低密度脂蛋白在2型糖尿病骨质疏松中的作用研究进展

2型糖尿病及骨质疏松已成为我国最主要的慢性代谢性疾病。2型糖尿病常伴有血脂紊乱，常表现为低密度脂蛋白升高，而越来越多的研究表明血脂通过不同的方式影响骨代谢，其机制可能是通过抑制骨髓间充质干细胞成骨分化，通过RANK/RNAKL/OPG信号通路及炎症反应调节破骨细胞等方式调节骨代谢。     

激素对骨骼系统的不良反应(Ⅱ)

1骨梗死 已知大量应用激素治疗可发生骨髓梗死[1].骨梗死就是骨髓坏死.可单发或多发,单侧或双侧,最常发生在股骨远段和胫骨近段的骨髓内.亦见有肱骨、不规则骨,甚至腰椎骨梗死.     

降钙素对骨性关节炎中软骨作用的研究进展

骨性关节炎的特征表现是关节软骨的进行性退变。实验研究和临床观察证实，完整的关节软骨形态取决于软骨下骨的转化、正常的软骨细胞功能和基本的生物力学刺激㈦。鉴于软骨下骨和关节软骨的关系十分密切，理论上理想的治疗药物应该着眼于生物力学刺激的干预和如何调整骨和软骨的代谢活性。     

经闭如狂治验1例

孙某，女，33岁，2003年5月14日就诊。自述月经闭止3月余。近来时常出现狂躁不安，有时无故对丈夫及女儿打骂，砸坏家什，夜间不能安眠，难以正常上班工作。诊见其心烦躁扰，坐立不安，不时捶胸顿足，诉记忆力很差，口苦口干，小腹硬满，月经不行，小便自利，大便色深黑，查舌质红、苔黄，脉沉涩。大便隐血试验阴性。证属下焦蓄血证，治宜破血祛淤，     

实验性骨折愈合中骨吸收活动的超微结构观察

将50只家兔造成实验性桡骨骨折,分批取骨痂标本,用光镜和电子显微镜观察表明,在骨折愈合过程中,破骨细胞是骨吸收的主要执行者,巨噬细胞能吞噬死骨,但不能吸收骨质。     

人外周血CD68^＋单核细胞体外的分选及诱导分化为破骨细胞

OBJECTIVE: To establish a method for obtaining highly purified primary human osteoclast precursors for the biochemical and molecular biological research. METHODS: CD68(+) mono/macrophages were separated from peripheral blood mononuclear cells (PBMCs) of healthy donors by means of immunomagnetic cell sorting for subsequent analysis with flow cytometry. The isolated cells were incubated on coverslips or bone slices in the presence of dexamethasone(10(-8) mol/L), macrophage colony-stimulating factor (25 microg/L ) and soluble receptor activator of nuclear factor (NF)-kappaB ligand (s-RANKL, 16 microg/L). Calcitonin receptor (CR) immunocytochemistry and tartrate-resistant acid phosphatase (TRAP) histochemistry were employed. The bone slices were also studied by scanning electron microscopy (SEM). RESULTS: Fluorescence-activated cytometric analysis showed that 93.06%+/-0.61% n=4 of the selected cells were CD68(+) cells. After 7 days of culture of the CD68(+) cells, VR+, TRAP+ multinucleated giant cells appeared, and resorption lacunae could be observed by SEM. CONCLUSION: Highly purified CD68(+) cells can be obtained from human PBMCs as the osteoclast precursors, and mature osteoclasts can be induced from CD68(+) mono/macrophages by RANKL.