OBJECTIVE: To verify the biologic links between progressive cellular and structural alterations within knee joint components and development of...
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[title] => Alteration of sensory neurons and spinal response to an experimental osteoarthri
[paragraph] => Alteration of sensory neurons and spinal response to an experimental osteoarthritis pain model.
[content] => Authors
H.-J. Im, J.-S. Kim, X. Li, N. Kotwal, D. Sumner et al.
Lab
Rush University Medical Center and University of Illinois, Chicago, USA.
Journal
Arthritis and Rhumatism
Abstract
OBJECTIVE: To verify the biologic links between progressive cellular and structural alterations within knee joint components and development of symptomatic chronic pain that are characteristic of osteoarthritis (OA), and to investigate the molecular basis of alterations in nociceptive pathways caused by OA-induced pain. METHODS: An animal model of knee joint OA pain was generated by intraarticular injection of mono-iodoacetate (MIA) in Sprague-Dawley rats, and symptomatic pain behavior tests were performed. Relationships between development of OA with accompanying pain responses and gradual alterations in cellular and structural knee joint components (i.e., cartilage, synovium, meniscus, subchondral bone) were examined by histologic and immunohistologic analysis, microscopic examination, and microfocal computed tomography. Progressive changes in the dynamic interrelationships between peripheral knee joint tissue and central components of nociceptive pathways caused by OA-induced pain were examined by investigating cytokine production and expression in sensory neurons of the dorsal root ganglion and spinal cord. RESULTS: We observed that structural changes in components of the peripheral knee joint correlate with alterations in the central compartments (dorsal root ganglia and the spinal cord) and symptomatic pain assessed by behavioral hyperalgesia. Our comparative gene expression studies revealed that the pain pathways in MIA-induced knee OA may overlap, at least in part, with neuropathic pain mechanisms. Similar results were also observed upon destabilization of the knee joint in the anterior cruciate ligament transection and destabilization of the medial meniscus models of OA. CONCLUSION: Our results indicate that MIA-induced joint degeneration in rats generates an animal model that is suitable for mechanistic and pharmacologic studies on nociceptive pain pathways caused by OA, and provide key in vivo evidence that OA pain is caused by central sensitization through communication between peripheral OA nociceptors and the central sensory system. Furthermore, our data suggest a mechanistic overlap between OA-induced pain and neuropathic pain.
BIOSEB Instruments Used
Dynamic Weight Bearing 2.0 (BIO-DWB-DUAL)
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[description_short] => The advanced version of our Dynamic Weight Bearing Test for rodents (rats and mice) allows for faster paw identification, based on a video solution taking advantage of the most advanced algorithms of morphologic analysis, weight distribution and postural changes in dynamic conditions. An efficient and advanced alternative to traditional incapacitance tests (i.e. the paw pressure test or the force plate test) for assessing pain sensitivity in your research on analgesia, hyperalgesia and nociception involving rats and mice, including work on osteoarthritis, bone cancer, analgesic substances, Parkinson disease, allodynia...


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[description_short] => Expand Your Analysis with Advanced Postural and Locomotor Calculations
BIOSEB’s renowned Dynamic Weight Bearing (DWB2) system is now more powerful than ever with the addition of the Postural Module. This optional software upgrade extends standard weight-bearing analysis by integrating unique calculations designed to quantify subtle aspects of postural balance, locomotor patterns, and compensatory behaviors.
Developed in collaboration with Dr. Tighilet’s lab from Aix Marseille Université-CNRS, the Postural Module improves your DWB2, providing valuable endpoints for studies on pain, neurology, vestibular dysfunction, and neurodegenerative disorders.


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