Innervation, Inflammation, and Hypermobility May Characterize Pathologic Disc Degeneration: Review of Animal Model Data

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 deg...

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Bibliographic Details
Published in:Journal of bone and joint surgery. American volume 2006-04, Vol.88 (suppl_2 Suppl 2), p.76-82
Main Authors: Lotz, Jeffrey C, Ulrich, Jill A
Format: Article
Language:English
Subjects:
Animals
Biomechanical Phenomena
Disease Models, Animal
Disease Progression
Intervertebral Disc - innervation
Intervertebral Disc - pathology
Intervertebral Disc - physiopathology
Joint Instability - physiopathology
Range of Motion, Articular - physiology
Risk Factors
Sensitivity and Specificity
Severity of Illness Index
Spinal Diseases - pathology
Spinal Diseases - physiopathology
Spondylitis - pathology
Spondylitis - physiopathology
Stress, Mechanical
Weight-Bearing
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Summary: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.
ISSN:0021-9355
1535-1386
DOI:10.2106/JBJS.E.01448