Major advances in oncology have led to significant improvements in survival and remission rates across many cancers. These therapeutic advances, however, are associated with adverse effects on bone, collectively termed cancer treatment-induced bone loss (CTIBL). Bone loss associated with anticancer therapies results from a combination of preexisting risk factors, the impact of the malignancy itself, and the direct or indirect effects of treatments on bone remodeling. The underlying mechanisms include therapy-induced hypogonadism, direct cellular toxicity on osteoblasts and osteoclasts, nutritional and digestive disturbances, and chronic inflammation. Clinically, CTIBL manifests as an early and accelerated decline in bone mineral density (BMD), greater than that observed in the general population, and an increased risk of osteoporotic fractures, particularly documented with endocrine therapy for breast and prostate cancers, glucocorticoids, and potentially immunotherapy. Conversely, certain targeted therapies, such as proteasome inhibitors, may exert partial protective effects on bone. Prevention requires a multidisciplinary approach involving both oncology and rheumatology: correction of nutritional deficiencies, calcium and vitamin D supplementation, promotion of physical activity, and the use of antiresorptive treatments (bisphosphonates, denosumab), whose efficacy in preserving BMD and reducing fracture risk is well established. Early attention to bone health at the initiation of anticancer therapies is essential to reduce fracture-related morbidity and improve patients’ quality of life.