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Pathophysiological mechanisms of persistent orofacial pain
Masamichi Shinoda1, Yoshinori Hayashi1, Asako Kubo1
1Department of Physiology, Nihon University School of Dentistry.
Journal of Oral Science
|March 6, 2020
Summary
Orofacial pain hypersensitivity is linked to neuroplastic changes in trigeminal ganglion (TG) neurons and other cells. These changes in the peripheral and central nervous system (CNS) contribute to abnormal pain perception.
Area of Science:
- Neuroscience
- Pain Research
- Cellular Biology
Background:
- Nociceptive stimuli in the orofacial region are processed by trigeminal ganglion (TG) neurons.
- Pain signals travel through the trigeminal spinal subnucleus caudalis, C1-C2, thalamus, and then to cortical and limbic systems.
- Abnormal orofacial pain is associated with neuroplastic changes throughout the pain pathway.
Purpose of the Study:
- To investigate the role of functional plastic changes in cells contributing to orofacial pain hypersensitivity.
Main Methods:
- Review of recent studies on cellular changes in orofacial pain.
- Analysis of functional plastic changes in TG neurons, glial cells (satellite cells, microglia, astrocytes), and immune cells (macrophages, neutrophils).
Main Results:
- Functional plastic changes in TG neurons, glial cells, and immune cells are implicated in orofacial pain.
- These cellular changes lead to neuronal sensitization and disinhibition in both peripheral and central nervous systems (CNS).
Conclusions:
- Neuroplasticity in various cell types, including TG neurons, glial cells, and immune cells, is a key factor in the development of orofacial pain hypersensitivity.
- Understanding these cellular mechanisms is crucial for addressing abnormal pain in the orofacial region.
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