目的观察TGFβ/Smad信号分子在大鼠腭中缝牵张成骨过程中的表达规律。方法实验选用36只5周龄雄性Wistar大鼠,分为实验组和对照组(包括阴性对照和空白对照)。将初始力值为0.49 N的腭中缝扩大簧黏接到大鼠两侧上颌牙列上建立大鼠腭中缝牵张模型。取牵张第1、4、7天标本,采用免疫组化方法分析TGFβ/Smad信号分子在腭中缝牵张各加力时间点的表达。结果大鼠腭中缝牵张过程中,TGFβ1、2、3及Smad2、3、4等分子表达增强,并主要集中于骨端边缘骨膜、成骨细胞、继发软骨层、髓腔及骨缝纤维层与骨边缘的间充质细胞中。Smad7始终处于较低表达水平,无明显变化。结论机械牵张力可能通过刺激骨缝细胞TGFβ/Smad表达水平的改变,促进其增殖,并介导了骨缝牵张成骨的过程。
Objective To investigate the law of TGFβ /Smad signal molecule expression in mid-palatal suture remodeling after subjecting to tensional strain loading.Methods 36 Wistar male rats of 5 weeks old were divided into experimental group and control group(including negative controls and blank controls).The expansion appliances were placed into rats in experimental group,with opening loops with an initial force of 0.49 N applied to mid-palatal suture.After expansion for periods of 1,4 and 7 days,IHC staining was used to investigate the expression of TGFβ / Smad signal molecules during mid-palatal suture expansion at different time points.Results In rat midpalatal suture expansion,expression of TGFβ1,2,3,Smad2,3 and 4 was up-regulated,especially in marginal periosteum cells,osteoblasts,secondary cartilage layer,pulp cavity and mesenchymal cells in sutura fiber layer and marginal bone.Expression of Smad7 was kept in a low level.Conclusions Mechanical tensil stress may regulate the expression pattern of TGFβ / Smad in suture cells to stimulate their proliferation,which leads to suture distraction osteogensis.