there is a strong evidence that a decreased nutritional supply to the dishes results in increased disk degeneration. You have been able to see this link at:

Sickle cell anemia
Gaucher disease
It is believed that the reason for finding a connection between smoking and back problems is

Carboxy-hemoglobin production
Reduced fibrinolytic activity resulting in altered blood flow.
Reduced permeability leading to increased amounts of lactate which lowers the pH value.

It has not been possible to determine completely whether nutritional deficiency or end plate classification is the primary cause of the degenerative changes.

Cellular aging
It is believed that premature aging of the cell may be a contributing cause of disk degeneration. With increasing age and degeneration, several non-fully functioning cells get into the disk. Apoptosis (programmed cell death) increases with increasing age and as the cell ages, the ability to replicate ceases. So it is still alive but has a different gene expression which makes it respond differently to stimulation. It can begin to secrete substances with a different effect on surrounding cells and matrix production. E.g. an increased secretion of catabolic enzymes that breaks down tissue.

Anabolic growth factors
Studies have shown that anabolic growth factors can have a regenerative effect in disk degeneration. The people you are talking about are:

In the disk matrix it has been seen that receptors for the growth factors are found on the surface of the nucleus pulposyus as well as the inner layer. It is believed that it can affect homeostasis (stability state) in the disk matrix.

Catabolic cytokines
Cytokines have been shown to play an important role in the degeneration of the cartilage in osteoarthritis (= osteoarthritis). The cytokines that are mentioned above are:

It is believed that these catabolic cytokines contribute to disk degeneration, disk hernias and nerve root pain by having a direct effect on the matrix cells. It is believed that they reduce the formation of matrix and increase degradation.

Epidemiological twin studies have shown that genetics is the most important factor for developing early disk degeneration. Recent studies have shown that the genetic factor affects the disk more than other biomechanical factors such as:

BMI (body mass index
Body length
disk Size

The biomechanical factors are believed to be more linked to lower disk height. Genetics also affect more than other physical external factors such as:

Heavy body work
Stressful leisure activities
Disk & pain
The outer third of the anulus is innervated in the normal disk. The rest of the anulus and nucleus are devoid of innervation and vascular supply. It has been seen that the growth of unmyelinated pain fibers of substance P can cause pain to patients. However, all patients with a nerve growth are in pain. Vessels that grow in from the cover plates can give rise to an ingrowth of nerves and thus cause pain.

In diagnostics, you can today use MR to provide the best precision. Common to look at in addition to common changes in the counter are:

Signal changes in the subcondral bone (Modic changes)
Type 1: decreased signal T1 signal and increased T2 signal – it is believed that there is an inflammatory edema at the end plates.
Type 2: increased T1 signal and slightly increased T2 signal. You can also see marrow fat and end plate cracking.
Type 3: lowered T1 and T2 signal. Correlates with subcondral sclerosis on smooth X-ray.
Disk degeneration (based on disk structure, signal intensity, disk height)
High-intensity zone which is meant by a rupture in the posterior anulus.
Biological treatment of degenerate disks
Today, there is poor support for biological treatment of a degenerate disc. The reason for being cautious about a biological treatment is because you are afraid to trigger an immunological response and have negative consequences for it. However, four variants are used:

Direct injection of an active substance (growth factors, cytokines) into the disc.
Gene therapy where you try to change the gene content in the disk cells
Autologous cell transplantation with or without prior gene modification
Transplantation of mesemkymal stem cells
Direct injection
An increased wash height and proteoglycan synthesis have been observed with an injection of unstable protein-1. However, this has happened in rabbits so not completely transmissible to humans. Today more research is needed on this in order to be able to use on people.

Gene therapy Treatment
An attempt is made to supply genetic material to the cells in the disk.

A vector is needed to supply or reimplant the gene-altered cells to the disk. The vectors used are viral vectors or non-viral vectors where the viral vectors are most effective. This technique is careful to try to tease out the body’s inflammatory response. The technique goes like this because you often do not get to the basic problem, which is often a reduced nutritional condition in the counter.

Autologous cell transplantation
Is an alternative to treat the existing cells in the disk. Autologous cells are taken from non-degenerate disks and inserted into the disc. Human studies have begun, but relatively far into this method of treatment can become a reality.

Transplantation of stem cells
Today we are in a very early stage of this type of treatment.