Idiopathic femoral head necrosis
Idiopathic femoral head necrosis, also known as ischemic femoral head necrosis, is a common disease. The causes of femoral head necrosis are varied, but the common pathological mechanism is bone tissue ischemia, so the pathogenesis and blood supply obstruction theory are the most easily accepted. This theory believes that due to various pathogenic factors inside and outside the bone, the nutrient blood flow to the bone tissue is reduced, the intraosseous vascular network is compressed, or the outflow vein is blocked, resulting in local blood supply obstruction. In severe cases, it can cause ischemic necrosis of bone tissue. At the beginning of the disease, it may only manifest as damage to a single major blood vessel. As the disease progresses, if the residual circulating blood volume is insufficient to maintain the normal blood supply needs of bone cells in the damaged area, the bone marrow tissue will be damaged first, followed by osteocyte necrosis. Pathological examination shows the phenomenon of emptiness in the bone lacuna caused by the lack of cellular components. Those with a small range of lesions can usually heal spontaneously and are difficult to detect clinically. Repeated physiological repair activities cause bone tissue hardening in the lesion area. For patients with a larger lesion range, only the necrotic bone tissue around the lesion is often replaced by new bone tissue, while the necrotic cancellous bone in other parts is covered by new bone tissue, which prevents the possibility of further growth of new bone tissue for replacement and repair. As the disease progresses, the subchondral bone plate and articular surface eventually collapse. The joint space is narrowed, and the bone tissue shows typical osteoarthritis changes such as cystic changes and sclerosis, and the joint is completely destroyed. Therefore, the key to treating idiopathic femoral head necrosis is early diagnosis and early treatment to promote local vascular regeneration, restore normal circulation and prevent articular surface collapse.