Periosteal reaction, also known as periosteal hyperplasia, is an increase in bone growth caused by stimulation of the periosteum and increased activity of osteoblasts in the inner layer of the periosteum, which usually indicates the presence of a lesion. Histologically, an increase in osteoblasts in the inner layer of the periosteum is seen, by new bone trabeculae. The periosteal reaction is not specific and is commonly seen in inflammation, tumors, trauma, and subperiosteal hemorrhage, as well as in normal growth and developmental stages. Diagnosis: 1. Periosteal edema Most studies have demonstrated that periosteal edema is an important sign to determine the presence of occult fractures and early occult fractures. t2WI and enhanced T1WI of MRI can clearly demonstrate periosteal edema, a linear high signal shadow next to the bone cortex. MRI dynamic enhancement scans of the lesion can also obtain a time-signal intensity profile of the edematous periosteum, i.e., the periosteum begins to gradually strengthen within 40 seconds of contrast injection, followed by a peak in strengthening. Pathologically, the edematous periosteum is seen to be lax in structure, with enlarged gaps in the collagen fibril bundles and no significant changes in the cell-forming layer. Periosteal edema often occurs in conjunction with bone marrow edema and peripheral soft tissue edema, and the mechanism may be congestive edema. In animal models of bone tumors, periosteal edema was seen within 15 days after implantation of the tumor in the bone marrow cavity, and during the late growth of the tumor, periosteal edema was also seen in the normal areas adjacent to the tumor, which is consistent with what is seen in clinical bone tumor cases. Therefore, it is believed that periosteal edema is an early periosteal reaction before the formation of new bone in the periosteum. With the development of lesion, pathological exudate and tumor tissue travel along volkmann’s canal to subperiosteum and lift up the periosteum, and stimulate periosteal proliferation and thickening. On MRI, the thickened periosteum is a linear shadow similar to soft tissue signal on T1WI and a higher signal linear shadow on T2WI (Figure 2a), which can be significantly enhanced. x-ray plain film cannot show periosteal thickening. Histologically, cellular hyperplasia of the inner and outer layers of the periosteum is seen, characterized by changes in the number and morphology of cells in the cell-forming layer, as well as thickening of the outer fibrous bundles. The mechanism of periosteal thickening is the transformation of the outer fibrous layer of the periosteum from surrounding soft tissues such as fascia, fat, and muscle, and the transformation of fibroblasts in the fibrous layer into osteoprogenitor cells through enlarged nuclei and increased cytoplasm, with further enlargement of the osteoprogenitor nuclei and mitosis to form a cell-forming layer with bone matrix-secreting cells. Periosteal thickening occurs prior to the formation of periosteal new bone, and a thickened periosteum is always seen covering the surface of periosteal new bone during the process of continuous formation of periosteal new bone. Therefore, periosteal thickening is both an early periosteal abnormality before the formation of periosteal new bone and a necessary preparation for the continuous formation of periosteal new bone. The destruction of periosteal bone is a common x-ray sign of malignant tumor. After the tumor destroys the periosteal bone, it can also destroy the periosteum. In the dynamic observation of the animal model of bone tumor, it was found that the bilayer structure of periosteum was not eroded by tumor at the same time, but the inner cell-forming layer of periosteum was replaced by tumor cells first, while the collagen fiber layer remained intact, which was shown as tumor pseudo-envelope on MRI. When the tumor continues to grow, the fibrous layer is destroyed and the periosteum is completely interrupted locally. The tumor invades into the surrounding fat and muscle from the interrupted periosteum, and then MRI can show the incomplete periosteum. This result is consistent with the “pseudo-envelope” that separates the tumor from normal tissues after the tumor breaks through the bone cortex in clinical bone tumor cases, which can be considered as the periosteal fibrous layer that has not been destroyed. Although whether the periosteum is invaded or not is not a clear indication of the prognosis of the tumor, the periosteum and periosteal new bone separating the diseased tissue from the normal tissue may have the effect of stopping and slowing down the growth of the tumor. The periosteal changes that can be observed by imaging scholars are not limited to the post-osteogenic stage, but include periosteal edema, periosteal thickening and periosteal destruction, which cannot be shown by conventional radiographs without calcification or inconspicuous calcification. If the term “periosteal reaction” is still equated with “periosteal new bone”, it cannot fully describe the various periosteal changes shown by modern imaging. Therefore, we propose to use “periosteal new bone” to represent the traditional “periosteal reaction” and “periosteal reaction” to represent periosteal edema, periosteal thickening and periosteal destruction that cannot be shown by x-ray. The “periosteal abnormalities” include periosteal reaction and periosteal new bone, so as to achieve a comprehensive and accurate description of periosteal changes.