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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
    Gereau, RW
    Guilak, Farshid
    Hong, Ji Hee
    Lee, SH
    Liedtke, Wolfgang Bernhard
    McNulty, Amy
    Moore, Carlene
    Parekh, Puja K
    Rothfusz, NE
    Taylor, Andrea
    Wang, Fan
    Williams, SH
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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
    http://hdl.handle.net/10161/12973
    Published Version (Please cite this version)
    10.1016/j.pain.2013.04.004
    Publication Info
    Chen, Yong; Gereau, RW; Guilak, Farshid; Hong, Ji Hee; Lee, SH; Liedtke, Wolfgang Bernhard; ... Williams, SH (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 http://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

    Assistant Professor in Neurology

    Farshid Guilak

    Lazlo Ormandy Professor of Orthopaedic Surgery
    Liedtke

    Wolfgang Bernhard Liedtke

    Professor 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 McNulty

    Assistant Professor in Orthopaedic Surgery
    The long term goals of the McNulty lab are to develop strategies to prevent osteoarthritis and to promote tissue repair and regeneration following joint injury.  In order to achieve these goals, we need to understand the mechanisms necessary for tissue repair and regeneration and how they are altered with aging and joint injury.  Specifically, we are working to enhance the integrative repair of meniscus to restore meniscal function and decrease the risk of osteoarthritis development. &
    Moore

    Carlene D Moore

    Assistant Professor of Neurology
    Wang

    Fan Wang

    Morris N. Broad Distinguished Professor
    My lab studies neural circuit basis of sensory perception and motor action.Specifically we are interested in determining functions as well as mapping the meso-scale connectivity of neural circuits involved in (1) voluntary movements; (2) touch and pain sensation; and (3) social interactions. We use a combination of genetic, viral, electrophysiology, and in vivo imaging (in free-moving animals) techniques to study these questions.
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