Unoki E
Department of Orthopedic Surgery, Akita University School of Medicine, Japan.
Nihon Seikeigeka Gakkai Zasshi. 1995 Oct;69(10):1064-75.
Serum and urine chemical analyses were combined with a bone histomorphometrical study of rat metaphyses to evaluate the osteogenetic effect of intermittent administration of human parathyroid hormone (h-PTH) on steroid-induced osteopenia. Seven-month-old female Wistar rats were divided into the following 4 groups: (1) a control group: age-matched and untreated; (2) a baseline control group (BL group): given 2.5 mg/kg prednisolone subcutaneously 6 times/week for 8 weeks, at the end of which the animals were sacrificed; (3) a PTH group: in the 9th week of continuous steroid administration, 6.0 micrograms/kg h-PTH was added to the regimen; and the animals were sacrificed in the 12th week; (4) a vehicle group, as a control for the h-PTH group: only the vehicle was administered instead of PTH. At the necropsy at the end of the experiment, both tibias were collected. The undecalcified sections were stained by Villanueva bone stain and labelled with tetracycline, and the decalcified sections were stained by TRAP, and examined histomorphometrically. Serum Ca and P were not changed by any treatment. Serum 1,25 (OH)2D3 values were significantly increased in rats treated with h-PTH. There was no significant change in urinary Ca, P, or hydroxyproline excretion in any group. Histomorphometrically, the parameters related to bone formation--osteoid surface, mineralized surface and bone formation rate--were all reduced in the BL group and in the vehicle group. The bone volume was significantly lower in these group than in controls. The PTH group, on the other hand, showed increases in the osteoid surface, mineral apposition rate, and bone formation rate and the bone volume was significantly higher than in controls. The PTH group showed no increases in the osteoclast number or in the osteoclast surface. These results suggested that intermittent administration of h-PTH activated bone formation only, and increased bone volume.
将血清和尿液化学分析与大鼠干骺端的骨组织形态计量学研究相结合，以评估间歇性给予人甲状旁腺激素（h-PTH）对类固醇诱导的骨质减少的成骨作用。将7月龄雌性Wistar大鼠分为以下4组：（1）对照组：年龄匹配且未接受治疗；（2）基线对照组（BL组）：每周皮下注射2.5mg/kg泼尼松龙6次，共8周，在第8周结束时处死动物；（3）PTH组：在持续给予类固醇的第9周，在给药方案中添加6.0μg/kg h-PTH；动物在第12周处死；（4）溶剂对照组，作为h-PTH组的对照：仅给予溶剂而非PTH。在实验结束时尸检时，收集双侧胫骨。未脱钙切片用Villanueva骨染色法染色并用四环素标记，脱钙切片用抗酒石酸酸性磷酸酶（TRAP）染色，并进行组织形态计量学检查。任何治疗均未改变血清钙和磷水平。h-PTH治疗的大鼠血清1,25（OH）2D3值显著升高。任何组的尿钙、磷或羟脯氨酸排泄均无显著变化。组织形态计量学方面，与骨形成相关的参数——类骨质表面、矿化表面和骨形成率——在BL组和溶剂对照组中均降低。这些组的骨体积显著低于对照组。另一方面，PTH组的类骨质表面、矿物质沉积率和骨形成率增加，且骨体积显著高于对照组。PTH组的破骨细胞数量或破骨细胞表面无增加。这些结果表明，间歇性给予h-PTH仅激活骨形成，并增加骨体积。
