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1 Orthopaedic Surgery, Indiana University, Indianapolis, Indiana, United States
2 Anatomy and Cell Biology, Indiana University, Indianapolis, Indiana, United States
3 Biomedical Engineering, Indiana University, Indianapolis, Indiana, United States
4 Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, California, United States
5 Department of Biomedical Engineering, Indiana University, Indianapolis, Indiana, United States
* To whom correspondence should be addressed. E-mail: turnerch{at}iupui.edu.
Mechanical loading caused by physical activity can stimulate bone formation and strengthen the skeleton. Estrogen receptors play some role in the signaling cascade that is initiated in bone cells after a mechanical load is applied. We hypothesized that one of the ERs, ER
, influences the responsiveness of bone to mechanical loads. To test our hypothesis, 16 week old male and female mice with null mutations in ER (ER-/-) had their right forelimbs subjected to short daily loading bouts. The loading technique used has been shown to increase bone formation in the ulna. Each loading bout consisted of 60 compressive loads within 30 sec applied daily for three consecutive days. Bone formation was measured by first giving standard fluorochrome bone labels one and six days after loading and using quantitative histomorphometry to assess bone sections from the mid-shaft of the ulna. The left non-loaded ulna served as an internal control for the effects of loading. Mechanical loading increased bone formation rate at the periosteal bone surface of the mid-ulna in both ER-/- and wildtype (WT) mice. The ulnar responsiveness to loading was similar in male ER-/- versus WT mice but, for female mice, bone formation was stimulated more effectively in ER-/- mice (p<0.001). We conclude that estrogen signaling through ER suppresses the mechanical loading response on the periosteal surface of long bones.
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