Tumor Necrosis Factor α and Nucleus-Pulposus-Induced Nerve Root Injury

Olmarker, Kjell; Larsson, Karin

doi:10.1097/00007632-199812010-00008

Cited by 318 publications

(193 citation statements)

References 57 publications

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“…Application of nucleus pulposus onto nerve roots has been shown to induce edema of the nerve roots and dorsal root ganglia, and to alter the conduction velocity [41]. Proinflammatory cytokines, including IL-1, IL-6, and TNF-alpha, as well as COX-2, are known mediators of the peripheral inflammatory response caused by nucleus pulposus [10,28,30,36]. These molecules are also synthesized and released during various types of nerve injury [26].…”

Section: Discussionmentioning

confidence: 99%

“…Radicular pain, a common symptom of lumbar disc herniation, is induced by mechanical compression and inflammation [28,29]. Prostaglandins (PGs) and cytokines generated at the site of inflammation are responsible for producing the associated pain [26].…”

Section: Introductionmentioning

confidence: 99%

“…Prostaglandins (PGs) and cytokines generated at the site of inflammation are responsible for producing the associated pain [26]. Recently, cytokines such as interleukins and tumor necrosis factor alpha (TNFalpha), and cyclooxygenase-2 (COX-2) have been strongly linked to the effects of nucleus pulposus on nerve roots [12,27,28]. It was recently reported that infliximab, a TNFalpha inhibitor, was effective in treating sciatic pain caused by lumbar disc herniation and that patients experienced no significant side effects [16].…”

Section: Introductionmentioning

confidence: 99%

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Nuclear factor-kappa B decoy suppresses nerve injury and improves mechanical allodynia and thermal hyperalgesia in a rat lumbar disc herniation model

et al. 2009

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Nuclear factor-kappa B (NF-jB) is a gene transcriptional regulator of inflammatory cytokines. We investigated the transduction efficiency of NF-jB decoy to dorsal root ganglion (DRG), as well as the decrease in nerve injury, mechanical allodynia, and thermal hyperalgesia in a rat lumbar disc herniation model. Forty rats were used in this study. NF-jB decoy-fluorescein isothiocyanate (FITC) was injected intrathecally at the L5 level in five rats, and its transduction efficiency into DRG measured. In another 30 rats, mechanical pressure was placed on the DRG at the L5 level and nucleus pulposus harvested from the rat coccygeal disc was transplanted on the DRG. Rats were classified into three groups of ten animals each: a herniation ? decoy group, a herniation ? oligo group, and a herniation only group. For behavioral testing, mechanical allodynia and thermal hyperalgesia were evaluated. In 15 of the herniation rats, their left L5 DRGs were resected, and the expression of activating transcription factor 3 (ATF-3) and calcitonin gene-related peptide (CGRP) was evaluated immunohistochemically compared to five controls. The total transduction efficiency of NF-jB decoy-FITC in DRG neurons was 10.8% in vivo. The expression of CGRP and ATF-3 was significantly lower in the herniation ? decoy group than in the other herniation groups.Mechanical allodynia and thermal hyperalgesia were significantly suppressed in the herniation ? decoy group. NFjB decoy was transduced into DRGs in vivo. NF-jB decoy may be useful as a target for clarifying the mechanism of sciatica caused by lumbar disc herniation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Nuclear factor-kappa B decoy suppresses nerve injury and improves mechanical allodynia and thermal hyperalgesia in a rat lumbar disc herniation model

et al. 2009

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“…Radicular pain is a common symptom of lumbar disc herniation and spinal stenosis induced by mechanical compression and inflammation [8,9]. Cytokines generated at the inflammatory site produce associated pain [6,10,11].…”

Section: Introductionmentioning

confidence: 99%

Proinflammatory cytokines in the cerebrospinal fluid of patients with lumbar radiculopathy

et al. 2010

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“…Proinflammatory cytokine pain mediators like substance P and tumor necrosis factor alpha (TNF-alpha) are released or activated by nervous structures in contact with the nucleus pulposus [2,23]. Substance P acts as a neuroregulator or neurotransmitter in the conduction of nociceptive stimuli, and is a modulator of neuroimmunoregulation.…”

Section: Introductionmentioning

confidence: 99%

Detection of bacterial DNA in painful degenerated spinal discs in patients without signs of clinical infection

2004

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A local inflammatory and potentially painful response, of which the ultimate cause is unknown, has been described in nervous tissues in contact with degenerated disc material in patients with low back and leg pain. With the rationale that a possible cause of such inflammation could be bacterial infection, we utilized PCR (polymerase chain reaction) amplification of the 16S rRNA (ribosomal RNA) gene followed by gene sequencing, to investigate whether bacterial DNA might be detected in the degenerative discs of 10 patients operated for disc herniation or post-discectomy syndrome. One patient with disc hernia harbored DNA homologous to Bacillus cereus, and in one patient suffering from post-discectomy syndrome, Citrobacter braakilfreundii DNA was detected. The finding demonstrates that 16S rRNA PCR can be a useful tool in search of bacterial DNA in degenerated discs, which in turn may be indicative of low-grade infection, manifesting itself only as pain rather than as clinical infection.

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Tumor Necrosis Factor α and Nucleus-Pulposus-Induced Nerve Root Injury

Cited by 318 publications

References 57 publications

Nuclear factor-kappa B decoy suppresses nerve injury and improves mechanical allodynia and thermal hyperalgesia in a rat lumbar disc herniation model

Nuclear factor-kappa B decoy suppresses nerve injury and improves mechanical allodynia and thermal hyperalgesia in a rat lumbar disc herniation model

Proinflammatory cytokines in the cerebrospinal fluid of patients with lumbar radiculopathy

Detection of bacterial DNA in painful degenerated spinal discs in patients without signs of clinical infection

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