This review systematically analyzes the bidirectional regulatory role of disulfidptosis in orthopedic diseases for the first time: on one hand, in degenerative conditions such as intervertebral disc degeneration and osteoporosis, the nutrient-deprived microenvironment may exacerbate cell loss by activating the disulfidptosis pathway; on the other hand, the dependency of malignant tumors like osteosarcoma on SLC7A11 can be transformed into a therapeutic target, enabling selective killing through the induction of disulfidptosis. This evidence concerns the gene SLC7A11 and Intervertebral disk degeneration.