高血糖通过增加破骨细胞陷窝密度和减少血管管腔体积来损害大鼠皮质骨。

Hyperglycemia compromises Rat Cortical Bone by Increasing Osteocyte Lacunar Density and Decreasing Vascular Canal Volume.

机构信息

Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON, Canada.

Department of Anatomy, Physiology and Pharmacology, University of Saskatchewan, Saskatoon, SK, Canada.

出版信息

Commun Biol. 2020 Jan 9;3(1):20. doi: 10.1038/s42003-019-0747-1.

Uncontrolled diabetes is associated with increased risk of bony fractures. However, the mechanisms have yet to be understood. Using high-resolution synchrotron micro-CT, we calculated the changes in the microstructure of femoral cortices of streptozotocin-induced hyperglycemic (STZ) Wistar Albino rats and tested the mechanical properties of the mineralized matrix by nanoindentation. Total lacunar volume of femoral cortices increased in STZ group due to a 9% increase in lacunar density. However, total vascular canal volume decreased in STZ group due to a remarkable decrease in vascular canal diameter (7 ± 0.3 vs. 8.5 ± 0.4 µm). Osteocytic territorial matrix volume was less in the STZ group (14,908 ± 689 µm) compared with healthy controls (16,367 ± 391 µm). In conclusion, hyperglycemia increased cellularity and lacunar density, decreased osteocyte territorial matrix, and reduced vascular girth, in addition to decreasing matrix mechanical properties in the STZ group when compared with euglycemic controls.

未控制的糖尿病与骨骨折风险增加有关。然而，其机制尚未被理解。我们使用高分辨率同步加速器微计算机断层扫描，计算了链脲佐菌素诱导高血糖（STZ）Wistar 白化大鼠股骨皮质微观结构的变化，并通过纳米压痕测试了矿化基质的力学性能。由于腔隙密度增加了 9%，STZ 组的股骨皮质总腔隙体积增加。然而，由于血管腔直径显著减小（7±0.3 对 8.5±0.4 µm），STZ 组的总血管腔体积减少。STZ 组的骨细胞性组织基质体积（14908±689 µm）小于健康对照组（16367±391 µm）。总之，与正常血糖对照组相比，高血糖症增加了细胞密度和腔隙密度，减少了骨细胞性组织基质，减少了血管周长，此外还降低了 STZ 组基质的力学性能。