Comparison of Clinical Characteristics in Myogenic, TMJ Internal Derangement and Atypical Facial Pain Patients

Harness, Dennis M.; Donlon, William C.; Eversole, Lewis R.

doi:10.1097/00002508-199003000-00003

Cited by 42 publications

(25 citation statements)

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“…The grid on which the rats can lie down and sleep is considered as an adequate environmental control [5]. Many studies have demonstrated that paradoxical sleep deprivation may induce psychological stress and activate the hypothalamic-pituitary-adrenal (HPA) axis [29], [30].…”

Section: Discussionmentioning

confidence: 99%

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Effects of Chronic Sleep Deprivation on the Extracellular Signal-Regulated Kinase Pathway in the Temporomandibular Joint of Rats

Wang

et al. 2014

PLoS ONE

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ObjectivesTo examine the possible involvement and regulatory mechanisms of extracellular signal-regulated kinase (ERK) pathway in the temporomandibular joint (TMJ) of rats subjected to chronic sleep deprivation (CSD).MethodsRats were subjected to CSD using the modified multiple platform method (MMPM). The serum levels of corticosterone (CORT) and adrenocorticotropic hormone (ACTH) were tested and histomorphology and ultrastructure of the TMJ were observed. The ERK and phospho-ERK (p-ERK) expression levels were detected by Western blot analysis, and the MMP-1, MMP-3, and MMP-13 expression levels were detected by real-time quantitative polymerase chain reaction (PCR) and Western blotting.ResultsThe elevated serum CORT and ACTH levels confirmed that the rats were under CSD stress. Hematoxylin and eosin (HE) staining and scanning electron microscopy (SEM) showed pathological alterations in the TMJ following CSD; furthermore, the p-ERK was activated and the mRNA and protein expression levels of MMP-1, MMP-3, and MMP-13 were upregulated after CSD. In the rats administered with the selective ERK inhibitor U0126, decreased tissue destruction was observed. Phospho-ERK activation was visibly blocked and the MMP-1, MMP-3, and MMP-13 mRNA and protein levels were lower than the corresponding levels in the CSD without U0126 group.ConclusionThese findings indicate that CSD activates the ERK pathway and upregulates the MMP-1, MMP-3, and MMP-13 mRNA and protein levels in the TMJ of rats. Thus, CSD induces ERK pathway activation and causes pathological alterations in the TMJ. ERK may be associated with TMJ destruction by promoting the expression of MMPs.

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Section: Discussionmentioning

confidence: 99%

“…The modified multiple platform method (MMPM) was selected to induce CSD in this study [5]. As shown in Figure 1, the rats were placed inside a tiled glass water tank containing 15 narrow circular platforms (6.5 cm in diameter) or a grid floor.…”

Section: Methodsmentioning

confidence: 99%

Effects of Chronic Sleep Deprivation on the Extracellular Signal-Regulated Kinase Pathway in the Temporomandibular Joint of Rats

Wang

et al. 2014

PLoS ONE

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“…In light of a recent study that showed the role of P2X 5 -ASIC3 interaction in muscle afferents under muscle ischemia condition (Birdsong et al, 2010) our data reinforces the notion that channel-channel interactions in sensory neurons provide mechanisms by which nociceptor function is dynamically modulated. TMD patients often suffer from mechanical hyperalgesia of masticatory musculature (Harness et al, 1990; Stohler, 1999). Unfortunately, currently available pharmacological interventions are often ineffective and produce undesirable side effects (Cowan et al, 1988; Sheldon et al, 1990; Cheng et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…Patients with temporomandibular disorders (TMD) often suffer from mechanical hyperalgesia arising in masticatory muscles (Harness et al, 1990; Stohler, 1999). Transient Receptor Potential V1 (TRPV1) are increasingly recognized as important players underlying mechanical hyperalgesia (Pomonis et al, 2003; Walker et al, 2003; Honore et al, 2005; Fujii et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

