Kimmel D, Ritz E, Krempien B, Mehls O
Metab Bone Dis Relat Res. 1981;3(3):191-8. doi: 10.1016/0221-8747(81)90008-4.
Bone cell kinetics and function and chondrocyte kinetics were evaluated in uremic rats and their pair-fed controls using quantitative histology and 3H-thymidine labeling. The principle histologic abnormality in the proximal tibial metaphysis of uremic rats was a relative abundance of proliferating and differentiated bone cells. No mineralization abnormalities were observed. There was increased proliferation of bone cells and an increased rate of differentiation of osteoblasts and osteoclast nuclei in uremic animals. There was no change in chondrocyte kinetics, indicating a dissociation of the normal bone elongation and bone maturation processes. The data on osteoclast number and hard tissue suggest individual osteoclasts in uremic animals have sub-normal resorbing efficiency. It is proposed that the cell kinetic alterations are due to secondary hyperparathyroidism. The cause of osteoclast inefficiency is uncertain, but may be related to (1) deficiency of active products of vitamin D; (2) chronic uremia; and/or (3) chronic secondary hyperparathyroidism.
使用定量组织学和3H-胸腺嘧啶核苷标记法，对尿毒症大鼠及其配对喂养的对照大鼠的骨细胞动力学与功能以及软骨细胞动力学进行了评估。尿毒症大鼠胫骨近端干骺端主要的组织学异常是增殖和分化的骨细胞相对增多。未观察到矿化异常。尿毒症动物的骨细胞增殖增加，成骨细胞和破骨细胞核的分化速率加快。软骨细胞动力学未发生变化，表明正常的骨骼生长和骨成熟过程出现分离。关于破骨细胞数量和硬组织的数据表明，尿毒症动物的单个破骨细胞重吸收效率低于正常水平。有人提出，细胞动力学改变是继发性甲状旁腺功能亢进所致。破骨细胞效率低下的原因尚不确定，但可能与以下因素有关：（1）维生素D活性产物缺乏；（2）慢性尿毒症；和/或（3）慢性继发性甲状旁腺功能亢进。
