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维生素D3过多症中的骨重塑。放射学-微血管造影-病理学相关性

Bone remodeling in hypervitaminosis D3. Radiologic-microangiographic-pathologic correlations.

作者信息

Jiang Y B, Wang Y Z, Zhao J, Marchal G, Wang Y X, Shen Y L, Xing S Z, Li R G, Baert A L

机构信息

Department of Radiologic Pathology, Beijing Institute of Traumatology and Orthopaedics, Beijing Ji Shui Tan Hospital, People's Republic of China.

出版信息

Invest Radiol. 1991 Mar;26(3):213-9. doi: 10.1097/00004424-199103000-00002.

DOI:10.1097/00004424-199103000-00002
PMID:1647377
Abstract

To investigate the mechanism of bone changes in hypervitaminosis D3, we compared contact radiographs, microangiograms by injection of Chinese ink, and corresponding histopathologic macrosections of 66 rabbits that received different doses of vitamin D3. In early stages, radiographs showed subperiosteal bone resorption and porotic cortical bone. The corresponding microangiograms showed proliferating vessels in the periosteum and cortical bone with associated dilatation of the Haversian and Volkmann's canals. When metastatic calcification fills these intracortical caverns or the intertrabecular spaces in the metaphysis and physis, the bone shows a diffuse increased density on radiographs. A dense band in the metaphysis reflects a thickening of calcified chondromatrix due to a hypotrophy of the distal metaphyseal capillaries. Six to 12 weeks after vitamin D3 withdrawal, radiographs showed further increased density of the cortical bone, due to newly formed bone and metastatic calcification. Alternating bands of increased and decreased density in the metaphysis and physis reflect the reinvasion of normal vasculature between growth cartilage and calcified chondromatrix, with normalization of endochondral ossification.

摘要

为研究维生素D3过多症时骨改变的机制,我们比较了66只接受不同剂量维生素D3的兔子的接触X线片、注射中国墨汁后的微血管造影照片以及相应的组织病理学大体切片。早期,X线片显示骨膜下骨吸收和骨质疏松性皮质骨。相应的微血管造影照片显示骨膜和皮质骨内血管增生,伴有哈弗斯管和福尔克曼管扩张。当转移性钙化填充这些皮质内空洞或干骺端和生长板的小梁间隙时,X线片上骨密度弥漫性增加。干骺端的致密带反映了由于远端干骺端毛细血管萎缩导致钙化软骨基质增厚。停用维生素D3 6至12周后,X线片显示皮质骨密度进一步增加,这是由于新形成的骨和转移性钙化所致。干骺端和生长板密度增加与降低交替的带反映了生长软骨和钙化软骨基质之间正常血管的重新侵入,软骨内成骨恢复正常。

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