P2X3 and TRPV1 functionally interact and mediate sensitization of trigeminal sensory neurons

Saloman

Chung

2013

Neuroscience

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Musculoskeletal pain conditions, particularly those associated with temporomandibular joint and muscle disorders (TMD) affect a large percentage of the population. Identifying mechanisms underlying hyperalgesia could contribute to the development of new treatment strategies for the management of TMD and other muscle pain conditions. In this study, we provide evidence of functional interactions between two ligand-gated channels, P2X3 and TRPV1, in trigeminal sensory neurons, and propose that the interactions serve as an underlying mechanism for the development of mechanical hyperalgesia. Mechanical sensitivity of the masseter muscle was assessed in lightly anesthetized rats via an electronic anesthesiometer (Ro et al., 2009). Direct intramuscular injection of a selective P2X3 agonist, αβmeATP, induced a dose- and time-dependent hyperalgesia. Mechanical sensitivity in the contralateral muscle was unaffected suggesting local P2X3 mediate the hyperalgesia. Anesthetizing the overlying skin had no effect on αβmeATP-induced hyperalgesia confirming the contribution of P2X3 from muscle. Importantly, the αβmeATP-induced hyperalgesia was prevented by pretreatment of the muscle with a TRPV1 antagonist, AMG9810. P2X3 was co-expressed with TRPV1 in masseter muscle afferents confirming the possibility for intracellular interactions. Additionally, in a subpopulation of P2X3/TRPV1 positive neurons, capsaicin-induced Ca2+ transients were significantly amplified following P2X3 activation. Finally, activation of P2X3 induced phosphorylation of serine, but not threonine, residues in TRPV1 in trigeminal ganglia cultures. Significant phosphorylation was observed at 15 min, the time point at which behavioral hyperalgesia was prominent. Previously, activation of either P2X3 or TRPV1 had been independently implicated in the development of mechanical hyperalgesia. Our data propose P2X3 and TRPV1 interact in a facilitatory manner, which could contribute to the peripheral sensitization known to underlie masseter hyperalgesia.

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“…In the test phase the ziconotide dose should be increased by 0.6 µg/day per week after an initial dose of 0.6-1.2 µg/day to avoid side-effects. [9]. Psychische Erkrankungen kommen bei Patienten mit anhaltendem idiopathischem Gesichtsschmerz gehäuft vor.…”

Section: Schlüsselwörterunclassified

Erfahrungen mit intrathekaler First-line-Therapie mit Ziconotide bei Patienten mit neuropathischen Gesichtsschmerzen

Lux

Rasche

2011

Schmerz

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We report on the intrathecal use of ziconotide in three patients with idiopathic facial pain after surgery of the mouth, jaw or face and one patient with neuropathic pain after damage of the lingual nerve. The therapy was successful in three patients but one patient with idiopathic facial pain had pain relief only during the test phase of ziconotide with an external pump and not after implanting the Synchromed® pump. With intrathecal morphine therapy this patient achieved good pain relief. We recommend that patients with neuropathic facial pain should be treated with ziconotide after implementation of guideline-based therapy. In the test phase the ziconotide dose should be increased by 0.6 µg/day per week after an initial dose of 0.6-1.2 µg/day to avoid side-effects.

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Comparison of Clinical Characteristics in Myogenic, TMJ Internal Derangement and Atypical Facial Pain Patients

Cited by 42 publications

References 0 publications

Effects of Chronic Sleep Deprivation on the Extracellular Signal-Regulated Kinase Pathway in the Temporomandibular Joint of Rats

Effects of Chronic Sleep Deprivation on the Extracellular Signal-Regulated Kinase Pathway in the Temporomandibular Joint of Rats

P2X3 and TRPV1 functionally interact and mediate sensitization of trigeminal sensory neurons

Erfahrungen mit intrathekaler First-line-Therapie mit Ziconotide bei Patienten mit neuropathischen Gesichtsschmerzen

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