Tian X Y, Zhang Q, Zhao R, Setterberg R B, Zeng Q Q, Ma Y F, Jee W S S
Division of Radiobiology, University of Utah School of Medicine, Salt Lake City, UT 84108-1218, USA.
J Musculoskelet Neuronal Interact. 2007 Oct-Dec;7(4):372-81.
It is well documented that intermittent PGE(2) treatment increases both trabecular and cortical bone mass. However, the effects of continuous PGE(2) administration remain undocumented. The aim of the study was to investigate the effects of continuous prostaglandin E(2) (PGE(2)) on different bone sites in skeletally mature rats. Six-month-old Sprague Dawley rats were treated with PGE(2) at 1 or 3 mg/kg/d continuously via infusion pump for 21 days. Two other groups of rats received PGE(2) at the same doses by intermittent (daily) subcutaneous injections and served as positive controls. Histomorphometry was performed on cancellous bone of the proximal tibial metaphysis and cortical bone of the tibial shaft. As expected, intermittent PGE(2) treatment increased both cancellous and cortical bone mass by stimulating bone formation at the cancellous, periosteal and endocortical bone surfaces. In contrast, continuous PGE(2) treatment decreased cancellous bone mass with bone resorption exceeding bone formation. In addition, continuous PGE(2) treatment increased endocortical and intracortical bone remodeling, inducing bone loss which was partially offset by stimulating periosteal expansion. We conclude that continuous PGE(2) treatment induces overall catabolic effects on both cancellous and cortical bone envelopes, which differs from intermittent PGE(2) treatment that is anabolic. Lastly, we speculate that superior bone mass may be achieved by co-treatment of continuous PGE(2) in combination with an anti-catabolic agent.
有充分文献记载，间歇性前列腺素E2（PGE2）治疗可增加小梁骨和皮质骨量。然而，持续给予PGE2的效果尚无文献报道。本研究的目的是调查持续给予前列腺素E2（PGE2）对骨骼成熟大鼠不同骨部位的影响。6月龄的Sprague Dawley大鼠通过输液泵以1或3 mg/kg/d的剂量持续给予PGE2，共21天。另外两组大鼠通过间歇性（每日）皮下注射给予相同剂量的PGE2，作为阳性对照。对胫骨近端干骺端的松质骨和胫骨干的皮质骨进行组织形态计量学分析。正如预期的那样，间歇性PGE2治疗通过刺激松质骨、骨膜和骨内膜骨表面的骨形成，增加了松质骨和皮质骨量。相比之下，持续PGE2治疗导致松质骨量减少，骨吸收超过骨形成。此外，持续PGE2治疗增加了骨内膜和皮质内骨重塑，导致骨丢失，而骨膜扩张刺激可部分抵消这种骨丢失。我们得出结论，持续PGE2治疗对松质骨和皮质骨包膜均产生总体分解代谢作用，这与具有合成代谢作用的间歇性PGE2治疗不同。最后，我们推测，联合使用抗分解代谢药物与持续PGE2治疗可能会实现更好的骨量。
