The pathophysiology of medication-related osteonecrosis of the jaw (MRONJ) is associated with microcirculatory dysfunction, direct toxicity to osteoblast, osteoclast and bone marrow stromal cells (BMSCs), bacterial infection, related factors, immune dysfunction, and transforming growth factor-beta (TGF-β1) pathway. MRONJ and osteoradionecrosis of the jaw (ORN) shared some histological characteristics, suggesting that improving blood flow, increasing blood supply to the lesion and regulating TGF-β1/BMP signaling can improve osteonecrosis of the jaw, thus PTX as non-selective PEDs inhibit, which can significantly improve microcirculation of ORN and anti-fibrotic drugs, have also similar preventive and therapeutic effects on MRONJ. However, as to whether PTX can treat and prevent phosphorous necrosis of the jaw(PNJ) remains to be further studied.