Lora Victor Ricardo Manuel Muñoz, Clemente-Napimoga Juliana Trindade, Abdalla Henrique Ballassini, Macedo Cristina Gomes, Canales Giancarlo de la Torre, Barbosa Celia Marisa Rizzatti
Department of Prosthodontics and Periodontology, Piracicaba Dental School, University of Campinas (UNICAMP), Av Limeira, 901, Piracicaba, São Paulo, zip code 13414-903, Brazil.
São Leopoldo Mandic Institute and Research Center, Rua Jose Rocha Junqueira, 13 - Swift, Campinas, São Paulo, zip code 13045-755, Brazil; Laboratory of Orofacial Pain, Department of Physiological Sciences, Piracicaba Dental School, University of Campinas (UNICAMP), Av Limeira, 901, Piracicaba, São Paulo, zip code 13414-903, Brazil.
Toxicon. 2017 Apr;129:52-57. doi: 10.1016/j.toxicon.2017.02.010. Epub 2017 Feb 14.
This study aimed to investigate the antinociceptive effects of Botulinum toxin type A (BoNT-A) on persistent inflammatory hypernociception induced by arthritis in the temporomandibular joint (TMJ) of rats.
Wistar rats were induced to persistent inflammatory hypernociception in the left TMJ. Then, animals were treated with intra-TMJ injections of BoNT-A, using doses of 3.5, 7 and 14 U/kg. Saline was used as control group. Behavioral tests were applied to evaluated the effect of BoNT-A in the inflammatory hypernociception. After that, animals were euthanized and samples from peri-articular tissues and trigeminal ganglia were obtained for further analyses.
BoNT-A reduced the persistent inflammatory hypernociception induced by arthritis in the TMJ of rats. BoNT-A significantly reduced the peripheral release of the neurotransmitters Substance P and Calcitonin gene related peptide; and the pro-inflammatory cytokine IL-1β. Otherwise, BoNT-A had no effect in the peripheral release of glutamate and the cytokine TNF-α.
These results demonstrate that intra-articular injection of BoNT-A reduces the albumin-induced arthritis persistent hypernociception in TMJ of rats by peripheral inhibition of neuropeptides release.
本研究旨在探讨A型肉毒杆菌毒素（BoNT-A）对大鼠颞下颌关节（TMJ）关节炎诱导的持续性炎性痛觉过敏的镇痛作用。
将Wistar大鼠诱导产生左侧TMJ持续性炎性痛觉过敏。然后，对动物进行TMJ内注射BoNT-A治疗，剂量分别为3.5、7和14 U/kg。生理盐水作为对照组。应用行为学测试评估BoNT-A对炎性痛觉过敏的影响。之后，对动物实施安乐死，并获取关节周围组织和三叉神经节的样本进行进一步分析。
BoNT-A减轻了大鼠TMJ关节炎诱导的持续性炎性痛觉过敏。BoNT-A显著降低了神经递质P物质和降钙素基因相关肽的外周释放；以及促炎细胞因子IL-1β。此外，BoNT-A对谷氨酸的外周释放和细胞因子TNF-α没有影响。
这些结果表明，关节内注射BoNT-A通过外周抑制神经肽释放减轻了白蛋白诱导的大鼠TMJ关节炎持续性痛觉过敏。
