• Luiz M Rocha-Neto, Jaime R Gamarra-Suárez, Fabiana F Freitas, Augusto Muzilli, Henrique B Abdalla, Cristina G Macedo, Marcelo H Napimoga, and Juliana T Clemente-Napimoga.
• Laboratory of Orofacial Pain, Department of Physiological Sciences, Piracicaba Dental School, University of Campinas-UNICAMP, Piracicaba, SP, Brazil.
• Neuroscience. 2019 Sep 15; 416: 229-238.

AbstractDiabetes is a chronic degenerative disease that represent a major threat to public health worldwide. Once the disease is established, one of the major concerns about the diabetes complications is the development of neuropathy. This study established an experimental model that evaluates the effect of type 1 diabetes on nociceptive challenges in the temporomandibular joint (TMJ). Streptozotocin-induced type 1 (STZ 75 mg/Kg) diabetes inhibited the responsiveness of C-fibers nociceptors located in the TMJ of Wistar rats since seventh day after the disease induction. Diabetes-induced hyporesponsiveness of C-fibers nociceptors was associated with significantly reduction of protein level of neuropeptides Substance P and Calcitonin Gene Related Peptide. Diabetic animals pre-treated with Protein Kinase C (PKC)-α and -β inhibitor (GO6976) or PKC-β inhibitor (LY333531) significantly increased capsaicin-induced nociception in the TMJ higher protein levels of Na+/K+-ATPase pump in the trigeminal ganglia. On the other hand, although diabetes inhibits formalin-induced nociception higher protein levels of pro-inflammatory cytokine IL1-β and chemokine CINC-1/CXCL-1 were observed. Overall, the results of the present work suggest that diabetes causes a hyporesponsiveness of C-fiber and a potentialization of the inflammatory response which may result in the degenerative process of periarticular tissues without pain perception.Copyright © 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

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