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BackgroundIn order to evaluate mechanisms that may underlie the sensitization of trigeminal spinal subnucleus caudalis (Vc; the medullary dorsal horn) and upper cervical spinal cord (C1-C2) nociceptive neurons to heat, cold and mechanical stimuli following topical capsaicin treatment of the facial skin, nocifensive behaviors as well as phosphorylation of extracellular regulated-kinase (pERK) in Vc and C1-C2 neurons were studied in rats.ResultsCompared to vehicle application, capsaicin application to the lateral facial skin produced 1 hour later a flare in the skin, and also induced significantly greater nocifensive behaviors to heat, cold or mechanical stimulus of the lateral facial skin. The intrathecal (i.t.) injection of the MEK inhibitor PD98059 markedly attenuated the nocifensive behaviors to these stimuli in capsaicin-treated rats. Moreover, the number of pERK-like immunoreactive (pERK-LI) cells in Vc and C1-C2 was significantly larger following the heat, cold and mechanical stimuli in capsaicin-treated rats compared with vehicle-treated rats. The number of pERK-LI cells gradually increased following progressive increases in the heat or mechanical stimulus intensity and following progressive decrease in the cold stimulus. The ERK phosphorylation in Vc and C1-C2 neurons was strongly inhibited after subcutaneous injection of the capsaicin antagonist capsazepine in capsaicin-treated rats.ConclusionThe present findings revealed that capsaicin treatment of the lateral facial skin causes an enhancement of ERK phosphorylation in Vc and C1-C2 neurons as well as induces nocifensive behavior to heat, cold and mechanical simulation of the capsaicin-treated skin. The findings suggest that TRPV1 receptor mechanisms in rat facial skin influence nociceptive responses to noxious cutaneous thermal and mechanical stimuli by inducing neuroplastic changes in Vc and C1-C2 neurons that involve in the MAP kinase cascade.

Zygomatic fractures can be associated with functional and esthetic problems. Recent improvements in surgical techniques and materials have enabled stable fixation of zygmomatic fractures. Multiple-point fixation is most commonly used for internal fixation. Generally, reduction and fixation are performed through lateral brow, subciliary, temporal, or intraoral incisions (three-point fixation). Our experience indicates that postoperative scarring and sensory disturbances are caused by a subciliary incision with inferior orbital rim fixation. It is thus recommended that inferior orbital rim fixation with mini- or microplates be avoided. In patients in whom the fracture does not involve the orbital floor, reduction of the zygoma and zygomatic arch through a temporal incision is performed at this institution. Fixation of the lateral zygomaticomaxillary buttress and anterior wall of the maxilla with miniplates through an intraoral incision is also performed. If necessary, zygomaticofrontal suture fixation with a miniplate or wire is performed through a lateral brow incision. The status of inferior orbital rim reduction is confirmed by palpitation. Inferior orbital rim fixation with mini- or microplates is recommended for reduction of comminuted fractures and orbital floor fractures with herniation of internal orbit components. Patients who did not undergo inferior orbital rim fixation were free of inferior orbital rim deformity, diplopia, and postreduction rotation.

Distraction osteogenesis has become a standard technique for craniomaxillofacial reconstruction. The authors performed gradual cranial vault distraction osteogenesis in 19 patients with craniosynostosis to study the outcome and complications of this procedure. Postoperative infections developed around the shaft puncture wounds in four patients, including one who required surgical removal of the device. Advanced bone was deformed in one patient. In another, the expansion device was exposed, resulting in a postoperative scar. Despite these complications, the cranium was successfully expanded in all patients.

To elucidate if microglial P2Y12 receptor (P2Y12R) mechanisms are involved in the trigeminal spinal subnucleus caudalis (Vc; also known as the medullary dorsal horn) in intraoral cancer pain, we developed a rat model of tongue cancer pain. Squamous cell carcinoma (SCC) cells were inoculated into the tongue of rats; sham control rats received the vehicle instead. Nociceptive behavior was measured as the head-withdrawal reflex threshold (HWRT) to mechanical or heat stimulation applied to the tongue under light anesthesia. On day 14 after the SCC inoculation, activated microglia and P2Y12R expression were examined immunohistochemically in the Vc. The HWRT was also studied in SCC-inoculated rats with successive intra-cisterna magna (i.c.m.) administration of specific P2Y12R antagonist (MRS2395) or intraperitoneal administration of minocycline, a microglial activation inhibitor. Tongue cancer was histologically verified in SCC-inoculated rats, within which the HWRT to mechanical stimulation of the tongue was significantly decreased, as compared with that of vehicle-inoculated rats, although the HWRT to heat stimulation was not. Microglia was strongly activated on day 14, and the administration of MRS2395 or minocycline reversed associated nocifensive behavior and microglial activation in SCC-inoculated rats for 14 d. The activity of Vc wide dynamic range nociceptive neurons was also recorded electrophysiologically in SCC-inoculated and sham rats. Background activity and noxious mechanically evoked responses of wide dynamic range neurons were significantly increased in SCC-inoculated rats versus sham rats, and background activity and mechanically evoked responses were significantly suppressed following i.c.m. administration of MRS2395 in SCC-inoculated rats as compared with sham. The present findings suggest that SCC inoculation that produces tongue cancer results in strong activation of microglia via P2Y12 signaling in the Vc, in association with increased excitability of Vc nociceptive neurons, reflecting central sensitization and resulting in tongue mechanical allodynia.