将羟基磷灰石（HA）涂层钛种植体延期植入狗颌骨，施以150g的正畸力，通过口内及X线照片测量，动态研究种植支抗在3个月内的稳定性。结果显示：判断种植支抗的移动应综合采用口内及通过X线照片测量两种方法；HA涂层钛种植支抗的骨内段无移位（P＞0.05），而基桩在受力后第2和第3个月倾斜移动。说明该类骨内种植体的体部承受正畸力时具有良好的稳定性，在将其颈部设计调整后作为种植支抗，可保证在短期正畸治疗时间内不移动。

目的探讨正畸牙移动骨改建过程中成骨细胞调控破骨细胞分化成熟的机制。方法分离培养大鼠股骨骨髓间充质干细胞来源的成骨细胞，采用膜式动态张应力加载体系进行体外细胞加力，RT-PCR技术检测不同强度、不同性质、不同作用时间张应力对成骨细胞ICAM-1mRNA表达的影响。结果张应力刺激对成骨细胞ICAM-1mRNA的表达有明显抑制作用,强度越大抑制作用越强，（依次为静、动态5kPa组，静、动态3kPa组，静态1kPa组，对照组）；静态张应力抑制效应明显弱于动态张应力（静态3kPa、5kPa组分别弱于动态3kPa、5kPa组）；ICAM-1mRNA的表达在动态张应力作用后3h即显著降低,12h最低（降至未加力时的23%），后有所回升但仍维持在一较低水平，具有时效性。结论机械张应力刺激通过抑制成骨细胞ICAM-1mRNA的表达限制破骨细胞的分化成熟。

This study was to examine the effects of mechanical stimuli alone and coupled with some inhibitors of related signaling pathways on early cellular responses. MG-63 cells were subjected to cyclic uniaxial compressive or tensile strain at 4000 lstrain, produced by fourpoint bending system. The effects of mechanical strains alone and coupled with inhibitors of microfilament and receptor tyrosine kinase (RTK) on activation of extracellular signal-regulated kinase (ERK), c-fos mRNA, and c-Fos protein were examined. ERK could be activated by mechanical stimuli in 5 min and so could be c-fos mRNA and c-Fos protein in 30 min. Tensile stress had a more obvious effect than compressive one. Early ellular responses were connected with cytoskeleton and RTK pathways during the transduction of mechanical signals. The property of strains was an influential factor for the activation effects.

Objective: Using type X collagen as a marker, this research was designed to examine the alteration of condylar growth in response to mandibular condylar forward positioning. Methods: One hundred female Sprague-Dawley rats with 5 weeks of age were randomly divided into five experimental and five control groups. In the experimental groups, bite jumping appliances created forward positioning of the condyle. The experimental rats, together with the age-matched controls, were sacrificed on days 3, 7, 14, 21 and 30, respectively. Tissue sections were cut in the sagittal plane through the mandibular condyle and were processed for in situ hybridization and immunostaining of type X collagen and then for quantitative imaging analyses. Results: (1) Both type X collagen mRNA in situ hybridization signals and type X collagen immunostaining were localized within the hypertrophic zone of the condylar cartilage. (2) With condylar forward positioning, the level of type X collagen mRNA signals (8541±74 μm2 at peak) was 300% higher than that in the controls (2117±78 μm2 at peak); type X collagen immunostaining in condylar advancing groups (54864±134 μm2 at peak) was 254% more than that in the controls (15470±121 μm2 at peak). (3) The amount of type X collagen mRNA signals and immunostaining in experimental and control groups reached the highest levels at day 14 and day 21, respectively, indicating that an increase in endochondral ossification occurred 21 days after condylar forward deviation. Conclusion: Condylar forward repositioning provokes an enhanced maturation of condylar chondrocytes resulting in increased synthesis of type X collagen, a extracellular protein that attributes to endochondral ossification.