Anabolic effect of prostaglandin E2 in bone is not dependent on pituitary hormones in rats.
Prostaglandin E2 (PGE2) is an anabolic agent of bone in vivo but the mechanism of its action still remains unclear. The aim of this study was to determine whether the effect of PGE2 on skeleton is mediated by pituitary hormones. Forty female, Sprague-Dawley rats were divided into four groups: baseline control (basal), age-matched intact control (CON), hypophysectomy (HX), and HX + PGE2 (2 mg/kg/day) with 10 animals in each group. The basal group was sacrificed at 2 months of age, and the remaining groups after 6 weeks of treatment. Cancellous and cortical bone histomorphometry was performed on double fluorescent-labeled 40 micron-thick sections of the proximal tibia and tibial shaft. Our results show that HX resulted in a cessation of bone growth, a decrease in cancellous bone volume, and cortical bone gain compared with the age-matched, intact CON rats. Compared with the HX group, the HX + PGE2 group had a significantly greater tibial bone density (mean +/- SE, HX + PGE2:1.595 +/- 0.007 versus HX:1.545 +/- 0.013), percent cancellous bone volume (21.4 +/- 2.0 versus 8.41 +/- 1.70), percent cortical bone area (87.2 +/- 0.85 versus 81.7 +/- 0.7), and ratio of cortical area to marrow area (7.14 +/- 0.56 versus 4.52 +/- 0.21). Increased bone masses by PGE2 in the HX animals were accompanied by an increase in the trabecular and endosteal-labeled surface and bone formation rate. The trabecular number and width were increased whereas trabecular separation was decreased in the HX + PGE2 group compared with the HX group (P < 0.05). PGE2 treatment also caused a decrease in the tibial endosteal eroded surface and medullar cavity of the HX animals. In conclusion, this study clearly demonstrates that PGE2 (2 mg/kg/day) in the HX rats increases both cortical and cancellous bones and improves trabecular architecture in the tibia after 6 weeks of treatment. These skeletal alterations are due to a stimulation of bone formation and a suppression of bone resorption activity. These findings suggest that the anabolic effect of PGE2 in bone is independent of pituitary hormones.
Chen
M M
MM
Department of Medicine, Metabolism Laboratory, Winthrop-University Hospital, Mineola, New York 11501, USA.
Yeh
J K
JK
Aloia
J F
JF
D000818:Animals; D001835:Body Weight / Q000187:drug effects; D001862:Bone Resorption; D001842:Bone and Bones / Q000187:drug effects / Q000378:metabolism*; D015232:Dinoprostone / Q000494:pharmacology*; D005260:Female; D006132:Growth Plate / Q000033:anatomy & histology / Q000187:drug effects; D010012:Osteogenesis / Q000187:drug effects / Q000502:physiology*; D005082:Physical Exertion / Q000187:drug effects; D010907:Pituitary Hormones / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley
D010907:Pituitary Hormones; D015232:Dinoprostone