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Osteocytic Osteolysis in PTH-treated Wild-type and Rankl-/- Mice Examined by Transmission Electron Microscopy, Atomic Force Microscopy, and Isotope Microscopy.
Journal of Histochemistry & Cytochemistry ( IF 1.9 ) Pub Date : 2020-09-18 , DOI: 10.1369/0022155420961375
Hiromi Hongo 1 , Tomoka Hasegawa 1 , Masami Saito 2 , Kanako Tsuboi 3 , Tomomaya Yamamoto 4 , Muneteru Sasaki 5 , Miki Abe 1 , Paulo Henrique Luiz de Freitas 6 , Hisayoshi Yurimoto 7 , Nobuyuki Udagawa 8 , Minqi Li 9 , Norio Amizuka 1
Affiliation  

To demonstrate the ultrastructure of osteocytic osteolysis and clarify whether osteocytic osteolysis occurs independently of osteoclastic activities, we examined osteocytes and their lacunae in the femora and tibiae of 11-week-old male wild-type and Rankl−/− mice after injection of human parathyroid hormone (PTH) [1-34] (80 µg/kg/dose). Serum calcium concentration rose temporarily 1 hr after PTH administration in wild-type and Rankl−/− mice, when renal arteries and veins were ligated. After 6 hr, enlargement of osteocytic lacunae was evident in the cortical bones of wild-type and Rankl−/− mice, but not so in their metaphyses. Von Kossa staining and transmission electron microscopy showed broadly demineralized bone matrix peripheral to enlarged osteocytic lacunae, which contained fragmented collagen fibrils and islets of mineralized matrices. Nano-indentation by atomic force microscopy revealed the reduced elastic modulus of the PTH-treated osteocytic perilacunar matrix, despite the microscopic verification of mineralized matrix in that region. In addition, 44Ca deposition was detected by isotope microscopy and calcein labeling in the eroded osteocytic lacunae of wild-type and Rankl−/− mice. Taken together, our findings suggest that osteocytes can erode the bone matrix around them and deposit minerals on their lacunar walls independently of osteoclastic activity, at least in the murine cortical bone. (J Histochem Cytochem 68: –XXX, 2020)



中文翻译:

通过透射电子显微镜、原子力显微镜和同位素显微镜检查 PTH 处理的野生型和 Rank1-/- 小鼠的骨细胞溶骨。

为了证明骨细胞溶骨的超微结构并阐明骨细胞溶骨是否独立于破骨细胞活动而发生,我们在注射人甲状旁腺后检查了 11 周龄雄性野生型和Rankl -/-小鼠股骨和胫骨中的骨细胞及其腔隙激素 (PTH) [1-34](80 µg/kg/剂量)。当结扎肾动脉和静脉时,在野生型和Rank1 -/-小鼠中施用 PTH 后 1 小时,血清钙浓度暂时升高。6 小时后,在野生型和Rankl -/-的皮质骨中,骨细胞腔隙扩大明显老鼠,但在他们的形而上学中并非如此。Von Kossa 染色和透射电子显微镜显示广泛脱矿的骨基质外围到扩大的骨细胞腔隙,其中包含破碎的胶原纤维和矿化基质的胰岛。原子力显微镜的纳米压痕揭示了经 PTH 处理的骨细胞周围基质的弹性模量降低,尽管对该区域矿化基质进行了微观验证。此外,通过同位素显微镜和钙黄绿素标记在野生型和Rankl -/-的侵蚀骨细胞陷窝中检测到44 Ca 沉积老鼠。综上所述,我们的研究结果表明,骨细胞可以侵蚀它们周围的骨基质,并将矿物质沉积在其腔隙壁上,而不受破骨细胞活动的影响,至少在小鼠皮质骨中是这样。 (J Histochem Cytochem 68:–XXX,2020)

更新日期:2020-09-20
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