Abstract
Mirror-image pain is a kind of pain that occurs on the contralateral side, but its pathogenesis remains unclear.ObjectiveTo develop an osteoarthritis mouse model for investigating mirror-image pain through observing nocifensive behaviors, histological changes, and nociceptive activity at days 3, 7, 14, 21, and 28 after the chemical induction of unilateral temporomandibular joint (TMJ) osteoarthritis.MethodologyWe randomly divided 6-week-old mice into sham and complete Freund adjuvant groups. To induce nocifensive behaviors, we applied 0.04 g of von Frey filament, 10 psi of air puff, and cold acetone on both sides of whisker pads at different days. The histology of TMJ on both sides was observed by hematoxylin/eosin staining and microcomputed tomography scanning. Furthermore, the nociceptive activity was evaluated using the phosphorylated cyclic AMP response element binding protein (pCREB) and a microglia marker at different days in the trigeminal subnucleus caudalis.ResultsNocifensive behaviors against mechanical and temperature stimuli on the contralateral side became stronger than the baseline on day 28, in agreement with the elevation of the pCREB and the microglia marker in the trigeminal subnucleus caudalis. Thus, hypernociception on the contralateral side occurred at day 28.ConclusionsClearly, the TMJ model with unilateral osteoarthritis exhibited mirror-image pain. Therefore, this model is useful in investigating the pathogenesis of pain and in developing treatments.
Highlights
Mirror-image pain is the pain found on the opposite side after acquiring peripheral nerve lesion.1,2 This type of pain is generally characterized by hypersensitivity to mechanical or thermal painful stimulus that responds even to a light touch or low-threshold stimulus.3 Mirror-image pain occurs in 8%–15% of patients with chronic temporomandibular joint (TMJ) osteoarthritis.4 the pathogenesis of mirror-image pain on TMJ osteoarthritis is insufficiently understood
The injection of complete Freund adjuvant certainly induced TMJ osteoarthritis associated with mirror-image pain, without affecting mouse’s bodyweight
Our study shows the development of mirror-image pain on TMJ osteoarthritis in mice induced by the unilateral injection of complete Freund adjuvant
Summary
Mirror-image pain is the pain found on the opposite side after acquiring peripheral nerve lesion. This type of pain is generally characterized by hypersensitivity to mechanical or thermal painful stimulus that responds even to a light touch or low-threshold stimulus. Mirror-image pain occurs in 8%–15% of patients with chronic temporomandibular joint (TMJ) osteoarthritis. the pathogenesis of mirror-image pain on TMJ osteoarthritis is insufficiently understood. Mirror-image pain is the pain found on the opposite side after acquiring peripheral nerve lesion.. Mirror-image pain is the pain found on the opposite side after acquiring peripheral nerve lesion.1,2 This type of pain is generally characterized by hypersensitivity to mechanical or thermal painful stimulus that responds even to a light touch or low-threshold stimulus.. For the pathophysiology of the pain pathway, the contralateral dorsal root ganglia or trigeminal ganglia upregulate the proinflammatory cytokines 3 weeks after the nerve injury.. The number of glia cells in the contralateral dorsal horn or trigeminal subnucleus caudalis increases 3 weeks after nerve damage.. All of the evidence about mirror-image pain condition in neuropathic pain models suggested that proinflammatory cytokines in the peripheral nerve injury were carried by the cerebrospinal fluid to the contralateral dorsal horn, activating glia cells in that horn.. Recent evidence of pain associated with mirror-image pain was mainly found on neuropathic animal models. In chronic constriction injury of the spinal nerve or the infraorbital nerve, pain hypersensitivity on the contralateral side appeared 3 weeks after the nerve lesion. The expression of proinflammatory cytokines (TGFβ1, IL-1β, TNFα, and IL-10) in the contralateral nerve, which was not directly injured, significantly increased 2 weeks after a nerve injury. For the pathophysiology of the pain pathway, the contralateral dorsal root ganglia or trigeminal ganglia upregulate the proinflammatory cytokines 3 weeks after the nerve injury. the number of glia cells in the contralateral dorsal horn or trigeminal subnucleus caudalis increases 3 weeks after nerve damage. All of the evidence about mirror-image pain condition in neuropathic pain models suggested that proinflammatory cytokines in the peripheral nerve injury were carried by the cerebrospinal fluid to the contralateral dorsal horn, activating glia cells in that horn. The activated glia cells might potentially stimulate other glia cells and increase the excitability of pain signals in the contralateral dorsal horn.
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