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破骨细胞

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However, the molecular events of osteoclasts in response to tensile stress are still not well understood so far.

但到目前为止,有关牵张应力导致破骨细胞生物学行为变化的分子机制尚不清楚。

Methods:The femur were removed aseptically from adult SD rat (aged 12 weeks).

目的:探讨IL-6对成年大鼠骨髓破骨细胞生成诱导的影响。

Figure 6 Bright fluorescence of condensed nuclear chromatin appeared around circumnuclear edge of apoptotic osteoclast,nonapoptotic nuclear fluorescence showed coherent distributed.

凋亡细胞核核周呈一亮环,而未凋亡细胞核染色均一(图6)。图6 凋亡破骨细胞胞核周缘呈环状亮色,而未凋亡细胞核荧光染色均一。

Inhibition of EGFR signaling can delay endochondral ossification,osteoclast recruitment and decrease osteoclast formation.

EGFR信号转导机制可能通过调节破骨细胞的生成,影响其向中心生长板的募集,从而影响小鼠初级软骨内骨化的进展。

At 96 h, the resorption lacunae become bigger. Conclusion: Osteoclasts showed resorption ability to PCCC in vitro.

破骨细胞在体外培养条件下对PCCC材料有明显吸收降解作用。

Scanning electron microscope showed that many resorption lacunae were generated on PCCC surface with the diameter less than 50 μm. Osteoclasts were located in the lacunae.

扫描式电子显微镜观察见在PCCC表面出现许多散在分布的吸收空隙,直径一般50μm,破骨细胞位于其中。96h见吸收空隙增大。

Results Six days after culture, a large number of multinuclear mature osteoclasts were formed, and TRAP staining confirmed them to be mature osteoclasts.

结果 混合培养6d后,体系中可见成熟破骨细胞出现。

They arise in settings of excess osteoclastic activity, such as hyperparathyroidism, and can cause bone pain.

它通常由过度的破骨细胞活性造成,例如甲状旁腺功能亢进,并且可以造成骨痛。

This review will outline up-to-date information regarding the signaling pathways and the regulating factors of osteoclast differentiation and some potential therapies that aim at curing the osteolytic diseases.

笔者将就破骨细胞在分化过程中的信号通路及其调节因素以及一些潜在可行的治疗骨量丢失相关疾病的方法予以综述。

The observation with histomorphology and phase contrast microscope: osteoclasts were large in size, multinucleus, foam-like cytoplasm with vacuole and pseudopodia, and movable. Acid Phosphatase reaction is positive.

经组织形态学、光镜和相差显微镜观察,破骨细胞具有胞体大,多核,胞浆泡沫状间有空泡,胞浆有伪足样突起,并可移动,酸性磷酸酶反应阳性。

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