Synonyms: Disk degeneration, degenerative disk disease, chondrosis intervertebralis.

The first stage of discosis begins with regression of the intradiscal vessels between the ages of 2 and 4 years.

Pathoanatomical changes within the disk tissue, including fiber disruption, tissue loss due to prolapse, and dehydration, produce a further manifestation of the second stage of discosis: segmental instability. Slackening of the initially tautly elastic disk tissue loosens the mechanical link between adjacent vertebrae, enabling movements of nonphysiological amplitude and direction. This kind of instability may not be directly visible. It can often be detected only with the aid of functional images, e. g., lateral radiographs on forward and backward bending. Degenerative instability also causes slippage (olisthesis) of the vertebrae relative to one another, either ventrally or dorsally (retrolisthesis). Symptoms are produced by impingement on the neural elements in the vertebral canal or the intervertebral foramen. Most therapeutic procedures are undertaken in the second stage of discosis, because it is in this stage that disk displacement and slackening most commonly produce intense local and radicular manifestations.

The spine of a quadruped consists, in principle, of a horizontal chain of identical segments supported at two points. The vertical human spine is subject to much greater gravitational stresses.

Schmorl’s nodes, i.e., circumscribed protrusions of disk tissue into the vertebral end plates, are not found in quadrupeds. The vertebral columns of certain flightless birds, whose bipedal stance places gravitational stress on the spine much as it does in humans, display abnormalities of a comparable type (Klapp 1958). Exner (1954) described severe forms of spondylosis deformans in anthropoid apes with upright posture. Yamada (1962), Wassilev and Dimova (1970), and Cassidy et al. (1988) forced mice to walk upright by amputating their forelegs. One year later, the anulus fibrosus and cartilaginous end plates displayed structural changes attributable to vertical stress. Similar observations in animals were made by Palmer and Lotz (1993), Edwards et al. (1998), and Unglaub et al. (2003).

The human intervertebral disk does not begin as bradytrophic tissue. In infancy, when the disk is not under any particular mechanical stress, intense metabolic exchange takes place across the intradiscal vessels. Twisting and bending of the trunk, as the infant crawls, further aid fluid exchange across the boundaries of the disk.

The assumption of an upright posture fundamentally alters the biomechanical situation of the disk. The intravertebral vessels are protected by the bony trabecular system, but the vertical compressive pressure on the disk (the sum of the weight of the body above the disk and the muscle tone across it) is transmitted directly to the blood vessel walls within the pulpy, homogeneous disk tissue. Because the arteriolar and venous pressure is lower than the hydrostatic pressure, the blood is pressed out of these vessels, which collapse, suffer pressure atrophy, and finally disappear. The nutrient supply of the fibroblasts and cartilage cells diminishes in a relatively short time because they are isolated from the bloodstream. Metabolic exchange can now take place only across long distances within the disk tissue, through transport mechanisms that are less effective than the previous normal vascularization.

Insufficient nutrient supply is associate with a lowered oxygen/glucose concentrations and acidic pH, and adversely affects the ability of disk cells to synthesize and maintain the disk matrix leading to disk degeneration (Mokhbi-Soukane 2006).

In most individuals, the active and passive transport mechanisms across the boundaries of the disk cannot sustain, over the decades, a constant, adequate supply of nutrients to its cells.

Trauma and transient overloading impair the nutrient supply of the disk cells much less than a prolonged absence of movement.

In addition to the verticality of the spine and invariance of posture, genetic factors also contribute to the early appearance of regressive changes in the intervertebral disks. An endogenous component is postulated by many authors (Hanraets 1959, Armstrong 1965, Schmorl and Junghanns 1968, Wilson 1968, Braun 1969, Brocher 1973, Töndury 1981, Idelberger 1984, Simmons 1996, Matsui 1998, Kawaguchi 2002, Battié 2004, Bernadino 2004, Lattermann 2004). According to Idelberger (1952), some individuals have a constitutional predisposition to premature disk fatigue. Hanraets (1959) and Wilson (1968) showed familial clustering of disk disease. According to Wilson (1968) and Beard and Stevens (1985), the quality and configuration of the collagen fibers in the anulus fibrosus are influenced by genetic factors. Battié and Videmann (2004) found that near relatives of patients with disk prolapses are more likely to have spine-related complaints than near relatives of normal control individuals. Hestbaek et al. (2006) in their twin study demonstrated a correlation between low back pain in childhood/adolescence and low back pain in adulthood.

The existence of an inherited predisposition to disk disease thus cannot be rejected out of hand, but there is no apparent connection to any particular habitus, as is the case for some other diseases (diabetes mellitus, peptic ulcer disease). Our own studies in a large set of patients have unequivocally shown that disk lesions are equally common in individuals of athletic, leptosomal, pyknic, or dysplastic build (Krämer 1978).

Videman et al. (2006) identified new genes associated with signs of disk degeneration and presents evidence of a multigenic etiology.

The worsened metabolic situation beginning in childhood alters not only the chemical composition, but also the anatomical structure of the intervertebral disk. Because of their inadequate supply of energy and nutrients, the fibroblasts form fibers and matrix of deficient quality, and finally disintegrate. Many histological studies of disk material from unselected autopsy cases have shown this to be the case. The degenerative process begins in the disk (Eubanks 2006).

Overview of the literature. Basic studies have been undertaken by Hirsch and Schajowitz (1952–1953), Hirsch et al. (1953, 1963), Hirsch and Nachemson (1954), Hirsch (1960, 1966), Hirsch and Bobechenko (1965), Feng (2000), Roughley (2004), Battié and Videmann (2004), An et al. (2004), Crock (2004), Hansson (2004), Naturajan et al. (2004), Haefeli et al. (2005), Roh et al (2005), An and Masuda (2006), Brisby (2006), Guehring et al. (2006), Natarajan (2006), Setton (2006), and Unglaub et al. (2006). Growth factors, such as bFGF and TGF-β1, macrophages, and mast cells may play a key role in the repair of the injured anulus fibrosus and subsequent disk degeneration (Peng 2006).

Biology offers several strategies for restoring the degenerating disk, including the use of recombinant or natural proteins that increase matrix accumulation and assembly, enhance the number of disk cells, or in other ways lead to restoration of the native healthy disk. Recombinant bone morphogenetic protein-7 (osteogenic protein-1) shows promise in this regard. Other growth factors, as well as cytokine antagonists such as the interleukin-1 receptor antagonist, are also good candidates (Evans 2006).