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目的:观察牙髓炎大鼠三叉神经节初级感觉神经元及牙周组织中疼痛及炎症相关因子的表达变化,探讨三叉神经参与牙髓病理改变及炎性疼痛的信号调节作用。方法:建立完全弗氏佐剂诱发的大鼠牙髓炎痛敏模型,应用免疫荧光标记法观察牙髓炎症及炎性痛敏过程神经元细胞体中CGRP的动态表达,检测牙髓及牙周组织中TNF-α的表达与分布。结果:完全弗氏佐剂诱发大鼠急性牙髓炎症,镜下可见牙髓成牙本质细胞层排列紊乱、空泡性变,根周牙槽骨骨髓腔内出现大量弥散性炎细胞浸润灶。炎症刺激24h后,三叉神经节初级感觉神经元CGRP表达明显增强,1周后显著性减少;牙周组织中TNF-α于牙髓炎24h后表达明显增加,持续至炎症刺激1周后。结论:三叉神经系统通过调节CGRP的表达参与牙髓的炎症及痛觉过敏过程;TNF-α不仅在牙髓炎的发生发展过程中具有重要的炎症介导作用,并且在炎性疼痛的发展和维持中起关键的作用。
OBJECTIVE: To observe the expression changes of pain and inflammation-related factors in the primary sensory neurons and periodontal tissues of the trigeminal ganglion in pulpitis rats and to explore the signal regulation effect of the trigeminal nerve on the pathological changes of dental pulp and inflammatory pain. Methods: Pain model of rat pulpitis induced by complete Freund’s adjuvant was established. Dynamic expression of CGRP in pulpitis and periodontitis was observed by immunofluorescence staining. Tissue TNF-α expression and distribution. Results: Complete Freund’s adjuvant induced acute pulpitis in rats. Microscopically, the dental pulp odontoblasts were disordered and vacuolated, and a large number of diffuse infiltration of inflammatory cells appeared in the root canal alveolar bone marrow cavity. The expression of CGRP in primary sensory neurons of trigeminal ganglion was significantly increased after 24-hour inflammation stimulation, and decreased significantly after one week. The expression of TNF-α in periodontal tissues increased significantly after 24-hour inflammation, and continued to one week after inflammation stimulation. Conclusion: The trigeminal nervous system participates in inflammation and hyperalgesia of dental pulp by regulating the expression of CGRP. TNF-α not only plays an important inflammatory mediating role in the development of pulpitis, but also plays an important role in the development and maintenance of inflammatory pain Play a key role.