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The author discusses the profound connection between dentistry and otolaryngology (ENT), highlighting how issues in one can significantly impact the other. He discusses the possible causes of earaches, the important role of the oral microbiome in overall health, and benefits of collaboration between dental practitioners and ENT specialists.

Background: Exercise is a known trigger of the inhibitory pain modulation system and its analgesic effect is termed exercise‐induced hypoalgesia (EIH). Previous studies have demonstrated that rats with deficient analgesic response following exercise develop more significant hypersensitivity following nerve injury compared to rats with substantial analgesic response following exercise. Objectives: A rat model of EIH as an indicator of the pain inhibitory system's efficiency was used to explore the association between EIH profiles and the effect of pharmacotherapy on rat's neuropathic pain. Methods: EIH profiles were assessed by evaluating paw responses to mechanical stimuli before and after exercise on a rotating rod. Rats with a reduction of ≤33% in responses were classified as low EIH and those with ≥67% as high EIH. Low and high EIH rats underwent sciatic nerve chronic constriction injury (CCI). Paw responses to mechanical stimuli were measured at baseline, following CCI, and after treatment with diclofenac, duloxetine or pregabalin. In a different group of low and high EIH rats, EIH was measured before and following treatment with the same medications. Results: Low EIH rats developed more significant hypersensitivity following CCI. Duloxetine and pregabalin successfully reduced hypersensitivity, although significantly more so in low EIH rats. Diclofenac had limited effects, and only on low EIH rats. Four days of duloxetine administration transformed low EIH rats' profiles to high EIH. Conclusions: The findings of this study suggest that EIH profiles in rats can not only predict the development of hypersensitivity following injury but may also support targeted pharmacological treatment. Significance: Exercise is a known trigger of the inhibitory pain modulation. Rats with deficient analgesic response following exercise develop more significant hypersensitivity following nerve injury. Pain modulation profiles in rats can also support targeted pharmacological treatment; rats with deficient analgesic response following exercise benefit more from treatment with duloxetine and gabapentin. Treatment with duloxetine can improve pain modulation profile. [ABSTRACT FROM AUTHOR]

Two cases of pain evoked by cold food ingestion, following root canal therapy, are presented. The source of pain was detected when cold application to the vestibular, periapical area corresponding to the teeth involved evoked strong pain of about 30-second durations. In the first case, the patient suffered from strong pain in the mandibular right area over the last 4 months. After successive root canal therapy of three mandibular right teeth, the spontaneous pain eased significantly, but strong pain evoked by cold food ingestion persisted. Cold application to the vestibular periapical area of teeth involved identified the source of pain, which was abolished by 80 mg/day of slow-release propranolol. In the second case, cold allodynia developed after root canal therapy. The root canal therapy was performed for prosthetic reasons with no prior pain. Pain could be duplicated by cold application to the vestibular area of the treated tooth. The patient preferred no treatment when the source of pain was explained. In both cases cold application did not produce any pain in other intraoral locations, including the contralateral vestibular area or the mid soft or hard palate. Pain mechanisms, neurovascular and neuropathic, which differ for each case are discussed.