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Prostaglandin E2 Prevents Disuse-Induced Cortical Bone LossThe 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.
Document ID
19970003807
Acquisition Source
Ames Research Center
Document Type
Reprint (Version printed in journal)
Authors
Jee, Webster S. S.
(Utah Univ. Salt Lake City, UT United States)
Akamine, T.
(Utah Univ. Salt Lake City, UT United States)
Ke, Hua Zhu
(Utah Univ. Salt Lake City, UT United States)
Li, Xiao Jian
(Utah Univ. Salt Lake City, UT United States)
Tang, L. Y.
(Utah Univ. Salt Lake City, UT United States)
Zeng, Q. Q.
(Utah Univ. Salt Lake City, UT United States)
Date Acquired
August 17, 2013
Publication Date
January 1, 1992
Publication Information
Publication: Bone
Publisher: Pergamon Press PLC
Volume: 13
ISSN: 8756-3282
Subject Category
Life Sciences (General)
Report/Patent Number
NAS 1.26:202681
NASA-CR-202681
Accession Number
97N70263
Funding Number(s)
CONTRACT_GRANT: NAG2-435
CONTRACT_GRANT: DE-AC02-76EV-00119
CONTRACT_GRANT: NIH-AR-38346
CONTRACT_GRANT: DE-FG02-89ER-60764
Distribution Limits
Public
Copyright
Public Use Permitted.
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