Anti-osteoporosis drugs and reduction of mortality in cancer patients

Abstract

Osteoporosis and cancer share a complex relationship, with each condition influencing the progression and outcomes of the other.1 Multiple factors, such as chemo- and hormonal therapies, and the direct invasion of bone tissue by malignant cells contribute to the accelerated bone loss seen in cancer patients.1 Various anti-osteoporosis drugs, including anti-resorptives such as bisphosphonates, denosumab and selective estrogen receptor modulators (SERMs), and anabolic agents such as teriparatide and romosozumab have demonstrated efficacy in preventing bone loss and reducing fracture risk in non-cancer populations. These medications exert their effects through different mechanisms, such as inhibiting osteoclast activity, modulating hormonal pathways or promoting bone formation.2 However, their effectiveness in cancer patients remains an area of ongoing research and debate. The interplay between cancer-related bone loss and the actions and potential benefits of anti-osteoporosis drugs is complex. The plausible biological mechanisms underlying the observed benefits of anti-osteoporosis drugs in cancer patients with osteoporotic fractures warrant exploration. Beyond their direct effects on bone density, these medications may influence the tumour microenvironment, immune response, and the release of factors that affect cancer progression.1,3