Pain in the head and face, which can be very severe and debilitating, often involves activation of trigeminal ganglion nerves. The craniofacial symptoms can manifest as acute or transient conditions such as toothaches and headaches, or can transform into more chronic conditions such as migraine, rhinosinusitis, temporomandibular joint (TMJ) disorder, or trigeminal neuralgia. Traditionally, it is known that peripheral tissue injury or inflammation leads to excitation of trigeminal nerves that release inflammatory molecules in the periphery as well as facilitate transmission of nociceptive signals to the central nervous system. However, findings from recent studies have demonstrated that peripheral tissue injury or inflammation also leads to increased interactions between neuronal cell bodies and satellite glial cells within the trigeminal ganglion. These cell-to-cell interactions, which involve the transfer of key regulatory mediators via channels or gap junctions as well as paracrine signaling, are thought to play an important role in the induction and maintenance of peripheral sensitization of trigeminal nociceptors. The focus of this review will be on understanding the importance of the increased signaling between neuronal cell bodies and satellite glia cells in trigeminal ganglia to the development of persistent pain.



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© Durham and Garrett; Licensee Bentham Open. This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.


Trigeminal, neuron, satellite glia, signaling, gap junctions-connexins, neuropathic, inflammation, acute, chronic, peripheral sensitization, comorbitity, migraine, TMJ, rhinosinusitus

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The Open Pain Journal