Breast cancer and osteoporosis are both diseases of aging. The "one in eight" lifetime risks of breast cancer occur primarily in the sixth, seventh, eighth, and ninth decades of life. One-third of postmenopausal women will experience an osteoporotic fracture. It is the coalescence of osteoporosis, breast cancer, and breast cancer treatments that, in some cases, increases the risks of osteoporotic fracture. That makes it imperative to assess risk factors, screen, and prevent or treat osteoporosis in postmenopausal women with breast cancer. Osteoporosis is primarily a genetic disease with a few modifiable risk factors. These risk factors include greater than two to three alcoholic drinks per day, current smoking, and decreased physical activity. The standard screening tool for osteoporosis is dual-energy x-ray absorptiometry (DXA) that gives a readout of T-scores of the lumbar spine, total hip, and femoral neck. The T-score is the number of standard deviations (SD) above or below the mean bone mineral density (BMD) of an average young adult of the same sex. For every SD below the mean BMD, the fracture risks double. Osteoporosis prevention and treatment do not differ in women with or without breast cancer. The difference is in breast cancer treatments, such as aromatase inhibitors (AI), which cause two to three-fold higher bone loss than average postmenopausal bone loss. Two classes of drugs for osteoporosis are oral and intravenous (iv) bisphosphonates and the receptor activator of nuclear factor kappa B ligand (RANKL) ligand inhibitor, subcutaneous (sc) denosumab. All three prevent bone loss and reduce the likelihood of fragility fractures. The treatment choice depends upon patient and provider preferences, specific contraindications (e.g., renal insufficiency), compliance, and costs. Despite guidelines and algorithms for AIinduced bone loss, the screening and treatment of osteoporosis remain suboptimal in postmenopausal women with breast cancer.
KeywordsOsteoporosis; breast cancer; postmenopausal women Table 4 Major Trials of Anti-Resorptive Drugs in Aromatase inhibitor-induced Bone Loss. Trial Treatments n Results (L/S BMD) † p-value Ref Brufsky ZA 4 mg iv q6 mo for 1 yr vs. delayed 502 2.0 vs. −2.5 <0.001 [59] Coleman ZA 4 mg iv q6 mo for 5 yrs vs. delayed 1065 4.3 vs. −5.4 <0.0001 [60] Ellis DEN 60 mg sc q6 mo for 2 years vs. placebo 262 6.0 vs. −1.6 <0.0001 [61] Gnant DEN 60 mg sc q6 mo for 5 years vs. placebo 3425 HR fractures = 0.50 95% CI 0.39-0.65 <0.0001 [62] Van Poznak Risedronate oral 35 mg/week for 2 years vs. placebo 111 2.2 vs. −1.85 <0.0001 [63] Sestak Risedronate oral 35 mg/week for 3 years vs. placebo 150 1.1 vs. −2.6 <0.0001 [64]Abbreviations: Zoledronic acid (ZA); denosumab (DEN); hazard ratio (HR); †percentage change in the lumbar spine per year.