Transient effects of subcutaneously administered prostaglandin E2 on cancellous and cortical bone in young adult dogs.
Transient effects of subcutaneously administered prostaglandin E2 on cancellous and cortical bone in young adult dogs.
复制标题
皮下注射前列腺素 E2 对年轻成年犬松质骨和皮质骨的短暂影响。
DOI：
10.1016/8756-3282(90)90091-c
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发表时间：
1990
期刊：
影响因子：
4.1
通讯作者：
Patterson-Buckendahl,P
中科院分区：
文献类型：
--
作者：
Li,XJ;Jee,WS;Li,YL;Patterson-Buckendahl,P
治疗31天后，评价了前列腺素E2（PGE 2）对9只完整年轻成年犬髂嵴和胫骨中段松质骨和皮质骨的短暂影响。组织形态计量学骨变化的特点是在体内荧光双标记的未脱钙骨标本。PGE 2引起松质骨重塑增加，表现为活化频率增加;侵蚀和形成表面百分比增加;矿物质沉积和骨形成速率增加;吸收、形成和总骨重塑期缩短。活化的松质骨重塑未导致松质骨质量降低，表明骨吸收和形成之间的失衡有利于重塑部位的形成（活化→吸收→刺激形成; A → R → F ↑）。PGE 2处理激活了骨膜和皮质内表面形成模式（激活→形成; A → F）的骨建模，并增加了胫骨干皮质内骨重建的激活频率。增加的建模激活将静止的骨表面转化为具有刺激的成骨细胞活性的形成表面（即，增加的百分比标记的骨膜和皮质内表面，矿物质沉积率，和编织和层状骨小梁形成），导致骨膜下，骨内膜下和骨髓区域的新形成的骨量增加9- 26倍。然而，增加的皮质内骨重塑增加了重塑空间（即，增加的皮质孔隙度），产生部分抵消骨获得的骨损失。与对照骨中的负骨平衡相比，组合事件导致PGE 2治疗的皮质骨中的正骨平衡。总之，我们的数据表明，在体内PGE 2是一个强大的活化剂的松质骨和皮质骨的形成，这可能是能够建立一个峰值骨量，以防止和/或纠正骨骼缺陷，治疗骨质疏松症。
The transient effects of prostaglandin E2(PGE2) on cancellous and cortical bone in iliac crests and mid-tibial shafts of nine intact young adult dogs were evaluated following 31 days of treatment. Histomorphometric bone changes were characterized from in vivo fluorescent double-labeled undecalcified bone specimens. PGE2caused an increase in cancellous bone remodeling evidenced by increased in activation frequency; increased percent eroded and formation surfaces; increased mineral apposition and bone formation rates; and shortened resorption, formation, and total bone remodeling periods. Activated cancellous bone remodeling did not lead to decreased cancellous bone mass, indicating an imbalance between bone resorption and formation in favor of formation (activation → resorption → stimulated formation; A → R → F ↑) at remodeling sites. The PGE2treatment activated bone modeling in the formation mode (activation → formation; A → F) at the periosteal and endocortical surfaces and increased activation frequency of intracortical bone remodeling in the tibial shaft. Increased modeling activation converted quiescent bone surfaces to formation surfaces with stimulated osteoblastic activity (i.e., increased percent labeled periosteal and endocortical surfaces, mineral apposition rates, and woven and lamellar trabecular bone formation) leading to 9- to 26-fold increases in newly formed bone mass in subperiosteal, subendosteal, and marrow regions, compared to controls. However, increased intracortical bone remodeling elevated remodeling space (i.e., increased cortical porosity), producing a bone loss that partially offsets the bone gain. The combined events lead to a positive bone balance in PGE2-treated cortical bone, compared to a negative bone balance in control bones. Collectively our data suggest that in vivo PGE2is a powerful activator of cancellous and cortical bone formation, which may be able to build a peak bone mass to prevent and/or correct the skeletal defects to cure osteoporosis.