Archives of oral biology · 2010
Involvement of microglial activation in the brainstem in experimental dental injury and inflammation.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
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Fan Wenguo, Huang Fang, Zhu Xiao, Dong Weiguo, Gao Zhixiong, Li Dongpei, He Hongwen
Аннотация
OBJECTIVE: The purpose of this study was to determine the effect of dental injury and inflammation on microglia in the trigeminal subnucleus caudalis (Vc).
METHODS: Pulp exposure (PX) was performed on the first maxillary molar of 35 rats. Specimens were collected at 1, 3, 7, 14, 21 and 28 days after PX. Teeth were processed for H&E staining and immunohistochemical staining for OX-42, a marker of microgial activation, in the Vc.
RESULTS: We observed that there was a progressive and persistent inflammation in the tooth. At 21-28 days after PX, the inflammation extended out into periodontal ligament. Simultaneously, significant microglial activation was observed which starting at 2 weeks and peaking at 4 weeks.
CONCLUSION: Dental injury and inflammation induced microglial activation in the Vc. The results indicate that activation of microglia may be implicated in the central mechanisms of pain that can be associated with dental inflammation.
METHODS: Pulp exposure (PX) was performed on the first maxillary molar of 35 rats. Specimens were collected at 1, 3, 7, 14, 21 and 28 days after PX. Teeth were processed for H&E staining and immunohistochemical staining for OX-42, a marker of microgial activation, in the Vc.
RESULTS: We observed that there was a progressive and persistent inflammation in the tooth. At 21-28 days after PX, the inflammation extended out into periodontal ligament. Simultaneously, significant microglial activation was observed which starting at 2 weeks and peaking at 4 weeks.
CONCLUSION: Dental injury and inflammation induced microglial activation in the Vc. The results indicate that activation of microglia may be implicated in the central mechanisms of pain that can be associated with dental inflammation.