Fibrous ankylosis is rare. With subluxation, osteochondrosis is complicated by deforming arthrosis of the intervertebral joints, which leads to a decrease in the horizontal and vertical dimensions of the intervertebral foramen.
However, while the clinical and morphological aspects of spinal osteochondrosis and the pathogenesis of its various manifestations are fairly well studied both in the clinic and in the experiment, the etiology is still largely unclear.
G.S. Yumashev and M.E. Furman in their monograph “Osteochondrosis of the spine” give a number of theories (infectious, rheumatoid, autoimmune, traumatic, involutive, muscle, endocrine and metabolic, theories of heredity, anomalies of the development of the spine and static disorders) explaining the cause of osteochondrosis, however, their multiplicity indicates that none of them is true.
Proponents of the infectious theory believed that the cause of damage to the roots of the spinal nerves are acute and chronic infections, and sometimes a cold (meaning rheumatism). However, already in 1924, Sicard noted that the radicular process is associated with damage to the spine, and currently the infection theory has practically no supporters.
Rheumatoid theory is more justified. This theory is most applicable for the common (generalized) form of osteochondrosis, when segments of different localization are involved in the process. The question of the role of rheumatoid changes in osteochondrosis has not yet been completely resolved. Autoimmune theory explains the origin of osteochondrosis by autoimmune changes in the body.
According to the traumatic theory, osteochondrosis develops due to micro- or macro-trauma. This theory is recognized by all. This is due to the predominance of the load on these segments.
The involutive theory explains the damage of the intervertebral disc to premature aging. It is known that in children, the nutrition of the disc occurs due to the vessels penetrating from the lateral vertebrae. By 20 years, they are completely obliterated. The disk is fed by diffusion through the hyaline plates of the vertebrae. Inadequate nutrition and high load on the discs lead to their aging (usually this happens by 50 years). The disk is dehydrated by approximately 22%, as a result, its elasticity and core turgor decrease. Osteoporosis develops, marginal osteophytes appear and the height of those departments of the vertebral bodies that have the greatest load decreases.
The causes of premature disc aging are not well understood. Perhaps they are hidden in biochemical shifts that can lead to local dehydration processes, which can be associated with an intensive fluid exchange in the intervertebral discs. The main substance of the disk consists of a complex of protein and hyaluronic acid. Violation of tissue metabolism leads to degenerative processes – a decrease in the buffer properties of the nucleus and a decrease in the elasticity of the fibrous ring. Due to the anatomical and morphological features, the discs are easier to degeneration and destruction than any other type of connective tissue, including cartilage.
In this regard, G. S. Yumashev and M. E. Furman consider promising a more detailed study of biochemical processes in discs with osteochondrosis and age-related changes. Endocrine and metabolic theories do not yet have reliable evidence. The theory of heredity is also not well argued.