Nucleus Reconstruction by Autologous Chondrocyte Transplantation

The structure of the spine is not unique to the human body, but one conserved in basic design across several classes of living organisms. Although interspecies variation occurs with regard to the number of individual vertebrae, the metameric nature of the spine permits continued axial growth. Both our uniqueness in upright posture and that of serpentine segmentation is accommodated by the spine. It is impossible to discuss an intervertebral disc without defining the integral unit of a motion segment. The term motion segment designates two hemivertebrae and the disc connecting them [7]. Within the motion segment, each intervertebral disc has two distinct components: a central nucleus pulposus and an outer ring of connective tissue described as the anulus fibrosus. Together the two components function to dissipate the compressive component of axial loading via the tensile, collagenous properties of the anular fibers. In balance the force exchange is efficient, coupling progressive recruitment of concentric, collagenous fibers radially in response to central deforming action of the nucleus centrally. Within the context of the two components lies amore subtle balance, with anatomical differences between the two components more a spectrum than an interface. Separate from these two main components lies the vertebral endplate of each vertebra, which itself has distinctions along its entire margin. It is disparate harmony between the structures that results in disc failure, andwithout adequate knowledge of the structure, designing an effective strategy for treating disc degeneration is not possible. Numerous scientific studies have provided observations concerning the biochemistry and biomechanics of the disc, offering insights and theories into structure-function-failure relationships [9, 11, 12]. Spine dysfunction, back pain, and an accompanying quality-of-life reduction are pervasive in the human population. Theories for the epidemic prevalence of lower back pain include anatomy, biochemistry, postural bias, obesity, and a host of other structural-functional paradigms. Strategies to repair the dysfunctional spinal segment have historically utilized symptomatic relief as an endpoint outcome, where functional recovery did not necessarily correlate with anatomical correction. A consensus of opinion exists that prosthetic replacement to restore motion is a necessary component of any strategy. Clearly, the development of prosthetic components for other applications has brought to the table a separate but similarly troubling set of patient symptoms. Component loosening, periprosthetic osteolysis, fibrosis, bursitis, and even unintended arthrosis, while limited in prevalence remain problems nonetheless in other applications of joint replacement. Our project summons two key intents in design and eliminates the dependence on a mechanical or prosthetic interface. The first goal is to retain spinal segment motion, and the second goal is to create a biological interface to promote repair even though complete restitution to native function currently does not seem possible. Most assessments of intervertebral disc failure have focused on degenerative change, changes in morphology that affect the biomechanical performance of the motion segment. In this consideration, mechanical failure is little more than a corollary of matrix structure, which in turn depends on balanced cell metabolism for efficient maintenance of the disc matrix. Given the value of cells to the metabolic health of the disc, our therapeutic strategy has been to replace, regenerate, or in some other manner augment the intervertebral disc cell with a goal of correcting matrix insufficiencies, thereby restoring normal segment biomechanics. If, however, the biological basis for function is removed, replaced, or fusion is performed, then no further option to a biological basis for treatment remains, and the potential loss of motion within the disc segment is virtually assured.