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Temporomandibular joint pain: a critical role for Trpv4 in the trigeminal ganglion.

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Date
2013-08
Authors
Chen, Yong
Williams, Susan H
McNulty, Amy L
Hong, Ji Hee
Lee, Suk Hee
Rothfusz, Nicole E
Parekh, Puja K
Moore, Carlene
Gereau, Robert W
Taylor, Andrea B
Wang, Fan
Guilak, Farshid
Liedtke, Wolfgang
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Abstract
Temporomandibular joint disorder (TMJD) is known for its mastication-associated pain. TMJD is medically relevant because of its prevalence, severity, chronicity, the therapy-refractoriness of its pain, and its largely elusive pathogenesis. Against this background, we sought to investigate the pathogenetic contributions of the calcium-permeable TRPV4 ion channel, robustly expressed in the trigeminal ganglion sensory neurons, to TMJ inflammation and pain behavior. We demonstrate here that TRPV4 is critical for TMJ-inflammation-evoked pain behavior in mice and that trigeminal ganglion pronociceptive changes are TRPV4-dependent. As a quantitative metric, bite force was recorded as evidence of masticatory sensitization, in keeping with human translational studies. In Trpv4(-/-) mice with TMJ inflammation, attenuation of bite force was significantly less than in wildtype (WT) mice. Similar effects were seen with systemic application of a specific TRPV4 inhibitor. TMJ inflammation and mandibular bony changes were apparent after injections of complete Freund adjuvant but were remarkably independent of the Trpv4 genotype. It was intriguing that, as a result of TMJ inflammation, WT mice exhibited significant upregulation of TRPV4 and phosphorylated extracellular-signal-regulated kinase (ERK) in TMJ-innervating trigeminal sensory neurons, which were absent in Trpv4(-/-) mice. Mice with genetically-impaired MEK/ERK phosphorylation in neurons showed resistance to reduction of bite force similar to that of Trpv4(-/-) mice. Thus, TRPV4 is necessary for masticatory sensitization in TMJ inflammation and probably functions upstream of MEK/ERK phosphorylation in trigeminal ganglion sensory neurons in vivo. TRPV4 therefore represents a novel pronociceptive target in TMJ inflammation and should be considered a target of interest in human TMJD.
Type
Journal article
Subject
Animals
Bite Force
Cell Size
Disease Models, Animal
Female
Freund's Adjuvant
Gene Expression Regulation
Glycoproteins
Green Fluorescent Proteins
Inflammation
MAP Kinase Kinase Kinases
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Nerve Tissue Proteins
Sensory Receptor Cells
Sex Factors
TRPV Cation Channels
Temporomandibular Joint Dysfunction Syndrome
Time Factors
Tomography, X-Ray Computed
Trigeminal Ganglion
Permalink
https://hdl.handle.net/10161/12973
Published Version (Please cite this version)
10.1016/j.pain.2013.04.004
Publication Info
Chen, Yong; Williams, Susan H; McNulty, Amy L; Hong, Ji Hee; Lee, Suk Hee; Rothfusz, Nicole E; ... Liedtke, Wolfgang (2013). Temporomandibular joint pain: a critical role for Trpv4 in the trigeminal ganglion. Pain, 154(8). pp. 1295-1304. 10.1016/j.pain.2013.04.004. Retrieved from https://hdl.handle.net/10161/12973.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Chen

Yong Chen

Associate Professor of Neurology

Farshid Guilak

Lazlo Ormandy Professor of Orthopaedic Surgery
This author no longer has a Scholars@Duke profile, so the information shown here reflects their Duke status at the time this item was deposited.
Liedtke

Wolfgang Bernhard Liedtke

Adjunct Professor in the Department of Neurology
Research Interests in the Liedtke-Lab: Pain/ nociception Sensory transduction and -transmission TRP ion channels Water and salt equilibrium regulated by the central nervous system Visit the lab's website, download papers and read Dr. Liedtke's CV here.
McNulty

Amy Lynn McNulty

Associate Professor in Orthopaedic Surgery
The McNulty Lab is working to develop strategies to prevent osteoarthritis and to promote tissue repair and regeneration following joint injury. In order to accomplish this, we are working in three main areas.  1) We are working to understand the pathways that are activated by normal and injurious mechanical loading of cartilage and meniscus and how these mechanotransduction pathways are altered during aging, injury, and tissue degeneration. A greater understanding of alterations in mech
Moore

Carlene D Moore

Assistant Professor in Neurology

Andrea Beth Taylor

Adjunct Professor in the Department of Orthopaedic Surgery
Wang

Fan Wang

Morris N. Broad Distinguished Professor
My lab studies neural circuit basis of sensory perception. Specifically we are interested in determining neural circuits underlying (1) active touch sensation including tactile processing stream and motor control of touch sensors on the face; (2) pain sensation including both sensory-discriminative and affective aspects of pain; and (3) general anesthesia including the active pain-suppression process. We use a combination of genetic, viral, electrophysiology, and in vivo imaging (in f
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Alphabetical list of authors with Scholars@Duke profiles.
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