Cancer-Associated Osteoporosis and Treatment-Induced Bone Loss: Mechanisms, Prevention, and Therapeutic Strategies

Abstract

Background. Cancer-associated osteoporosis and cancer treatment-induced bone loss (CTIBL) are important causes of skeletal morbidity. Fracture risk reflects the interaction of treatment-related bone loss, endocrine disruption, and deterioration of the muscle–bone unit and may not be adequately captured by bone mineral density (BMD) alone.

Aim. To critically synthesize current evidence on the mechanisms, risk assessment, prevention, and treatment of cancer-associated osteoporosis and CTIBL.

Material and methods. A narrative review of international guidelines, randomized trials, systematic reviews, meta-analyses, and key observational studies was conducted.

Results. Aromatase inhibition and androgen deprivation are major drivers of CTIBL, with additional risk from glucocorticoids, gonadal dysfunction, sarcopenia, and physical deconditioning. Management requires integration of BMD with clinical and treatment-specific fracture risk. Bisphosphonates and denosumab remain the principal pharmacological strategies, while structured exercise complements treatment by targeting the muscle–bone unit. Treatment selection, safety, and appropriate therapeutic sequencing are essential for effective fracture prevention.

Conclusions. Cancer-associated skeletal fragility should be regarded as a dynamic, treatment-modified fracture-risk state rather than a BMD-defined complication. Integrating treatment-specific risk assessment, bone-directed therapy, and preservation of musculoskeletal function provides a coherent framework for fracture prevention throughout cancer care.