1.Microfracture and osteoporosis
Various causes, including chronic renal failure, alcoholism, organ transplantation, systemic skin disease, metabolic endocrine abnormalities, neoplastic hematological disease and long-term application of corticosteroids, can cause the bone tissue to gradually decrease its resistance to external forces. Repeated microfractures can be followed by multiple microangiopathy, causing necrosis of the brittle and incompletely repaired bone tissue due to ischemia.
2. Hyperlipidemia and fat embolism
Long-term steroid treatment and alcohol abuse can cause hyperlipidemia and fatty liver. Clinical data show that most patients with femoral head necrosis are often complicated by fat metabolism disorders or fat embolism, so it is believed that fat embolism in bone overload with reduced fat clearance and intravascular coagulation is the likely pathogenesis of skin erosion.
3.Intravascular coagulation and osteonecrosis
The intravascular coagulation and thrombosis stimulated by various diseases, including fat embolism, is the intermediate mechanism that leads to osteonecrosis.
4.Lesions originating from arteries
Clinical study found that asymptomatic early necrosis cases femoral head medullary heart histological examination found that there is intra-medullary hemorrhage and small arterial wall muscle layer destruction, while no fat embolism and thrombosis in the lumen. This arteritis change is a very common lesion in cases of connective tissue disease and renal transplantation, and can also be the result of the direct destructive effect of steroids on the vessel wall.
5. Progressive ischemia theory
In addition to the obstruction of intramedullary vessels due to various reasons, the deterioration of intraosseous blood circulation can be aggravated by extravascular compression due to steroid-induced hypertrophy of intramedullary adipocytes, tissue edema due to bone tissue hypoxia, abnormal cell infiltration, intramedullary cell proliferation and intramedullary hemorrhage. All intraosseous vessels are thin-walled vessels, and the whole is buried in the hard bone canal. The intraosseous volume is constant, with no room for concession, and is an interstitial compartment that cannot be expanded. Both internal and external compression of the intramedullary vessels and their secondary changes can block the outflow of the bone marrow veins and increase the intramedullary pressure. It can also lead to insufficient blood supply to the bone due to reflex spasm of the nutrient artery of the bone, which further aggravates the circulatory disorder of the bone and leads to bone necrosis. The rationale for treating this disease with medullary decompression is to attempt to interrupt the above vicious cycle, improve venous outflow, descend the medullary cavity filling, and thus promote the recanalization of necrotic trabeculae.
1. Microfracture and osteoporosis
Various causes, including chronic renal failure, alcoholism, organ transplantation, systemic skin disease, metabolic endocrine abnormalities, neoplastic hematological disease and long-term application of corticosteroids, can cause the bone tissue to resist the effect of external forces to gradually diminish. Repeated microfractures can be followed by multiple microangiopathy, causing necrosis of the brittle and incompletely repaired bone tissue due to ischemia.
2. Hyperlipidemia and fat embolism
Long-term steroid treatment and alcohol abuse can cause hyperlipidemia and fatty liver. Clinical data show that most patients with femoral head necrosis are often complicated by fat metabolism disorders or fat embolism, so it is believed that fat embolism in bone overload with reduced fat clearance and intravascular coagulation is the likely pathogenesis of skin erosion.
3.Intravascular coagulation and osteonecrosis
The intravascular coagulation and thrombosis stimulated by various diseases, including fat embolism, is the intermediate mechanism that leads to osteonecrosis.
4.Lesions originating from arteries
Clinical study found that asymptomatic early necrosis cases femoral head medullary heart histological examination found that there is intra-medullary hemorrhage and small arterial wall muscle layer destruction, while no fat embolism and thrombosis in the lumen. This arteritis change is a very common lesion in cases of connective tissue disease and renal transplantation, and can also be the result of the direct destructive effect of steroids on the vessel wall.
5. Progressive ischemia theory
In addition to the obstruction of intramedullary vessels due to various reasons, the deterioration of intraosseous blood circulation can be aggravated by extravascular compression due to steroid-induced hypertrophy of intramedullary adipocytes, tissue edema due to bone tissue hypoxia, abnormal cell infiltration, intramedullary cell proliferation and intramedullary hemorrhage. All intraosseous vessels are thin-walled vessels, and the whole is buried in the hard bone canal. The intraosseous volume is constant, with no room for concession, and is an interstitial compartment that cannot be expanded. Both internal and external compression of the intramedullary vessels and their secondary changes can block the outflow of the bone marrow veins and increase the intramedullary pressure. It can also lead to insufficient blood supply to the bone due to reflex spasm of the nutrient artery of the bone, which further aggravates the circulatory disorder of the bone and leads to bone necrosis. The rationale for treating this disease with medullary decompression is to interrupt the above vicious cycle, improve venous outflow, and reduce marrow congestion, thus promoting the revascularization of necrotic trabeculae.