Abstract

Lumbar disc degeneration occurs because of a variety of factors and results in a multitude of conditions. Alterations in the vertebral endplate cause loss of disc nutrition and disc degeneration. Aging, apoptosis, abnormalities in collagen, vascular ingrowth, loads placed on the disc, and abnormal proteoglycan all contribute to disc degeneration. Some forms of disc degeneration lead to loss of height of the motion segment with concomitant changes in biomechanics of the segment. Disc herniation with radiculopathy and chronic discogenic pain are the result of this degenerative process.

Introduction

Lumbar disc degeneration occurs commonly in humans. There are a variety of factors that contribute to this condition. The disc itself is active tissue that contains significant mechanisms for self-repair.^[26] Reviewing the available literature concerning the normal and abnormal physiology of the disc is useful in understanding why degeneration occurs, why certain conditions are painful, and which mechanisms can be used to prevent further degeneration.

The intervertebral disc is composed of at least three elements. The central portion of the disc contains the nucleus pulposus, which is composed of cells from the primitive notochord. The outer portion of the disc is the anulus fibrosis, and it is composed of concentric layers of intertwined anular bands. These anular bands are arranged in a specific pattern to resist forces placed on the lumbar spine. The anular bands are subdivided into inner fibers, which are connected to the cartilaginous endplate, and outer Sharpy fibers, which are attached to the VB (Fig. 1). The ALL and PLL further strengthen the disc space. The ALL attaches more strongly to the VB edges than to the anulus. It provides a tension band to resist forces applied in extension and is a stronger ligament than the PLL. The PLL is not as strong as the ALL, but it provides a tension band to resist flexion forces. The PLL strongly attaches to the anulus fibrosis, and frequently is torn in cases of free fragment disc herniation.

A meningeal branch of the spinal nerve, better known as the recurrent sinuvertebral nerve, innervates the area around the disc space (Fig. 2). This nerve exits from the dorsal root ganglion and enters the foramen, where it then divides into a major ascending and lesser descending branch.^[6] It has been shown in animal studies that further afferent innervation to the sinuvertebral nerve arises via the rami communicantes from multiple superior and inferior dorsal root ganglia.^[43] In both human and animal studies, the outer anular regions are innervated, but the inner regions and nucleus pulposus are not innervated.^[37,48] In addition studies have demonstrated that the ALL also receives afferent innervation from branches that originate in the dorsal root ganglion.^[7] The PLL is richly innervated by nociceptive fibers from the major ascending branch of the sinuvertebral nerve. These nerves also innervate the adjacent outer layers of the anulus fibrosis.^[7,37] Degenerated human lumbar discs have been shown to contain more nerve tissue and to be more vascular than normal discs.^[9,12,48]