Abstract
Chemotactic cytokines or chemokines are a large family of secreted proteins able to induce chemotaxis. Chemokines are categorized according to their primary amino acid sequence, and in particular their cysteine residues that form disulphide bonds to maintain the structure: CC, CXC, CX3C, and XC, in which X represents variable amino acids. Among their many roles, chemokines are known to be key players in pain modulation in the peripheral and central nervous systems. Thus, they are promising candidates for novel therapeutics that could replace current, often ineffective treatments. The spinal and trigeminal systems are intrinsically different beyond their anatomical location, and it has been suggested that there are also differences in their sensory mechanisms. Hence, understanding the different mechanisms involved in pain modulation for each system could aid in developing appropriate pharmacological alternatives. Here, we aim to describe the current landscape of chemokines that have been studied specifically with regard to trigeminal pain. Searching PubMed and Google Scholar, we identified 30 reports describing chemokines in animal models of trigeminal pain, and 15 reports describing chemokines involved in human pain associated with the trigeminal system. This review highlights the chemokines studied to date at different levels of the trigeminal system, their cellular localization and, where available, their role in a variety of animal pain models.
Highlights
Pain is defined as an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage (1)
We explored results returned by searching PubMed and Google Scholar using the terms “chemokines AND trigeminal pain,” “chemokines AND migraine,” and “chemokines AND trigeminal neuralgia,” as well as permutations of “each chemokine” (e.g., CCL2, CX3CL1, etc.), AND the terms “Trigeminal Pain” or “temporomandibular joint (TMJ)” or “Tooth Pain” or “Dental pain” or “Trigeminal Ganglion” or “Trigeminal Pain.”
These authors suggest that shortly following injury, CCL2 expression is triggered in the neurons, which may signal to GFAPpositive astrocytes through CCR2
Summary
Pain is defined as an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage (1). Orofacial pain (OP) can be classified into seven categories: (i) OP attributed to disorders of dentoalveolar and anatomically related structures, (ii) myofascial OP, (iii) temporomandibular joint pain, (iv) OP attributed to lesion or disease of the cranial nerves, (v) OP resembling presentations of primary headaches, (vi) idiopathic OP, and (vii) psychosocial (2). Orofacial pain originates from the trigeminal nerve (cranial nerve V), which innervates facial, oral and nasal structures, and the meninges surrounding the brain. The peripheral branches of the trigeminal nerve merge to form the ophthalmic, maxillary, and mandibular nerve divisions. Most trigeminal sensory A-delta and C-fibres enter the pons and descend to form the spinal trigeminal tract, which extends caudally into the upper cervical cord with terminals synapsing on neurons of the spinal trigeminal nucleus, located medially to the spinal trigeminal tract. The afferent fibres respond to a range of thermal, mechanical, and chemical nociceptive stimuli (3)
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