Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Department of Orthopaedic Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Department of Trauma and Reconstructive Surgery, Asklepios Clinic St. Georg, Hamburg, Germany.
Bone. 2017 Oct;103:78-87. doi: 10.1016/j.bone.2017.06.022. Epub 2017 Jun 27.
Osteocytes are the most abundant bone cells and are highly regulated by external stimuli. Vitamin D and osteocytes cooperatively regulate bone remodeling as well as phosphate and calcium homeostasis. However, it is unclear if vitamin D regulates osteocyte number, connectivity or size in the setting of altered bone formation or impaired mineralization. Sixty iliac crest biopsies of patients with varying vitamin D levels were examined to analyze osteocyte number, osteocyte connectivity and osteocyte viability using high-resolution imaging. Osteocyte parameters were also quantified in mice lacking the vitamin D receptor (Vdr-/-) and in wildtype littermates. The cortical and cancellous bone of patients with vitamin D deficiency exhibited a significant decrease in the number of viable osteocytes, as well as increased osteocyte apoptosis and impaired osteocyte connectivity, based on evaluation of the canalicular network. The number of osteocytes was also decreased in Vdr-deficient mice, in comparison to wildtype controls, and this was accompanied by enlargement of osteocyte lacunae. A high calcium diet normalized the osteocyte lacunar area in Vdr-deficient mice, but failed to normalize osteocyte number. Thus, a diet-independent decrease in osteocyte number in Vdr-deficient mice suggests a mechanism that is directly dependent on the VDR, since vitamin D may promote the transition from osteoblasts to osteocytes. The increase in lacunar area the in Vdr-deficient mice, which is normalized by the high calcium diet suggests this phenotype is due to osteocytic osteolysis. These investigations demonstrate that vitamin D plays a role in the regulation of osteocyte number and perilacunar remodeling.
成骨细胞是最丰富的骨细胞，受外部刺激的高度调节。维生素 D 和成骨细胞共同调节骨重塑以及磷酸盐和钙的动态平衡。然而，目前尚不清楚维生素 D 是否会在改变骨形成或矿物质化受损的情况下调节成骨细胞的数量、连接或大小。对来自不同维生素 D 水平患者的 60 个髂嵴活检进行了检查，使用高分辨率成像分析成骨细胞数量、成骨细胞连接性和成骨细胞活力。还在缺乏维生素 D 受体（Vdr-/-）的小鼠和野生型同窝仔鼠中定量了成骨细胞参数。维生素 D 缺乏症患者的皮质骨和松质骨表现出活的成骨细胞数量显著减少，以及成骨细胞凋亡增加和连接性受损，基于对管腔网络的评估。与野生型对照相比，Vdr 缺陷型小鼠的成骨细胞数量也减少，并且骨陷窝增大。高钙饮食使 Vdr 缺陷型小鼠的骨陷窝面积正常化，但未能使成骨细胞数量正常化。因此，Vdr 缺陷型小鼠中成骨细胞数量的减少与饮食无关，这表明这一机制直接依赖于 VDR，因为维生素 D 可能促进成骨细胞向成骨细胞的转化。Vdr 缺陷型小鼠中骨陷窝面积的增加被高钙饮食所纠正，这表明这种表型是由于成骨细胞的骨溶解。这些研究表明，维生素 D 在调节成骨细胞数量和骨陷窝周围重塑中发挥作用。
