Bone Fragility After Breast Cancer Therapy (#52)
Breast cancer is the most common cancer among women worldwide. As survival continues to improve, preserving bone health has become an increasingly important aspect of survivorship. Bone fragility is a major complication in both early and metastatic breast cancer, in part arising from the effects of cancer therapies. Hormone receptor-positive early breast cancer is commonly treated with aromatase inhibitors (AIs), tamoxifen and ovarian function suppression. AI therapy accelerates bone remodelling and bone loss and increasing fracture risk, while tamoxifen exerts contrasting skeletal effects depending on menopausal status.
Current approaches to fracture prevention include clinical risk factor review, bone mineral density (BMD) assessment, optimising diet and exercise, in addition to antiresorptive therapy. In early breast cancer, zoledronic acid is recommended for women receiving ovarian suppression to reduce treatment-induced bone loss. In metastatic breast cancer, denosumab or zoledronic acid are used to prevent skeletal-related events. However, important challenges remain, including accurate assessment of fracture risk across a woman’s lifespan, optimal bone health assessment and management after AI completion, and optimal transition from denosumab to a bisphosphonate if denosumab cessation is planned.
Future research is necessary to examine fracture prediction using breast cancer-specific risk assessment tools, identifying novel predictors of bone fragility, defining optimal duration and sequencing of antiresorptive therapy as well as use and safety of romosozumab. An additional research priority is atypical femoral fractures (AFFs), a rare but serious complication associated with prolonged BMA exposure. Ongoing work is investigating the incidence, risk factors and imaging characteristics of AFFs in breast cancer populations to inform prevention strategies, optimise surveillance, and improve long-term skeletal outcomes.
ANZBMS 2026