Pain
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Although most cases of temporomandibular muscle and joint disorders (TMJD) are mild and self-limiting, about 10% of TMJD patients develop severe disorders associated with chronic pain and disability. It has been suggested that depression and catastrophizing contributes to TMJD chronicity. This article assesses the effects of catastrophizing and depression on clinically significant TMJD pain (Graded Chronic Pain Scale [GCPS] II-IV). ⋯ In addition, in the multivariable analysis adjusted by the same covariates previously described, the onset of clinically significant pain (GCPS II-IV) at the 18-month follow-up was associated with catastrophizing (odds ratio [OR] 1.72, P=0.02). Progression of clinically significant pain was related to catastrophizing (OR 2.16, P<0.0001) and widespread pain at baseline (OR 1.78, P=0.048). Results indicate that catastrophizing and depression contribute to the progression of chronic TMJD pain and disability, and therefore should be considered as important factors when evaluating and developing treatment plans for patients with TMJD.
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The perception of pain is initiated by the transduction of noxious stimuli through specialized ion channels and receptors expressed by primary nociceptive neurons. The molecular mechanisms that orchestrate the expression and function of ion channels relevant for pain processing are poorly understood. We demonstrate here a central role of the transcription factor Smad-interacting protein 1 (Sip1/Zfhx1b/Zeb2), a 2-handed zinc finger DNA-binding protein with essential functions in neural crest and forebrain development, in controlling nociceptive neuron excitability and pain sensitivity. ⋯ Analysis of the voltage-gated currents underlying repetitive firing revealed a significant increase in persistent sodium currents and a reduction in delayed rectifier potassium currents. Modeling experiments in conjunction with experimental results suggest that these changes cause a depolarization-induced block of action potential propagation past the DRG axon T-junction. These data suggest that Sip1 controls the transduction properties of heat-sensitive primary sensory neurons and thus thermal pain sensitivity in a novel manner via coordinated changes in DRG-neuron voltage-gated ion channels.
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This study examined the influence of patients' likability on pain estimations made by observers. Patients' likability was manipulated by means of an evaluative conditioning procedure: pictures of patients were combined with either positive, neutral, or negative personal traits. Next, videos of the patients were presented to 40 observers who rated the pain. ⋯ The effect on pain estimations was only found with regard to patients expressing high-intensity pain. There was no effect on response bias (i.e., the overall tendency to indicate pain). These findings suggest that we take the pain of patients we do not like less seriously than the pain of patients we like.
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Odontoblasts form the outermost cellular layer of the dental pulp where they have been proposed to act as sensory receptor cells. Despite this suggestion, evidence supporting their direct role in mediating thermo-sensation and nociception is lacking. Transient receptor potential (TRP) ion channels directly mediate nociceptive functions, but their functional expression in human odontoblasts has yet to be elucidated. ⋯ Using a gene silencing approached we further confirmed a role for TRPA1 in mediating noxious cold responses in odontoblasts. We conclude that human odontoblasts express functional TRP channels that may play a crucial role in mediating thermal sensation in teeth. Cultured and native human odontoblasts express functional TRP channels that may play a crucial role in mediating thermal sensation in teeth.