• Ricardo Bonfante, Marcelo Henrique Napimoga, Cristina Gomes Macedo, Henrique Ballassini Abdalla, Victor Pieroni, and Juliana Trindade Clemente-Napimoga.
• Laboratory of Orofacial Pain, Department of Physiological Sciences, Piracicaba Dental School, University of Campinas - UNICAMP, Piracicaba, SP, Brazil.
• Neuroscience. 2018 Nov 1; 391: 120-130.

AbstractTemporomandibular joint (TMJ) is frequently involved with rheumatoid arthritis with a high prevalence that could result in a chronic pain state. Once the disease is established in the joint, the antigen-specific immune reaction initiates a neuro-immune cascade of events that causes sensitization of the central nervous system. This study establishes animal experimental models that evaluate the chronicity of albumin-induced arthritis hypernociception in the TMJ. Antigen-induced arthritis was generated in rats with methylated bovine serum albumin (mBSA) diluted in complete Freund's. Intra-articular injection of mBSA (10 µg/TMJ/week) during 3 weeks resulted in a persistent inflammatory hypernociception which was characterized by an inflammatory episode characterized by the increased of lymphocytes, macrophages and pro-inflammatory interleukins IL-12 and IL-18. The persistent model of inflammatory hypernociception induced by arthritis in the TMJ elicited protein levels of P2X7 receptors, cathepsin S and fractalkine in the trigeminal subnucleus caudalis. Overall, the results of the present work suggest that a persistent inflammatory hypernociception of albumin-induced arthritis in the TMJ leads to the activation of the central nervous system signaling by P2X7/cathepsin S/fractalkine pathway.Copyright © 2018 IBRO. Published by Elsevier Ltd. All rights reserved.

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