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Estrogen and the Skeleton

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Despite the critical importance of estrogen for bone, it has proven to be remarkably challenging to define the precise mechanism s by which estrogen regulates bone metabolism. At the clinical level, treatment of postmenopausal women with estrogen leads to a marked and sustained reduction in urine or serum markers of bone resorption 6. Changes in bone formation markers are more complex: Bone biopsy data, which is generally obtained months or years after starting estrogen replacement, correlate well with the bone marker data, with a reduction in indices of bone resorption osteoclast [see Glossary] numbers, percent eroded surface and bone formation osteoblast numbers, bone formation rates 7.

Withdrawal of estrogen as in oophorectomy or menopause leads to exactly the opposite changes: However, the increase in bone resorption following estrogen deficiency outstrips the increase in bone formation, leading to net bone loss.

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Based on these fundamental clinical observations, basic research attempting to define the skeletal actions of estrogen has focused on defining how estrogen a inhibits bone resorption and b regulates bone formation. The latter is particularly challenging since, as noted above, estrogen treatment results overall in a decrease in bone formation, while chronic estrogen deficiency is associated with increased bone formation.

And yet, early after initiating estrogen therapy, there is a transient increase in bone formation before the subsequent decrease.

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The complexity of this problem can be summarized as follows: With this issue in mind, the subsequent sections summarize our current mechanistic understanding of estrogen effects on bone resorption and formation. Prior to doing so, however, it is important to briefly review the fundamental mechanisms of bone remodeling and the key role of the osteocyte in regulating bone turnover. This remodeling process occurs in basic multicellular units BMUs which include osteoclasts, osteoblasts, and osteocytes within the bone remodeling cavity Figure 1.

In turn, these bone lining cells are in communication with osteocytes embedded within the bone matrix This is accompanied by significant reductions in circulating estradiol E2 levels, although in contrast to humans 1the changes in circulating E2 levels in aging female mice are more difficult to detect. Thus, Nelson et al. Thus, female aging mice do develop E deficiency, although this is clearly not as profound as that observed in postmenopausal women.

Interestingly, age-related declines in vertebral and femoral trabecular bone begin in female mice by 2 months of age 15at a time of sex steroid sufficiency, again suggesting that trabecular bone loss in mice, as in humans, may be relatively sex steroid independent.

Recognizing that aging female mice only develop mild-moderate E deficiency manifested at certain days of the estrus cycle 14we sought to dissociate, as definitively as possible, effects of aging per se versus those of age-related E deficiency in mice on trabecular versus cortical bone loss over life. To do so, we compared the skeletal phenotype of young control mice age 6 months to that of normally aged mice to age monthsaged mice with lifelong E deficiency ovariectomized at 6 months of age and aged to monthsor aged mice who had been ovariectomized at the age of 6 months but continuously replaced with fixed doses of E between the ages of 6 months and months.

Thus, by maintaining relatively constant E levels over life in the latter group, we essentially eliminated possible effects of even subtle decrements in E levels with aging in female mice and isolated effects of aging alone on the various skeletal parameters. In addition, in order to better understand possible changes in osteoprogenitor cells with aging, we harvested hematopoietic lineage negative lin- cells from bone marrow of young and aged mice for analysis of osteoblastic genes and pathways.

Effects of Chronic Estrogen Treatment on Modulating Age-Related Bone Loss in Female Mice

These cells have recently been shown to be highly enriched for osteoprogenitor cells which mineralize in vitro, form bone in vivo, and express bone-related genes 16thereby providing a useful cell population for evaluation of effects of aging on osteoblast progenitor cells.

However, for every skeletal endpoint examined, changes in the two E groups relative to young control mice were virtually identical, so all data are presented for the two E groups combined.

For technical and cost reasons, specific analyses were done in random subsets of the Control and Aged groups; thus, the number of animals used in each analysis are indicated in the respective Figures and Tables.

During the experiments, animals had free access to water and were pair fed. At the end of the study, the animals were euthanized by cervical dislocation and the bones were harvested see below.

Effects of Chronic Estrogen Treatment on Modulating Age-Related Bone Loss in Female Mice

Slice images were measured 1 mm proximal to the tibial and fibula junction. The femoral scans were carried out in an area corresponding to the secondary spongiosa in the metaphyseal region, 0. Bone histomorphometry The femurs and lumbar spines L1-L4 were processed for histomorphometry as previously described 18 The total area scanned was 1.