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Occlusal Trauma Induces Neuroimmune Crosstalk for a Pain State

下调和上调 三叉神经节 P物质 疼痛 伤害 谷氨酸受体 医学 内科学 化学 神经肽 受体 神经科学 生物 感觉系统 外科 基因 生物化学
作者
Henrique Ballassini Abdalla,Marcelo Henrique Napimoga,Carlos Antônio Trindade‐da‐Silva,Morgana Rodrigues Guimarães,Míriam Teresa Paz Lopes,Paulo César Vieira dos Santos,W.A. Buarque e Silva,F. Andrade e Silva,Juliana Trindade Clemente‐Napimoga
出处
期刊:Journal of Dental Research [SAGE Publishing]
卷期号:101 (3): 339-347 被引量:9
标识
DOI:10.1177/00220345211039482
摘要

Temporomandibular joint (TMJ) disorder caused by occlusal trauma is one of the most controversial topics in dentistry. Experimental traumatic occlusion (ETO) induced by metal crowns cemented to mandibular first molars in rats causes a long-lasting nociceptive response. This study aimed to elucidate whether ETO generates an increase in inflammatory mediators in the TMJ. In addition, the impact of ETO on trigeminal ganglia, neurotransmitter release, and satellite glial cell (SGC) activation was investigated. ELISA revealed enhanced inflammatory mediators, including TNF-α, IL-1β, IL-6, CX3CL1, and ADAM-17 by Western blotting, in periarticular TMJ tissue after 28 d of ETO. In the trigeminal ganglia, ETO groups increased the release of the neurotransmitters substance P and glutamate. Overexpression of the AMPA receptor and upregulation of NMDA were observed in the 0.4- and 0.7-mm ETO groups, respectively, highlighting enhanced neuronal excitation. Increased IL-1β and COX-2 mRNA levels in the 0.7-mm ETO group confirmed trigeminal ganglia SGC activation. Immunofluorescence and electrophoresis of SGC revealed increased pERK expression in the 0.7-mm ETO group. ERK phosphorylation was shown to be nociceptive specific, with its upregulation occurring in cases of chronic inflammatory pain. Increased PKA mRNA levels were observed in the 0.4-mm ETO group, while CREB mRNA levels were upregulated for both ETO groups. Electrophoresis showed overexpression of sodium channel Nav 1.7 in the 0.7-mm ETO group, while immunofluorescence revealed that Nav 1.7 is expressed in sensory trigeminal ganglia cells. The results of this study suggest that occlusal trauma induces neuroimmune crosstalk, with synthesis of proinflammatory/pronociceptive mediators, which increases neuronal activity in trigeminal ganglia via the activation of an inflammatory response cascade to develop a persistent neuroinflammatory state that leads to central sensitization.
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