兔咬合创伤时咬肌损伤与线粒体Ca2+载的研究

目的研究咬合创伤导致咬肌损伤的作用和线粒体Ca2+超载在损伤机制中的作用.方法在兔一侧前磨牙粘固(牙合)板造成咬合创伤,皮下注射乙二胺四乙酸(ethylenediarninetetraaceticAcid,EDTA),同时建立对照组,10天后检测兔咬肌线粒体Ca2+含量,观察咬肌的组织学改变,并进行比较分析.结果戴(牙合)板而不注射EDTA兔的(牙合)板侧咬肌线粒体Ca2+含量明显升高,并有明显的超微结构改变;(牙合)板对侧及戴(牙合)板并注射EDTA兔的双侧咬肌线粒体Ca2+含量均与对照组无显著性差异,组织学改变亦不明显.结论咬合创伤是咬肌损伤的致病因素之一,而线粒体Ca2+超载则是咬肌损伤发生机制中的一个重要环节.

Ca2+ overload in mitochondria and injury in rabbit'''' s masseter muscles induced byocclusal trauma

Objective: To study the role of mitochondrial Ca2+ overload in mechanism of masticatory muscle injury induced by occlusal trauma. Methods: The model of traumatic occlusion was established by way of the wrought crown of unilateral mandibular molars of rabbits. Some of them were injected subcutaneously with EDTA. Mitochondrial Ca2+ of masticatory muscle was measured and histologic changes were observed ten days later. The data were compared with control groups and analysed. Results: In the group of rabbits with saline and metal splint, mitochondrial Ca2+ contents of masseter muscle ipsilateral to splint increased significantly (P<0.05) and the changes of masticatory muscle ultrastructure were obvious. Mitochondrial Ca2+ contents and the ultrastructure of masseter muscle contralateral to splint didn't change significantly. In the group with EDTA and splint, the increase of mitochondrial Ca2+ contents and injury of masseter muscle both ipsilateral and contralateral to splint were attenuated. Conclusion: Mitochondrial Ca2+ overload may have a role in the etiology of injury of masticatory muscle induced by occlusal trauma.