ISSLS Prize Winner
Autor: | Kenichi Murakami, Sumihisa Orita, Tomoaki Toyone, Gen Arai, Mamoru Kawakami, Hiroto Kamoda, Yasuhiro Oikawa, Gou Kubota, Yoshihiro Sakuma, Tomoyuki Ozawa, Gen Inoue, Yawara Eguchi, Masayuki Miyagi, Tetsuhiro Ishikawa, Masataka Shibayama, Yasuchika Aoki, Seiji Ohtori, Kazuhisa Takahashi, Miyako Suzuki |
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Rok vydání: | 2012 |
Předmět: |
musculoskeletal diseases
Pathology medicine.medical_specialty biology business.industry Regeneration (biology) Neuropeptide Nerve injury musculoskeletal system Nerve growth factor medicine.anatomical_structure Downregulation and upregulation Calcitonin Anesthesia biology.protein Medicine Orthopedics and Sports Medicine Neurology (clinical) medicine.symptom business Interleukin 6 Sensory nerve |
Zdroj: | Spine. 37:1810-1818 |
ISSN: | 0362-2436 |
DOI: | 10.1097/brs.0b013e31824ffac6 |
Popis: | Study design Animal model of intravertebral disc (IVD) degeneration. Objective To examine production of inflammatory mediators in IVDs and neuropeptides in dorsal root ganglia (DRGs) in rat models of IVD compression and injury. Summary of background data Sensory nerve fibers in IVDs and inflammatory mediator responses have been verified in animal models of IVD injury. However, the IVD injury in animals incompletely models degenerated human IVDs causing discogenic low back pain, because human IVDs are also subject to compression. Methods Experimental groups (controls, IVD injury, IVD compression, and their combination) of Sprague Dawley rats were prepared. Fluoro-Gold (FG; Fluorochrome, Denver, CO) was applied into coccygeal IVDs. Inflammatory mediators in IVDs, including nerve growth factor, tumor necrosis factor α, interleukin 1β, and interleukin 6, were quantified using enzyme-linked immunosorbent assays. DRGs were immunostained for calcitonin gene-related peptide, activating transcription factor 3, and growth-associated phosphoprotein 43. Results The upregulation of inflammatory mediators was transient in the IVD injury group but delayed and long-lasting in the IVD compression group. When the IVD injury and compression were combined, the upregulation of inflammatory mediators was long-lasting through 8 weeks. The proportion of calcitonin gene-related peptide-immunoreactive neurons among Fluoro-Gold-labeled neurons remained significantly higher in the IVD injury, compression, and combination groups than in the controls. In contrast, increases in the proportions of activating transcription factor 3-immunoreactive or growth-associated phosphoprotein 43-immunoreactive neurons in the IVD injury group animals were transient but long-lasting in the compression and combination groups compared with controls. Conclusion Disc injury in rats produces persistent increases in neuropeptides in DRGs but only transient increases in inflammatory mediators in IVDs. On the contrary, disc compression in rats produces a long-lasting increase in inflammatory mediators in IVDs and neuropeptides in DRGs. Moreover, disc compression induces persistent nerve injury and regeneration of the afferent fibers innervating IVDs. |
Databáze: | OpenAIRE |
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