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Human parathyroid hormone-(1-38) restores cancellous bone to the immobilized, osteopenic proximal tibial metaphysis in ratsThe purpose of this study was to determine if human parathyroid hormone-(1-38) (PTH) can restore cancellous bone mass to the established osteopenic, immobilized proximal tibial metaphyses (PTM) of female rats. The right hindlimbs of six-month-old female Sprague-Dawley rats were immobilized by bandaging the right hindlimbs to the abdomen. After 30 days of right hindlimb immobilization (RHLI), the rats were subcutaneously injected with 200 microgram hPTH(1-38)/kg/day for 15 (short-term) or 75 (longer-term) days. Static bone histomorphometry was performed on the primary spongiosa, while both static and dynamic histomorphometry were performed on the secondary spongiosa of the right PTM. Immobilization for 30 days without treatment decreased trabecular bone area, number and thickness in both primary and secondary spongiosa, and induced an increase in eroded perimeter and a decrease in tissue referent-bone formation rate (BFR/TV) in the secondary spongios. These changes reached a new steady state thereafter. Treatment with 200 microgram hPTH(1-38)/kg/day for 15 days, beginning at 30 days post immobilization (IM), significantly increased trabecular bone area, thickness and number in both primary and secondary spongiosa despite continuous IM when compared to the age-related and IM controls. The short-term (15 days) PTH treatment significantly increased labeling perimeter, mineral apposition rate and BFR/TV in the secondary spongiosa and stimulated longitudinal bone growth as compared to the age-related and IM controls. PTH treatment for longer-term (75 days) further increased trabecular bone area, thickness and number as compared to aging and IM controls and short-term (15 days) PTH treated groups. The bone formation indices in the secondary spongiosa of these longer-term treated rats were lower than that of short-term (15 days) PTH treated group, but they were still higher than those of IM and age-related controls. Our findings indicate that PTH treatment stimulates cancellous bone formation, restores and adds extra cancellous bone to the established, disuse-osteopenic proximal tibial metaphysis of continuously RHLI female rats. These results suggest that PTH may be a useful agent in treatment disuse-induced osteoporosis in humans.
Document ID
19950018136
Acquisition Source
Legacy CDMS
Document Type
Contractor Report (CR)
Authors
Ma, Y. F. (Utah Univ. Salt Lake City, UT, United States)
Jee, W. S. S. (Utah Univ. Salt Lake City, UT, United States)
Ke, H. Z. (Pfizer Central Research Groton, CT., United States)
Lin, B. Y. (Guangdong Medical Coll. Guangdong Province, China)
Liang, X. G. (Helen Hayes Hospital NY., United States)
Li, M. (Florida Univ. Gainesville, FL., United States)
Yamamoto, N. (Niigata Univ. Niigata, Japan)
Date Acquired
September 6, 2013
Publication Date
September 1, 1994
Subject Category
Aerospace Medicine
Report/Patent Number
NASA-CR-197709
NAS 1.26:197709
Accession Number
95N24556
Funding Number(s)
CONTRACT_GRANT: NAG2-435
CONTRACT_GRANT: NIH-AR-38346
CONTRACT_GRANT: DE-AC02-76EV-00119
Distribution Limits
Public
Copyright
Work of the US Gov. Public Use Permitted.

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