Articles: chronic.
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Temporomandibular disorders (TMD) are the most common reason for chronic pain in the orofacial area and significantly impact the lives of those affected. The role of lifestyle factors in TMD, however, remains less explored. This cohort study aims to estimate TMD prevalence by addressing potential selection biases and to evaluate the association between TMD and lifestyle factors with a specific focus on sick leave and health related quality of life. ⋯ The findings provide insight into how TMD affect individuals, by incorporating lifestyle factors, social determinants and the impact of sick leave at a population level. By incorporating these areas into the study of TMD, we can deepen our understanding of how TMD affects individuals' lives. This approach may also create opportunities to develop more comprehensive strategies to address TMD, focusing on broader implications beyond the clinical symptoms.
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Myofascial trigger points (MTrPs) are the primary etiological characteristics of chronic myofascial pain syndrome. Receptor tyrosine kinases (RTKs) are associated with signal transduction in the central mechanisms of chronic pain, but the role of RTKs in the peripheral mechanisms of MTrPs remains unclear. The current study aimed to identify RTKs expression in MTrPs and elucidate the molecular mechanisms through which platelet-derived growth factor receptor-α (PDGFR-α) induces contraction knots and inflammatory pain-like behavior in a rat model of myofascial trigger points. ⋯ COL1A1-induced phosphorylation of PDGFR-α and the subsequent activation of the JAK2/STAT3 pathway may induce dysfunctional muscle contraction and increased nociception at MTrPs.
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Microglia take on an altered morphology during chronic opioid treatment. This morphological change is broadly used to identify the activated microglial state associated with opioid side effects, including tolerance and opioid-induced hyperalgesia (OIH). Microglia display similar morphological responses in the spinal cord after peripheral nerve injury (PNI). ⋯ After PNI, we identify an early proliferative transcriptional event across models that precedes the upregulation of histological markers of microglial activation. However, we found no proliferative transcriptional response associated with opioid-induced microglial activation, consistent with histological data, indicating that the number of microglia remains stable during morphine treatment, whereas their morphological response differs from PNI models. Collectively, these results establish the diversity of pain-associated microglial transcriptomic responses and point towards the targeting of distinct insult-specific microglial responses to treat OIH, PNI, or other central nervous system pathologies.