Oestradiol depletion in premenopausal women with breast cancer linked to bone structure decline
Oestradiol depletion in premenopausal women with early breast cancer who were treated with ovarian suppression (OS) plus aromatase inhibition (AI) endocrine therapy was associated with severely deteriorated cortical and trabecular microstructure in their bones, according to preliminary data of an ongoing study presented at the 6th Asia-Pacific Osteoporosis Meeting (IOF Regionals 2016) held in Singapore.
“[The] severe and perhaps irreversible microstructural deterioration and the longevity of these women suggest there is a need to investigate the role of early intervention to preserve bone strength,” said researchers from the Departments of Endocrinology and Medicine at Austin Hospital in Heidelberg, Victoria, Australia.
The case-control study enrolled 23 premenopausal cases (mean age 42.3 years) with breast cancer who were treated with OS+AI for a median duration 1.5 years, 42 healthy age-matched premenopausal women (mean age 44.4 years), and 35 healthy women who were 10 years post natural menopause (mean age 62.4 years). Women who had been on tamoxifen therapy for >6 months or prior bone-related therapy were excluded from the study. [IOF 2016, abstract P174]
Microarchitecture and matrix mineral density (MMD) of distal radius and tibia were assessed using high-resolution peripheral quantitative computed tomography.
OS+AI endocrine therapy for breast cancer led to more rapid oestradiol depletion than natural menopause, said the researchers.
Cases treated with OS+AI had higher cortical porosity in the distal radius in all measured outcomes of porosity including total cortex, compact cortex, outer and inner transitional zones, and lower MMD than premenopausal age-matched controls (p<0.001 for all).
Despite being almost two decades younger than women who were 10 years postmenopause, cases had similar cortical porosity in all measured outcomes mentioned above in the distal radius as postmenopausal controls. MMD was also significantly lower in premenopausal cases than postmenopausal controls (p<0.001).
In addition, trabecular bone volume (BV/TV) in the distal radius was 1.47 percent lower in cases compared with premenopausal controls (p=0.008), and 0.67 percent lower compared with postmenopausal controls (p=0.07), which was due to fewer but not thinner trabeculae.
Similar results were also seen for measurements in the tibia, according to the researchers, although these were not included in the presentation.
Previous studies have shown that oestrogen deficiency can increase bone remodelling rate by increasing the lifespan of osteoclasts while decreasing that of osteoblasts. (Endocr Rev 2000;21:115-137) The rapid remodelling will reduce MMD and eventually lead to severe microstructural deterioration, according to the researchers.