THEORIES OF THE ORIGIN OF OSTEOCHONDRITIS AND INTERVERTEBRAL HERNIA

1. INVOLUTIONAL THEORY

With age, trophic tissue disturbances develop in the body, especially in tissues lacking a well-developed network of blood vessels. The intervertebral disc is one such tissue. According to the involutional theory, age-related changes lead to qualitative alterations in the composition of the nucleus pulposus of the intervertebral disc, which immediately affects its function, as an important factor—intrinsic disc pressure—changes.

Normally, when pressure on the spine increases, internal pressure also rises until it balances external forces. If this compensation does not occur, excessive pressure causes the disc to flatten, which irritates nerve receptors. If, by this time, there are also dystrophic changes in the fibrous ring, its fibers may rupture under excessive load.

2. HORMONAL THEORY

Supporters of this theory believe that hormonal disturbances in the human body initially manifest, followed by dystrophic changes, with involvement of the intervertebral discs being part of this overall process.

The main argument is that clinical symptoms of spinal hernia often appear against the background of developing hormonal imbalances. Hormonal disruptions evidently play a role in the development of both dystrophic changes and the disease itself.

3. VASCULAR THEORY

With impaired segmental blood circulation in the spinal motor segment, disturbances in water-salt metabolism occur, negatively affecting ionic exchange. Subsequently, due to circulatory disorders, dystrophic changes develop in various organs and tissues, including intervertebral discs. This suggests that dystrophic changes in the spine mostly occur in individuals with segmental blood circulation impairments.

According to this theory, there are four stages of dystrophic changes in the intervertebral disc:

  1. In the first stage, changes accumulate in the vascular system due to both external and internal factors.
  2. The second stage is characterized by impaired blood flow in the spinal motor segment and vascular regulation.
  3. The third stage involves worsening trophic processes and lymph flow in the disc.
  4. Finally, the fourth, terminal stage manifests with dystrophic changes of the disc.

4. INFECTION-RELATED THEORY

Intervertebral disc herniation often occurs as a consequence of a past infectious disease, such as tonsillitis or pharyngitis. Pathogenic bacteria accumulate in the cartilage tissue of the spine, increasing the concentration of mineral salts formed during the breakdown of dead cells. These form “salt islands,” which cause the development of osteochondrosis, leading to intervertebral hernias and other degenerative changes in the spine.

5. INFECTION-ALLERGIC THEORY

When an infectious process develops in the body, the activity of tissue enzymes in the disc changes accordingly. As a result of these and other complex biochemical changes, the supply of nutrients to the disc decreases, leading to dystrophic changes within it. The altered disc becomes less resistant to mechanical impacts, which under physical load can cause damage to the fibrous ring’s integrity. In response, lymphocytes accumulate in the affected spinal motion segment tissues, leading to cellular immune reactions. Antibodies to the affected disc tissues may appear in the blood, potentially triggering immune responses.

Thus, this theory mainly considers trophic (nutritional) factors. However, immunological changes in patients with spinal osteochondrosis can influence the formation of intervertebral hernias.

6. BIOELECTRIC THEORY

Proponents of this hypothesis believe that injuries, overloads, and temperature fluctuations cause inversion of the vector forces of the bioelectric fields in the intervertebral disc. Changing the direction of polarization vectors of these fields alters the activity of enzyme systems, which subsequently leads to dystrophy and ultimately to the development of osteochondrosis and spinal hernias.

7. ANOMALY THEORY

This theory is essentially a specific case of the mechanical theory but emphasizes various spinal anomalies. These include anomalies in the development of vertebral bodies and their structural parts, abnormalities in the positioning of articular surfaces, and fusion of vertebral bodies in areas where it is not anatomically typical (e.g., the sacrum). It is assumed that discs located near such anomalies experience overloads, which in turn lead to the development of dystrophic changes in the discs.

8. FUNCTIONAL THEORY

Supporters of this theory assign great importance to changes in the functioning of the spinal muscle apparatus in the development of dystrophic lesions of the intervertebral disc. Changes in motor function may be due to both congenital and acquired factors.

