Until the confirmation of biologic techniques, mechanical interventions are our primary means of action against degenerative disc disease.

Acute or progressive disc lesions create instability of the motion segment. This instability is best characterized by a loss of stiffness, which contributes to further deterioration leading to a vicious cycle exacerbated by a concentration of stress on the posterior portion of the disc.

As in any mobile, dynamic system submitted to a force, intervertebral segments undergo acceleration inversely proportional to the moment of inertia. The stiffness of the segment dampens this movement. This braking action preserves a margin of security and contributes to protection of the disc and intervertebral ligaments. Stiffness is a mechanical parameter defined in terms of load for a given displacement. It corresponds to the derivative of the load/deformity curve.

Ebara et al. (5) and Mimura et al. (6) demonstrated that segmental laxity or loss of stiffness is constant in degenerative disc disease. This is observed throughout the course of the degenerative process. Early on, before loss of disc height, bending studies reveal a wider range of motion corresponding to increased laxity (7). Even in advanced lesions in which intervertebral mobility is reduced because of disc narrowing, the system still exhibits loss of stiffness. This decrease in rigidity corresponds to an increase in the neutral zone of disc loading over displacement.

The stretching of the connective tissues uniting two vertebrae leads to a force resisting the displacement. The dissipation of kinetic energy in the form of heat is mediated by the visco-elastic properties of these connective tissues. This passive damping would, in fact, be quite insufficient to protect the disc if it were not constantly supplemented by the much more effective active damping provided by the reflex contraction of the powerful paravertebral muscles. Although the dynamic equilibrium of the intervertebral articular system is dependent on a combination of muscle activity and tension of the passive elements of union, the active system constantly protects the passive elements, which consequently remain within the limits of their elasticity under healthy physiologic conditions.

The mechanically mediated changes we attempt to achieve in degenerative disc disease are influenced by the biologic environment.

The disc and intervertebral ligaments can be overloaded and fail when loading is excessive or the active system of damping is deficient. Sustained excessive stresses on the connective tissues of the disc and ligaments prevent normal healing, because the cells can only persist and fulfill their functions under a restricted range of mechanical stresses. Under mechanical conditions outlined previously, the intervertebral disc cells that synthesize the extracellular matrix exhibit normal activity. Lotz and Chin (8) have shown that disc cells function normally only within a precise range of mechanical loading. Too much or too little loading leads to direct cell destruction and programmed cell death (apoptosis).

Discs consist almost entirely of connective tissue, with a disappearance of notochord remnants by 20 years of age (9). As in all connective tissues, notably the annulus, cell activity can repair damage if lesions are limited or if the lesional process takes place over time in a manner analogous to stress fractures. In fact, an indisputable healing process can be observed in the intervertebral disc, with a fibroelastic reaction and neovascularization, at least during early degenerative change. However, just as in pseudarthrosis of long bones and in meniscal lesions, when deleterious conditions persist, the healing process can be overwhelmed.

Based on these mechanical and biologic aspects of degenerative disc disease, different working hypotheses were involved in the concept of nonrigid stabilization and development of the Wallis system. One was that, by increasing the stiffness of
the damaged intervertebral segment and by limiting the amplitude of mobility, one provides mechanical normalization, which should slow the progression of degenerative lesions. Moreover, provided that disc height is sufficiently preserved, creation of the proper range of loading stresses on the disc by the interspinous process implant should foster the healing process of the disc tissue. Finally, although many years of follow-up will be necessary for confirmation, it is anticipated that dynamic stabilization will slow the domino effect of accelerated degenerative change in the segments adjacent to the treated level, especially in comparison to treatment by fusion. This brings us to the third aspect fundamental to the Wallis system.

One should not propose radical surgical solutions for early degenerative changes.

Surgery rarely affords definitive solutions. If the threshold of surgery is low and if a surgical procedure leaves other options open, it is beneficial to adopt a step-by-step strategy to treat low back pain without compromising future solutions. More and more patients are turning to the Internet health sites and may be aware of the advent of biologic methods of treating degenerative discs with the patients’ own stem cells or fibroblasts (10). How many spinal surgeons would compromise their own access to such future techniques by accepting an arthrodesis, or even a disc prosthesis, as long as other viable solutions exist? This is no far distant perspective. Stem cell injection is already being used for tendon and ligament lesions (11).