Abstract
IntroductionDegeneration of the interverterbral disk is as a cause of low-back pain is increasing. To gain insight into relationships between biological processes, structural alterations and behavioral pain, we created an animal model in rats.MethodsDisk degeneration was induced by removal of the nucleus pulposus (NP) from the lumbar disks (L4/L5 and L5/L6) of Sprague Dawley rats using a 0.5-mm-diameter microsurgical drill. The degree of primary hyperalgesia was assessed by using an algometer to measure pain upon external pressure on injured lumbar disks. Biochemical and histological assessments and radiographs of injured disks were used for evaluation. We investigated therapeutic modulation of chronic pain by administering pharmaceutical drugs in this animal model.ResultsAfter removal of the NP, pressure hyperalgesia developed over the lower back. Nine weeks after surgery we observed damaged or degenerated disks with proteoglycan loss and narrowing of disk height. These biological and structural changes in disks were closely related to the sustained pain hyperalgesia. A high dose of morphine (6.7 mg/kg) resulted in effective pain relief. However, high doses of pregabalin (20 mg/kg), a drug that has been used for treatment of chronic neuropathic pain, as well as the anti-inflammatory drugs celecoxib (50 mg/kg; a selective inhibitor of cyclooxygenase 2 (COX-2)) and ketorolac (20 mg/kg; an inhibitor of COX-1 and COX-2), did not have significant antihyperalgesic effects in our disk injury animal model.ConclusionsAlthough similarities in gene expression profiles suggest potential overlap in chronic pain pathways linked to disk injury or neuropathy, drug-testing results suggest that pain pathways linked to these two chronic pain conditions are mechanistically distinct. Our findings provide a foundation for future research on new therapeutic interventions that can lead to improvements in the treatment of patients with back pain due to disk degeneration.
Highlights
Degeneration of the interverterbral disk is as a cause of low-back pain is increasing
The intervertebral disk has a unique structure composed of a tough outer ring, the annulus fibrosus (AF), as well as a gelatinous inner core, the nucleus pulposus (NP)
We developed an animal model for chronic discogenic back pain that is amenable to assessment of behavioral hyperalgesia
Summary
Degeneration of the interverterbral disk is as a cause of low-back pain is increasing. To gain insight into relationships between biological processes, structural alterations and behavioral pain, we created an animal model in rats. There are many causes of low-back pain, symptomatic degeneration of the intervertebral disk is thought to be the leading cause of chronic discogenic. Animal pain models are essential for understanding the complexities of pain and the development and testing of new therapies. The rabbit disk puncture model has been beneficial in the study of biological mechanisms of disk degeneration and in testing therapeutics for disk regeneration. The rabbit disk slowly and progressively degenerates [2]. Rabbits tend to show minimal pain behavior during disk degeneration in this model. Rabbits do not display assessable pain behavior; they are not suitable for the study of discogenic back pain
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