| Innervation, inflammation, and hypermobility may characterize pathologic disc degeneration: review of animal model data. | |
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MedLine Citation:
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PMID: 16595449 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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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Authors:
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Jeffrey C Lotz; Jill A Ulrich |
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Publication Detail:
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Type: Comparative Study; Journal Article; Review |
Journal Detail:
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Title: The Journal of bone and joint surgery. American volume Volume: 88 Suppl 2 ISSN: 0021-9355 ISO Abbreviation: J Bone Joint Surg Am Publication Date: 2006 Apr |
Date Detail:
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Created Date: 2006-04-05 Completed Date: 2006-05-22 Revised Date: 2010-10-25 |
Medline Journal Info:
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Nlm Unique ID: 0014030 Medline TA: J Bone Joint Surg Am Country: United States |
Other Details:
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Languages: eng Pagination: 76-82 Citation Subset: AIM; IM |
Affiliation:
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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, USA. jlotz@itsa.ucsf.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Biomechanics Disease Models, Animal Disease Progression Intervertebral Disk / innervation*, pathology*, physiopathology Joint Instability / physiopathology* Range of Motion, Articular / physiology* Risk Factors Sensitivity and Specificity Severity of Illness Index Spinal Diseases / pathology*, physiopathology Spondylitis / pathology, physiopathology Stress, Mechanical Weight-Bearing |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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