The Journal of Bone and Joint Surgery (American). 2006;88:76-82.
doi:10.2106/JBJS.E.01448
© 2006 The Journal of Bone and Joint Surgery, Inc.
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Innervation, Inflammation, and Hypermobility May Characterize Pathologic Disc Degeneration: Review of Animal Model Data

Jeffrey C. Lotz, PhD and Jill A. Ulrich, BS

Corresponding author:
Jeffrey C. Lotz, PhD
Orthopaedic Bioengineering Laboratory, Department of Orthopaedic Surgery, University of California at San Francisco, Box 0514, 533 Parnassus Avenue, University Hall U-454, San Francisco, CA 94110.
E-mail address: jlotz{at}itsa.ucsf.edu

The authors did not receive grants or outside funding in support of their research for or preparation of this manuscript. They did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

Animal models provide important clues to the pathomechanisms of human intervertebral disc degeneration. Previous reviews on this topic have highlighted the fact that loss of nuclear volume (and, consequently, pressure) is a common trigger for tissue-remodeling and anatomic change consistent with degeneration in humans. Unfortunately, a large gap still exists in the medical knowledge base that serves to distinguish symptomatic from asymptomatic degeneration. Because disc degeneration per se is not a basis for clinical intervention, identification of specific features underlying discogenic pain is of the utmost importance to advance the current level of care and identify novel therapeutic targets. This article presents animal-model evidence that pathologic, or painful, degeneration is characterized by ineffective injury-healing of peripheral tissue. Because the disc is only vascularized at the vertebral end plate and the outer part of the anulus, these are the likely sites for focal damage, inflammation, neoinnervation, and nociceptor sensitization. Consequently, while nuclear insufficiency is likely the root of degenerative change, the end plate and peripheral part of the anulus are more likely the source of patient discomfort.


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