Acquired disorders can arise from reflex or mechanical factors. Mechanical factors include muscle overload and, consequently, disruption of the coordinated interaction of muscles in the spinal motion segment. Uneven contraction of muscles located in the same plane leads to areas of increased pressure on corresponding parts of the fibrous ring. As a result of frequent repetitive loads, dystrophic changes develop in the disc.

9. HEREDITARY THEORY

The possibility of hereditary factors contributing to the development of osteochondrosis and spinal hernia is often discussed. Differences in the incidence rates among relatives of patients of various degrees of kinship have been identified, which somewhat supports this viewpoint. However, this is more of a special case, and it is not possible to consider hernia solely a genetically caused disease.

10. MECHANICAL THEORY

This theory acknowledges the obvious fact that mechanical impacts on the spine, such as trauma or significant overloads, lead to disruption of the fibrous ring’s integrity and an increase in dystrophic changes in the disc. Doctors are increasingly concerned about the “younger age” of patients: cases of intervertebral disc hernias are increasingly found in adolescents aged 12-15 years and even younger. Sitting in poor posture at a desk or school bench, they do not realize how many problems back issues can cause. Poor posture over time can lead to conditions such as scoliosis and intervertebral hernias. Sometimes, intervertebral hernias in children can arise due to hereditary predisposition to these and other spinal diseases.

Supporters of this theory rely on the following points:

  1. Clinical symptoms of osteochondrosis often appear after mechanical factors act. Thus, trauma, sudden sharp blows, or increased pressure on the spine can lead to a hernia, causing increased pressure inside the disc, with the pulposus nucleus protruding through cracks formed within the vertebra.
  2. Intervertebral hernias often occur during periods when significant mechanical forces are present.
  3. Osteochondrosis and spinal hernias most often form in those spinal motion segments subjected to constant overload. Frequent causes of fibrous disc injury include repetitive uniform movements, such as lifting heavy objects, prolonged vibration exposure, or sports injuries.

All this is valid, but most often, the provoking mechanical factors are everyday loads the patient encounters almost daily—for example, bending over to put on shoes. The fibrous ring’s fiber structure is designed for a certain volume and direction of spinal movements. If the direction and volume of physical load on the disc differ from normal, gradual destruction of the fibrous ring occurs. This process can take years, and the “last straw” can be an awkward movement, sneezing, bending, extending, or another minor physical strain.


RISK FACTORS FOR HERNIA DEVELOPMENT:

Risk factors can be divided into those that can be avoided and those that cannot.

Non-avoidable risk factors include:

✓ The natural aging process. As intervertebral discs age and wear out, they are more susceptible to injury.

✓ Female sex. It is noted that intervertebral disc hernias occur more frequently in women.

✓ Previous spinal injuries, surgical interventions, and existing disc hernias.

Risk factors that can be influenced by lifestyle changes or medical treatment:

✓ Work or physical activity that increases the risk of disc hernia, such as prolonged sitting, frequent lifting of heavy objects, frequent spinal bending, generally heavy physical labor, repetitive monotonous movements, or vibration exposure.

✓ Lack of regular physical exercise, which helps strengthen spinal ligaments and intervertebral discs, or intensive exercise after a long period of inactivity.

✓ Smoking. Nicotine destroys the cartilage tissue of discs. Smoking damages the blood supply, reducing oxygen delivery, and as a result, the intervertebral discs lose their main “nutrition.”

✓ Obesity and excess weight. It has not yet been scientifically proven that excess weight alone places strain on the spine, but obesity reduces the ability to engage in physical exercise.

✓ Hypodynamia (lack of movement). Intervertebral discs lack blood vessels. The disc is nourished by diffusion (“soaking”) through tissues surrounding the vertebra. Nutrients enter the disc more actively when there are pressure fluctuations inside it (i.e., spinal movements). A typical sedentary lifestyle does not provide sufficient spinal movement, so lack of movement leads to poorer nutrition of intervertebral discs, resulting in reduced strength and rupture.