A mechanobiological hypothesis on bone cement-induced progression of bone metastases.

We propose the hypothesis that long-term alterations in the local biomechanical environment (a significant increase in stiffness and changes in stress distribution) induced by the implantation of bone cement for treating bone metastases may, by activating mechanotransduction pathways in tumor cells, potentially promote their proliferation, invasion, and therapy resistance, thereby affecting long-term disease progression. This effect is particularly noteworthy in specific patient populations with extended survival, low tumor burden, and radiosensitivity. For such patients without immediate structural instability risks, prioritizing non-invasive treatments like stereotactic radiotherapy can achieve effective symptom relief while avoiding the potential adverse biological effects associated with altering the bone's natural mechanical properties, which may lead to better long-term tumor control. This hypothesis does not challenge the critical role of bone cement in managing acute or impending pathological fractures. Instead, it advocates for a reassessment of its status as the "default" treatment option in certain specific patient populations, aiming to promote a more comprehensive balance between short-term symptom relief and long-term disease modulation in clinical decision-making.