颞下颌关节软骨对咬合力刺激响应特征的动物实验启示

Responses of the Temporomandibular Joint Cartilage to Occlusion Alterations:the Obtaining from Animal Investigation

关节软骨主要的功能之一是承受一定的运动负荷,颞下颌关节髁突软骨所承受的功能负荷与咬合密切相关,因而颞下颌关节髁突软骨可以随咬合的变化而进行相应的改建。我们利用大鼠、小鼠进行的实验研究显示,用佩戴金属冠的方法加高小鼠双侧前牙咬合(bilateral anterior elevation,BAE),可导致小鼠髁突软骨明显增厚;而用金属冠制作单侧前牙反[牙合](unilateral anterior crossbite,UAC)不良修复体,则可导致髁突软骨出现明显的退行性变,直至髁突变形。我们利用这些可导致髁突软骨出现增殖性或退行性改建的动物模型进行在体基因修饰实验,探索髁突软骨改建过程中与细胞自噬、凋亡、终末分化等活动密切相关的信号通路,例如哺乳动物雷帕霉素靶蛋白(mammalian target of rapmycin,mTOR)信号,印第安刺猬信号(India hedgehog,Ihh),以及甲状旁腺素及其相关蛋白受体信号等,其结论有望指导临床工作中在纠正异常咬合基础上,从细胞和分子水平干预软骨细胞功能,预防和治疗颞下颌关节软骨退变。

One of the main functions of the articular cartilage is to bear loads during various joint movements.The loads suffered by the temporomandibular joint(TMJ)are linked with occlusion.The mandibular condylar cartilage remodels in response to dental occlusion alterations.Through applying metal tubes onto incisors of rodents,we had reported that the bilateral anterior elevation(BAE)bite increases the condylar cartilage thickness,while unilateral anterior crossbite(UAC)relation leads to degenerative remodeling in the mandibular condylar cartilage which ends in deformation of the condyles.Through application of these dental stimulations,BAE and UAC,onto the mice with different genetic mutations,we investigated the signaling pathways such as mammalian target of rapamycin(mTOR),Indian hedgehog(Ihh),and parathyroid hormone receptor-1(PTHR1)which involve in chondrocytes autophagy,apoptosis and cellular terminal differentiation.The obtaining will bring a new insight in treatment of TMJ osteoarthritis,that is,dental occlusion correct in combined with molecular and cellular interventions.