Abstract
The effects of estrogen deficiency on bone mineral density (BMD) are well described. At the menopause, there is an accelerated phase of bone loss, and this can be prevented by the administration of menopausal hormonal therapy (MHT). There has recently been a technical advance that allows us to observe the effect of estrogen deficiency and replacement on bone microstructure, namely high-resolution peripheral quantitative computed tomography (HR-pQCT). Quantitative computed tomography (QCT) allows the study of bone in 3 dimensions and hence allows us to study the 2 major types of bone (cortical and trabecular) separately. This contrasts with the most commonly used method for studying bone, dual-energy x-ray absorptiometry, which allows the study of bone in 2 dimensions and so provides no separation of the 2 bone types. QCT methods have advanced and now have higher resolution, and dedicated devices are available that allow the measurement of the peripheral skeleton (radius and tibia) at high resolution (voxel size, 82 m). This allows us to study bone microstructure measures such as cortical thickness and trabecular number. In this issue of the JCEM, Farr et al (1) report on the changes in bone microstructure in response to MHT in women shortly after the menopause. They measured the radius using HR-pQCT over 4 years of treatment with MHT or placebo. They report significant effects of MHT (as compared to placebo) on volumetric BMD of the radius, significant for the cortical but not trabecular bone. The relative increase in cortical volumetric bone density was accompanied by a relative decrease in cortical porosity but no change in cortical thickness. The predominant effect of MHT on cortical bone was somewhat surprising because the fractures that result from postmenopausal osteoporosis usually occur at sites rich in trabecular bone, and estrogen deficiency is considered to be the principal cause of this trabecular bone loss. The introduction of HR-pQCT has extended our knowledge about bone modeling and bone loss across life and has given new insights into the basis of bone fragility. Particularly, these studies have shown that trabecular and cortical bone compartments behave differently during skeletal development and during aging. During skeletal development, trabecular modeling of the radius is completed at around the end of longitudinal growth at the end of puberty, but the cortex is still porous at the end of linear growth (ages 15–17 y). There is a significant decrease in radial cortical porosity between the end of adolescence and the end of the third decade (2). Cortical bone density remains stable from skeletal maturity to middle age, but there is some evidence that trabecular bone loss may begin in young adulthood, soon after skeletal maturity (thus before the menopause) (3). Trabecular bone at the radius is lost with aging, and the patternof lossdiffersbetweenmenandwomen.Menshow a decrease in trabecular thickness, and women show a decrease in trabecular number (3, 4). This may represent a greater rate of trabecular perforation in women. Trabecular microstructural properties in older women are associated with circulating estrogen levels (5). The extension of HR-pQCT to the study of cortical microstructure has demonstrated the importance of cortical bone loss in ageand menopause-related decrease in bone strength. At the radius, cortical porosity increases and cortical BMD decreases with age in men and women. However, the bone loss is more rapid in women than in
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call