Journal of dental research
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It recently became evident that activation of the complement system also contributes to tissue regeneration after infection/injury. The complement-derived fragment C5a induces vascular modifications and attracts cells expressing its receptor (C5aR/CD88) to the site of infection and tissue injury. Besides inflammatory cells, various tissue cells express this receptor. ⋯ RT-PCR on STRO-1-sorted pulp progenitor cells, co-expressing both STRO-1 and C5aR, revealed high C5aR mRNA levels. Experiments with the C5aR antagonist W54011 revealed that C5a specifically bound to progenitor cells via C5aR, inducing their selective migration toward the C5a gradient. Since we could also demonstrate C5b-9 formation by immunohistochemistry in carious teeth, our findings suggest that, upon local complement activation, C5a induces pulp progenitor cell migration, which may be critical in initiating the regenerative process after dentin/pulp injury.
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Healthcare professionals use race, gender, and age cues when making pain management decisions. Use of these demographic cues, therefore, is an important topic in the study of healthcare disparities. This study used virtual human (VH) technology to investigate the effects of VH patients' demographic cues on dentists' pain management decisions. ⋯ Currently, there are no guidelines for decision- making practices for gender-, race-, or age-related pain. Since dentists see thousands of patients during their careers, the use of demographic cues could affect a substantial portion of the population. The findings could improve future training programs for dentists and dental students.
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The whisker pad area (WP) is innervated by the second branch of the trigeminal nerve and experiences allodynia and hyperalgesia following transection of the mental nerve (MN; the third branch of the trigeminal nerve). However, the mechanisms of this extra-territorial pain remain unclear. The ionotropic P2X(7) ATP receptor (P2X(7)) in microglia is known to potentiate, via cytokines, the perception of noxious stimuli, raising the possibility that P2X(7) and cytokines are involved in this extra-territorial pain. ⋯ Allodynia/hyperalgesia after MNT was blocked by intracisternal administration of etanercept, a recombinant TNF-α receptor (p75)-Fc fusion protein. Intracisternal A438079, a P2X(7) antagonist, also attenuated allodynia/hyperalgesia and blocked up-regulation of mTNF-α and sTNF-α in the TNC. We conclude that sTNF-α released by microglia following P2X(7) activation may be important in both the initiation and maintenance of extra-territorial pain after MNT.
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Pain is associated with anxiety in a dental setting. It has remained unclear how cognitive-affective factors modulate pain and anxiety in a stressful context, such as receiving dental procedures. We hypothesized that both the situational factor (unpredictability about painful stimuli) and the trait factor (pain catastrophizing, i.e., the tendency to interpret pain in negative orientation) account for dental pain. ⋯ The score of the Pain Catastrophizing Scale was positively correlated with the increased pain modulated by unpredictability. Brain activation at the right posterior hippocampus, a region critically related to associative learning of aversive stimuli and context, was correlated with the individual catastrophizing level. Our findings suggest that both the situational factor (unpredictability) and the trait factor (catastrophizing) influence dental pain, highlighting the role of cognitive-affective factors in pain control of dental patients.
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Discomfort and pain encountered during orthodontic treatment are major problems for patients, but the details of the underlying neural processes and molecular mechanisms are not well-understood. Here we show that noxious tooth mechanical pressure induced by orthodontic elastics resulted in a rapid and transient activation of extracellular signal-regulated protein kinase (ERK) in the trigeminal spinal subnucleus interpolaris and caudalis transition zone (Vi/Vc), trigeminal spinal subnucleus caudalis (Vc), and upper cervical spinal cord (Vc/C2). ⋯ In addition, the tooth mechanical pressure led to Fos expression in the pERK-positive Vc neurons that would be suppressed by intrathecal administration of an MEK1/2 inhibitor (PD98059). Taken together, these findings suggest that activation of the ERK signaling cascade following noxious mechanical pressure on the teeth regulates Fos expression in Vc neurons and may thereby contribute to pain associated with orthodontic treatment.