Bone marrow edema syndrome is a relatively rare and self-limiting disease of unknown etiology. 1959 Curtis and Kincaid first reported three cases of pregnant women with hip pain in the last trimester of pregnancy and diffuse osteoporosis of the femoral neck on imaging, which they called temporary demineralization of the hip. 1968 Lequesne named it temporary osteoporosis and Banas et al. In 1968, Lequesne named it temporary osteoporosis, while Banas et al. called it regional migratory osteoporosis, and later many other names emerged, such as migratory osteolysis, painful joint atrophy, and bone marrow edema syndrome. The confusion of names reflects the lack of understanding of this disease. The term “bone marrow edema” was first used by Wilson et al. because MRI could show abnormal signals in the bone marrow before the abnormalities on radiographs. It is believed that bone marrow edema does not necessarily develop into osteoporosis on radiographs, and in many cases bone marrow edema does not migrate, so the term “bone marrow edema syndrome” seems to be more accurate than temporary osteoporosis or migrating osteoporosis, and has become a more common name. In 1969, Duncan et al. first reported myeloid edema syndrome in multiple joints, including the knee. Currently, it is not uncommon to see osteoarthritis or meniscal and articular cartilage damage in the knee joint, resulting in misdiagnosis and mismanagement. This article provides a review of the bone marrow edema syndrome of the knee, with the aim of raising awareness and attention. The literature on bone marrow edema syndrome of the knee is mostly case by case, with Fertakos et al. and Wambeek et al. each reporting a case in which the bone marrow edema first occurred in the medial femoral condyle and then migrated to the lateral femoral condyle. Stamp et al. reported a case of bone marrow edema in both knees in a woman in late pregnancy, and Ma et al. reported a case of bone marrow edema in the hip followed by bone marrow edema in the knee and ankle, also in a woman in late pregnancy. The bone marrow edema occurred only in the knee joint. The clinical manifestations of knee bone marrow edema syndrome are not specific, but mainly consist of knee pain and pressure, ranging from mild to moderate, with generally normal joint mobility. Patients usually have no history of trauma. X-rays are usually unremarkable in the early stages of the disease and may show limited or diffuse osteoporosis as the disease progresses. MRI is a specific method for the diagnosis of bone marrow edema because it can detect abnormalities at an early stage, and is characterized by low signal in T1WI and irregular areas of high signal in T2WI, with generally poorly defined borders and a heterogeneous distribution of abnormal signal intensity. The etiology of knee bone marrow edema syndrome remains unclear, with Curtis and Kincaid hypothesizing that it is due to neurovascular compression and some suggesting reflex sympathetic dystrophy. However, Banas refuted this view and suggested that reflex sympathetic dystrophy is usually seen after trauma, mostly in the upper extremities, but rarely in the hip and knee joints. These clinical features are not consistent with the manifestations of bone marrow edema syndrome. Earlier, it was speculated that bone marrow edema may be caused by local stasis due to obstruction of venous return. Dunstan et al. suggested that local ischemia causes necrosis of fat and hematopoietic stem cells in the bone marrow, but does not involve bone cells, as a way to distinguish it from osteonecrosis, and this theory is now more supported. In contrast, McCarthy et al. found through histological studies that bone marrow edema in the bone marrow cavity was accompanied by reactive bone formation, but no signs of osteoclastic resorption, fat necrosis, or osteonecrosis were seen, bone morphometry did not reveal osteoporosis, and reduced hydroxyapatite content could explain the reduced bone density on X ray. Although histological studies can objectively reveal the pathological mechanisms of the disease, they are limited by their invasive nature, which is difficult for patients to accept. Only a few case biopsy histological studies have been reported in the national and international literature. In addition Rodriguez et al. reported that myeloid edema syndrome is associated with vitamin C deficiency, which has attracted attention. The exact etiology of bone marrow edema syndrome of the knee joint still needs further study. In recent years, some people have discussed post-traumatic subchondral fractures also under the umbrella of myeloid edema syndrome. The author believes that myeloid edema syndrome is different from traumatic myeloid edema, and the former is not caused by trauma, whereas myeloid edema caused by trauma is usually called bone contusion, which has been described in a separate article by the author [18]. However, it is difficult to distinguish patients with subchondral fractures or bone contusions due to osteoporosis, even without significant trauma. In addition, the disease should be differentiated from osteoarthritis, joint infections, peripheral neuropathy, soft tissue injuries, and osteonecrosis. It is not very difficult to diagnose osteoedema syndrome with a detailed history (presence of trauma), careful physical examination, and careful reading of films (especially MRI films). Usually there is no history of trauma in osteoedema syndrome of the knee, and MRI examinations are usually not accompanied by abnormalities of articular cartilage, menisci and ligaments, except for abnormalities of the bone marrow. In contrast, osteoarthritis is based on articular cartilage disease, and MRI can show abnormal signals close to the articular cartilage, especially in T1-weighted images. Treatment of osteoarthritis consists of protective weight-bearing or non-weight-bearing braking for the first 1-2 weeks of the disease, and symptomatic pain management. There is no evidence that weight bearing aggravates the disease or causes poor prognosis. Some authors have applied diphosphonates, calcitonin, and glucocorticoids to treat bone marrow edema syndrome of the hip with good results, but there is less literature on pharmacologic treatment of the knee, which could theoretically be applied to the knee as well, but clinical confirmation is needed. Theoretically, these methods can also be applied to the knee, but clinical evidence is needed. Inspired by the treatment of femoral head necrosis, many authors have applied core decompression to treat hip oedema syndrome, which also provides rapid pain relief and normalizes MRI images within 3 months. All of these authors concluded that the benefits of medullary core decompression outweighed the disadvantages. In contrast, Guerra et al. concluded that decompression therapy was not necessary because of the good prognosis of myeloid edema syndrome. The authors believe that choosing the right patient with significant pain and unsatisfactory conservative treatment can lead to decompression therapy, which can provide rapid pain relief through minimally invasive decompression therapy (e.g., arthroscopic or percutaneous decompression) and is still desirable from a health economics perspective. Of course, if the symptoms are mild and conservative treatment is effective, decompression therapy is not always necessary. In general, the prognosis of myeloid edema syndrome is good. Regardless of conservative or surgical treatment, it can be basically cured (clinical symptoms disappear and MRI images return to normal) after 3-6 months.