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The Journal of Pain

Cover Image - The Journal of Pain, Volume 23, Issue 11

The Journal of Pain publishes original articles, reviews, and focus articles related to all aspects of pain, including basic, translational, and clinical research, epidemiology, education, and health policy. The journal is the scientific publication of the United States Association for the Study of Pain (USASP), whose mission is to promote scientific advances that reduce the burden of pain.

The Journal of Pain follows the ICMJE's Recommendations for the Conduct, Reporting, Editing and Publication of Scholarly Work in Medical Journals.

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The goal of the United States Association for the Study of Pain is to bring together diverse perspectives on pain science to directly improve the lives of people with pain.

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The Journal of Pain Early Career Editorial Fellowship Program to Promote Diversity in Editorial Leadership

Journal Club: Featured Article

Spinal CCK1 Receptors Contribute to Somatic Pain Hypersensitivity Induced by Malocclusion via a Reciprocal Neuron-Glial Signaling Cascade

Recent studies have shown that the incidence of chronic primary pain including temporomandibular disorders (TMD) and fibromyalgia syndrome (FMS) often exhibit comorbidities. We recently reported that central sensitization and descending facilitation system contributed to the development of somatic pain hypersensitivity induced by orofacial inflammation combined with stress. The purpose of this study was to explore whether TMD caused by unilateral anterior crossbite (UAC) can induce somatic pain hypersensitivity, and whether the cholecystokinin (CCK) receptor-mediated descending facilitation system promotes hypersensitivity through neuron-glia cell signaling cascade.

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Recent studies have shown that the incidence of chronic primary pain, including temporomandibular disorders (TMD) and fibromyalgia syndrome, (FMS) often exhibit comorbidities. This study explored whether TMD caused by unilateral anterior crossbite can induce somatic pain hypersensitivity, and whether the cholecystokinin (CCK) receptor-mediated descending facilitation system promotes hypersensitivity through neuron-glia cell cascade signaling. These findings indicate that the signaling transduction between neurons and glia at the spinal cord level contributes to the descending pain facilitation through CCK1 receptors during the development of the comorbidity of TMD and FMS. See Xiang, et al, Page 1629

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