Osteoporosis is frequently regarded as a complication associated with androgen deprivation therapy (ADT) in patients with prostate cancer. Nevertheless, a notably higher incidence of osteoporosis has been observed in prostate cancer patients even in the absence of ADT, when compared to age-matched healthy individuals. This phenomenon is likely attributable to the synergistic effects of aging, chronic inflammation, and tumor-related factors, which collectively contribute to accelerated bone loss in this population. Accumulating evidence has demonstrated that signaling pathways such as RANKL/RANK/OPG, Wnt, CXCL12/CXCR4, TGF-β, and IGF-1, play critical roles in both prostate cancer and osteoporosis. These pathways may provide potential targets for the concurrent treatment of the two diseases. Despite this, existing reviews have provided only limited examination of the overlapping molecular mechanisms underpinning both diseases. This review aims to elucidate the interplay between osteoporosis and prostate cancer, offering a comprehensive analysis of the shared signaling pathways implicated in the progression of both conditions. In addition, prevailing treatment strategies for the prevention of osteoporosis in prostate cancer patients are evaluated, and the potential for the development of dual-action pharmacological agents targeting the RANKL/RANK/OPG, Wnt, and CXCL12/CXCR4 pathways is discussed. These emerging approaches may yield more effective therapeutic modalities for individuals with prostate cancer.
Jiang et al. (Mon,) studied this question.