There are many names for this disease, but Gorham-Stout syndrome or massive osteolysis is the more appropriate name. So far, it is difficult to count the number of cases reported in the literature. From the reports, it is basically an individual case and should be a rare disease. There is no significant gender difference in Gorham-Stout syndrome. It occurs in a wide range of ages, with most patients developing the disease in their youth. Any bone can be involved, commonly the trunk bones and long tubular bones, such as the pelvis, ribs, scapula, femur, etc. The lesions can be solitary and transcend joints and multiple lesions. Trauma is not directly related to the onset of the disease, and some patients are found to have lesions as a result of trauma visits. No family history of the disease has been reported. The present data support the opinion of most scholars that the disease has a slow onset and a long course, which can last for decades, with self-limiting progression to a certain stage, often over a year and often taking several years, with unforeseen self-cessation. Some scholars [6,7] have also discussed the invasion of vital organs, poor healing and critical life in severe cases, and even some scholars believe that most patients die in about a year and survive up to 4 years. More examples are needed to demonstrate the healing of this disease, and it is important to strengthen the follow-up and follow up. Second, the etiology and pathogenesis of the disease is still not very clear, and may be related to the following factors. First, genetic, traumatic and other factors cause disorders in the differentiation and regulation of osteoclasts, with an increase in highly active osteoclasts and osteoclast precursors [9], or an increase in the sensitivity of these cell precursors to humoral factors such as calcitonin secreted by thyroid C cells. Second, the presence of hemangioma or lymphoma of bone leads to bone resorption, a view supported by many scholars. There are also dissenters in recent years, with studies such as Ricalde [11] finding no association with genetics, metabolism, immunity, or tumor, and KawSaki [12] suggesting that some cases do not have abundant vascular tissue. Regardless of the debate on the etiology, the overall pathological change is the process of bone resorption, which, as in osteoporosis, is influenced by many factors and is extremely complex.DicKson studied alkaline phosphatase and acid phosphatase in the ultrastructure of tissue sections of patients, and the results indicated that the two enzymes may contribute to the imbalance between bone formation and resorption. Also acid phosphatase biochemistry indicates that mononuclear macrophages, multinucleated osteoblasts and vascular endothelial cells are associated with bone resorption. Gorham also demonstrated that congestion, pH changes, mechanical forces, and trauma producing granulation tissue can cause resorption without an increase in the number of osteoclasts. Clinical manifestations There is mild pain and swelling at the lesion site and corresponding dysfunction, and the local skin is generally unchanged. Lesions located in the thoracic vertebrae, clavicle, lower ribs, or invasion of the thoracic duct may cause celiac disease, hemothorax, and systemic symptoms such as anemia and malnutrition [14]. There are no special complications, and the blood biochemical examination is usually normal. In the early stage, osteoporosis appears in the medullary cavity and subcortex, with speckled or small foveal translucent areas, followed by fusion and enlargement to indistinct boundaries. The lesion further develops with thinning of the bone cortex, collapsing into the medullary cavity, thinning of the bone, and finally loss of bone or defect [4], without sclerosis, periosteal reaction or new bone around the lesion, without bone crust growth in the pathological fracture, without soft tissue masses, and without multiple lesions across the joint and into adjacent bone. Pathological examination In pathological sections, the basic manifestation is tumor-like extensive proliferation of connective tissue containing capillaries instead of bone tissue, with sinus-like or sponge-like vessels. The vessel wall is composed of a single layer of flattened endothelial cells and filled with blood cells. Some authors [15] suggest that typically the bone cortex is thin and the medullary cavity is empty. Microscopic atrophy of the trabeculae is replaced by proliferating connective tissue, which is interspersed with proliferating lacunar vessels that branch and interconnect into grooves. Few osteoclasts were found, although some osteoblasts were found and no new bone appeared. Inflammatory cell infiltration was rare, mostly lymphocytes, plasma cells and neutrophils, and no malignant neoplastic cells. Diagnosis and differential diagnosis: Diagnostic points: 1. Local pain and corresponding functional limitation, generally no systemic symptoms. 2.Blood biochemical examination is within the normal range. 3.X-ray film with bone resorption, no periosteal reaction. 4, Pathology with vascular and fibrous connective tissue hyperplasia and bone loss. This disease is differentiated from the following diseases. Chronic septic osteomyelitis: there is usually a history of acute inflammation; local and systemic inflammatory symptoms, mostly dead bone, sinus tracts and new bone. Sodeck’s syndrome (post-traumatic reactive bone atrophy): local history of trauma, osteoporosis on imaging, and intact bone cortex. Hyperparathyroidism: elevated blood calcium, decreased blood phosphorus, increased urinary calcium and urinary phosphorus, calcification of soft tissue around bone resorption areas, often with urolithiasis, parathyroid hyperplasia or adenoma. Bone hemangioma, cystic lymphadenoma of bone, bone cyst: limited lesions, no progressive osteolysis, mostly with bone expansion and osteogenic reaction. Bone and joint tuberculosis: mostly seen in a single joint, usually with systemic symptoms, blood clots, and cold cysts. Various benign and malignant bone tumors: local mass with tumor bone, malignant with heavy local symptoms, may have systemic symptoms, special imaging changes. Myeloma blood biochemistry and bone marrow aspiration have specificity. Bone metastases may have a primary focus, heavy pain, and pathology to confirm the final diagnosis. Idiopathic osteolysis: similar name, with chronic bone resorption, highly misdiagnosed. The disease is divided into hereditary and non-hereditary, fatal nephropathy, mainly invades the fingers, toes, wrists and ankles and presents with ulceration, often with other congenital malformations. In the literature, a total of 13 out of 37 patients in 4 generations of a family have been reported to have chromosomal dominant inheritance. Most patients receive surgery and radiotherapy. If the lesion is not large in scope, it is expected to improve and be cured by bone cutting and bone grafting or prosthesis replacement, but the lesion should be removed completely, otherwise it is also easy to recur. If the lesion is in the lower extremity, it is not easy to repair, amputation and prosthesis can also be considered. Some parts can be protected by stents. Stöve] reported a patient who chose 40Gy dose of radiation therapy, which can make the pain relieved and osteolytic destruction temporarily stopped. Recently, calcitonin and bisphosphonates have been used to inhibit osteolytic activity. Gorham-Stout syndrome is rare, of unknown etiology, spontaneous and self-limiting. The clinical symptoms are atypical, and the X-ray shows osteolytic destruction, which is highly misdiagnosed. On the basis of pathological histology, the diagnosis needs to be confirmed by combining clinical manifestations and imaging data, and excluding other bone resorption diseases. In this case, the patient was treated with third-generation bisphosphonates orally, and the clinical symptoms were relieved. Whether this class of drugs is effective in preventing the process of osteolysis remains to be further observed and demonstrated.