Prostaglandin E2 prevents disuse-induced cortical bone loss.
The object of this study was to determine whether prostaglandin E2 (PGE2) can prevent disuse (underloaded)-induced cortical bone loss as well as add extra bone to underloaded bones. Thirteen-month-old retired female Sprague-Dawley breeders served as controls or were subjected to simultaneous right hindlimb immobilization by bandaging and daily subcutaneous doses of 0, 1, 3, or 6 mg PGE2/kg/d for two and six weeks. Histomorphometric analyses were performed on double-fluorescent labeled undecalcified tibial shaft sections (proximal to the tibiofibular junction). Disuse-induced cortical bone loss occurred by enlarging the marrow cavity and increasing intracortical porosity. PGE2 treatment of disuse shafts further increased intracortical porosity above that in disuse alone controls. This bone loss was counteracted by enhancement of periosteal and corticoendosteal bone formation. Stimulation of periosteal and corticoendosteal bone formation slightly enlarged the total tissue (cross-sectional) area and inhibited marrow cavity enlargement. These PGE2-induced activities netted the same percentage of cortical bone with a different distribution than the beginning and age-related controls. These findings indicate the PGE2-induced increase in bone formation compensated for the disuse and PGE2-induced bone loss, and thus prevented immobilization-induced bone loss.
Jee
W S
WS
Division of Radiobiology, University of Utah School of Medicine, Salt Lake City 84112.
Akamine
T
T
Ke
H Z
HZ
Li
X J
XJ
Tang
L Y
LY
Zeng
Q Q
QQ
D000704:Analysis of Variance; D000818:Animals; D016723:Bone Remodeling / Q000187:drug effects; D001862:Bone Resorption / Q000517:prevention & control*; D001842:Bone and Bones / Q000187:drug effects*; D015232:Dinoprostone / Q000494:pharmacology*; D005260:Female; D007103:Immobilization / Q000009:adverse effects; D051381:Rats; D011919:Rats, Inbred Strains
D015232:Dinoprostone