本综述旨在揭示乳腺癌和前列腺癌患者在接受激素剥夺疗法（HDTs）过程中，体成分的改变是骨脆性发生的关键，而机制基于骨质的改变而非骨量。临床前和临床数据表明，通过多种可溶性介体，骨骼、脂肪和肌肉组织之间存在紧密联系，可能导致（1）骨质量恶化的肥胖性肌营养不良患者的骨吸收和骨质量恶化，（2）健康锻炼人群的骨矿物质沉积。接受HDTs治疗的癌症患者常常处于第一种情况，称为骨肌肉不良性肥胖。目前的临床指南主要侧重于骨密度（BMD）作为主要预测骨折风险的因素，以预防治疗引起的骨质疏松症；然而，HDTs诱导的骨脆性的病理生理学与原发性和绝经后骨质疏松症的不同，暗示骨质量变化起主导作用。基于临床试验的现有数据，我们在本综述中建议将骨肌肉不良性肥胖作为HDTs相关代谢和骨骼并发症的常见目标，超越以BMD为中心的方法。©2023. 作者。

This review paper is intended to show that changes in body composition are key in the pathogenesis of bone fragility amongst patients with breast and prostate cancer receiving hormone deprivation therapies (HDTs) and that the mechanism is based on the development of alterations in bone quality rather than in bone quantity.Preclinical and clinical data suggest a tight connection amongst bone, adipose and muscular tissues by means of several soluble mediators, potentially leading to (1) bone resorption and bone quality deterioration in sarcopenic obese subjects, (2) bone mineral deposition in healthy trained subjects. Cancer patients treated with HDTs frequently fall into the first condition, named osteosarcopenic obesity. Current clinical guidelines for the prevention of treatment-induced osteoporosis focus on bone mineral density (BMD) as a main predictive factor for fracture risk; however, the pathophysiology underlying HDT-induced bone fragility differs from that of primary and postmenopausal osteoporosis, suggesting a prevalent role for bone quality alterations. Focusing on available data from clinical trials, in our review we suggest osteosarcopenic obesity as a common target for the prevention and treatment of HDTs-related metabolic and skeletal complications, beyond a BMD-centred approach.© 2023. The Author(s).