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首页> 外文期刊>Italian Journal of Anatomy and Embryology >Effect of PTH (1-34) on trabecular bone of rat vertebral body in induced-biochemical osteoporosis by calciumdeprived diet
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Effect of PTH (1-34) on trabecular bone of rat vertebral body in induced-biochemical osteoporosis by calciumdeprived diet

机译：缺钙饮食引起的生化性骨质疏松症中PTH（1-34）对大鼠椎体小梁骨的影响

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Rats fed calcium-deprived diet were used as experimental model for studying bone modelling alterations during biochemical osteoporosis and recovery of bone loss. Such model is suitable to evaluate the possible effects exerted by PTH(1-34) in preventing as well as in recovering metabolic osteoporosis. Three-month-old Sprague Dawley male rats were divided in different groups: some fed normal diet or calcium- deprived diet with/without 40μg/Kg/day PTH(1-34), provided by Eli Lilly-USA, for 4 weeks and some with restoration of normal diet with/without PTH (1-34) for further 4 weeks. To evaluate the occurrence of osteogenesis during the first 4 weeks of the experimental period, rats received three labels of bone deposition at 1st, 20th and 27th day (and then were sacrificed); during the successive 4 weeks (in which those rats previously fed with calcium-deprived diet had restoration of normal diet), animals received three labels of bone deposition at 1st, 7th and 14th day. Histomorphometrical analyses were performed on cortical and trabecular bone taken from the central level of the 5th lumbar vertebral body, transversely sectioned. The results showed that differences among the groups were observed mainly in trabecular bone with respect to cortical one, thus underlining the different role of the two types of bone architecture in mineral and skeletal homeostasis. Concerning trabecular bone, the observations showed that administration of PTH (1-34) during calcium-deprived diet and/or during the restoration of normal diet induces higher deposition of trabecular bone with respect to that recorded in rats that never received PTH(1-34), neither during calcium-deprived diet nor during restoration of normal diet. Since increments of trabecular bone are detectable only after the period of diet restoration (but not before), the authors suggest that a chronic administration of PTH (1-34) is necessary to achieve appreciable results on bone mass recovery.
机译：饲喂缺钙饮食的大鼠用作实验模型，用于研究生化性骨质疏松症和骨质流失恢复期间骨模型的改变。这种模型适合评估PTH（1-34）在预防和恢复代谢性骨质疏松症中可能发挥的作用。将3个月大的Sprague Dawley雄性大鼠分为不同的组：由Eli Lilly-USA提供的一些普通饮食或缺钙的饮食，含/不含40μg/ Kg /天PTH（1-34），持续4周，有些恢复了正常饮食，有/无PTH（1-34）持续了4周。为了评估在实验期的前4周内成骨的发生，大鼠在第1、20和27天接受了3种骨沉积标记（然后处死）。在连续的4周内（其中那些先前饲喂缺钙饮食的大鼠恢复了正常饮食），动物在第1、7和14天接受了三个骨沉积标记。对从第5个腰椎椎体中央水平截取的皮质和小梁骨进行组织形态计量学分析。结果表明，各组之间的差异主要体现在小梁骨和皮质骨之间，从而突显了两种类型的骨结构在矿物质和骨骼稳态中的不同作用。关于小梁骨，观察结果表明，相对于从未接受过PTH（1- 34），既不缺钙饮食也不恢复正常饮食。由于小梁骨的增加仅在饮食恢复期后才可检测到（但未在此之前），因此作者建议长期服用PTH（1-34）对于获得明显的骨量恢复效果是必要的。

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