Tian X Y, Zhang Q, Zhao R, Setterberg R B, Zeng Q Q, Iturria S J, Ma Y F, Jee W S S
Division of Radiobiology, Department of Radiology, University of Utah School of Medicine, 729 Arapeen Dr., Suite 2338, Salt Lake City, UT, 84108-1218, USA.
Bone. 2008 May;42(5):914-20. doi: 10.1016/j.bone.2007.12.228. Epub 2008 Feb 5.
The present study examined the effects of continuous and intermittent PGE2 administration on the cancellous and cortical bone of lumbar vertebral bodies (LVB) in female rats. Six-month-old Sprague-Dawley female rats were divided into 6 groups with 2 control groups and 1 or 3 mg PGE2/kg given either continuously or intermittently for 21 days. Histomorphometric analyses were performed on the cancellous and cortical bone of the fourth and fifth LVBs. Continuous PGE2 exposure led to bone catabolism while intermittent administration led to bone anabolism. Both routes of administration stimulated bone remodeling, but the continuous PGE2 stimulated more than the intermittent route to expose more basic multicellular units (BMUs) to the negative bone balance. The continuous PGE2 caused cancellous bone loss by stimulating bone resorption greater than formation (i.e., negative bone balance) and shortening the formation period. It caused more cortical bone loss than gain, the magnitude of the negative endocortical bone balance and increased intracortical porosity bone loss was greater than for periosteal bone gain. The anabolic effects of intermittent PGE2 resulted from cancellous bone gain by positive bone balance from stimulated bone formation and shortened resorption period; while cortical bone gain occurred from endocortical bone gain exceeding the decrease in periosteal bone and increased intracortical bone loss. Lastly, a scheme to take advantage of the marked PGE2 stimulation of lumbar periosteal apposition in strengthening bone by converting it to an anabolic agent was proposed.
本研究检测了连续和间歇性给予前列腺素E2（PGE2）对雌性大鼠腰椎椎体松质骨和皮质骨的影响。将6月龄的斯普拉格-道利雌性大鼠分为6组，其中2个对照组，其余组连续或间歇性给予1或3mg PGE2/kg，持续21天。对第四和第五腰椎椎体的松质骨和皮质骨进行组织形态计量学分析。连续暴露于PGE2会导致骨分解代谢，而间歇性给药则会导致骨合成代谢。两种给药途径均刺激骨重塑，但连续给予PGE2比间歇性给药刺激更强，使更多基本多细胞单位（BMUs）处于负骨平衡状态。连续给予PGE2通过刺激骨吸收大于骨形成（即负骨平衡）并缩短形成期，导致松质骨丢失。它导致皮质骨丢失多于增加，内皮质骨负平衡的程度以及皮质内孔隙率增加导致的骨丢失大于骨膜骨增加。间歇性PGE2的合成代谢作用源于松质骨通过刺激骨形成的正骨平衡和缩短吸收期而增加；而皮质骨增加则源于内皮质骨增加超过骨膜骨减少以及皮质内骨丢失增加。最后，提出了一种利用PGE2对腰椎骨膜附着的显著刺激作用，通过将其转化为合成代谢剂来强化骨骼的方案。
