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After menopause, remodeling becomes unbalanced and rapid. Each of the many remodeling transactions deposits less bone than it resorbed, producing microstructural deterioration. Trabecular bone is said to be lost more rapidly than cortical bone. However, because 80% of the skeleton is cortical, we hypothesized that most menopause-related bone loss and changes in bone microstructure are cortical, not trabecular in origin, and are the result of intracortical remodeling. Distal tibial and distal radial microstructure were quantified during 3.1 years (range, 1.5 to 4.5 years) of follow-up using high-resolution peripheral quantitative computed tomography and StrAx software in 199 monozygotic and 125 dizygotic twin pairs aged 25 to 75 years in Melbourne, Australia. The annual increases in tibial cortical porosity accelerated, being 0.44%, 0.80%, and 1.40% in women remaining premenopausal, transitioning to perimenopause, and from perimenopausal to postmenopause, respectively. Porosity increased in the compact-appearing, outer, and inner transitional zones of the cortex (all p<0.001). The annual decrease in trabecular bone volume/tissue volume (BV/TV) also accelerated, being 0.17%, 0.26%, and 0.31%, respectively. Little bone loss was observed before menopause. The reduction in BV/TV was due to a decrease in trabecular number (p<0.001). The greatest bone loss, 7.7mg hydroxyapatite (HA) annually, occurred in women transitioning from perimenopausal to postmenopause and of this, 6.1mg HA (80%) was cortical. Results were similar for the distal radius. Despite microarchitectural changes, no significant bone loss was observed before menopause. Over 90% of appendicular bone loss occurs during and after menopause, over 80% is cortical, and this may explain why 80% of fractures are appendicular.


Mary MacKillop Institute for Health Research

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Journal Article

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