Low-dose estrogen treatment suppresses periosteal bone formation in response to mechanical loading
Bone, ISSN: 8756-3282, Vol: 39, Issue: 6, Page: 1261-1267
2006
- 40Citations
- 36Captures
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Metrics Details
- Citations40
- Citation Indexes40
- 40
- CrossRef32
- Captures36
- Readers36
- 36
Article Description
Estrogen and exercise influence cortical bone formation. Both affect bone during growth, but with complex interactions. We hypothesized that estrogen reduces the osteogenic response caused by exercise at the periosteal surface of bone, while it enhances bone formation on the endocortical surface. To test our hypothesis, 16 young (8 weeks old) male Sprague-Dawley rats were randomized into two groups: (1) low-dose 17-α ethynylestradiol treatment + bone loading (EE 2 ) or (2) vehicle-treated + bone loading (vehicle). We applied controlled loading to the right ulna at a peak force of 17 N, 2 min/day, 3 days/week for 5 weeks to simulate exercise. The left nonloaded ulna served as an internal control for loading. Mechanical loading increased cortical area (7.7%) and bone mineral content (8%) in the vehicle-treated group ( P < 0.05) but only slightly increased cortical area in the EE 2 group ( P = 0.08). Histomorphometry showed 1 week of mechanical loading increased periosteal bone formation rate by 29% in the vehicle group and this response was reduced ( P < 0.05) to only 15% in the EE 2 group. At the endocortical surface, there were no differences in the loading response between the vehicle and EE 2 -treated groups. We conclude low-dose EE 2 suppresses the mechanical loading response on the periosteal surface of long bones, but had no effect on the loading response at the endocortical bone surface in growing male rats.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S8756328206005709; http://dx.doi.org/10.1016/j.bone.2006.06.030; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34547623094&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/16934543; https://linkinghub.elsevier.com/retrieve/pii/S8756328206005709; https://dx.doi.org/10.1016/j.bone.2006.06.030
Elsevier BV
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