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Occlusal Trauma Induces Neuroimmune Crosstalk for a Pain State
H B Abdalla1, M H Napimoga1, C A Trindade-da-Silva1
1Faculdade São Leopoldo Mandic, Instituto e Centro de Pesquisas São Leopoldo Mandic, Laboratoy of Neuroimmune Interface of Pain Research, Campinas, SP, Brazil.
Journal of Dental Research
|October 1, 2021
Summary
Occlusal trauma triggers inflammatory responses in the temporomandibular joint (TMJ) and trigeminal ganglia. This leads to neuroinflammation and central sensitization, contributing to persistent pain.
Area of Science:
- Neuroscience
- Immunology
- Dentistry
Background:
- Temporomandibular joint (TMJ) disorder from occlusal trauma is controversial.
- Experimental traumatic occlusion (ETO) in rats causes prolonged nociceptive responses.
Purpose of the Study:
- Investigate if ETO increases inflammatory mediators in the TMJ.
- Examine ETO's impact on trigeminal ganglia, neurotransmitter release, and satellite glial cell (SGC) activation.
Main Methods:
- ELISA and Western blotting to detect inflammatory mediators in TMJ tissue.
- Analysis of neurotransmitter release, receptor expression, and SGC activation markers (IL-1β, COX-2, pERK, Nav 1.7) in trigeminal ganglia.
- mRNA analysis for PKA, CREB.
Main Results:
- ETO enhanced inflammatory mediators (TNF-α, IL-1β, IL-6, CX3CL1, ADAM-17) in TMJ tissue.
- Increased substance P and glutamate release, with altered AMPA/NMDA receptor expression in trigeminal ganglia.
- Confirmed SGC activation and increased pERK, Nav 1.7 expression, indicating a neuroinflammatory cascade.
Conclusions:
- Occlusal trauma induces neuroimmune crosstalk, generating proinflammatory mediators.
- This increases neuronal activity in trigeminal ganglia, leading to persistent neuroinflammation and central sensitization.
- Findings suggest a mechanism for chronic pain development in TMJ disorders.
Keywords:
central nervous systeminflammationpaintemporomandibular disordertemporomandibular jointtraumatic dental occlusionMore Related Videos
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