Femoral head necrosis is the end result of impaired blood supply to the femoral head due to different causes. It has attracted more and more attention from orthopedic surgeons because it causes hip pain, serious dysfunction, high disability rate, and is more difficult to treat. At the same time, the incidence of femoral head necrosis has been increasing year by year in recent years, which also makes it one of the common clinical diseases. The disease was not recognized by medical workers until the beginning of this century. With the progress of science and technology. People began to the causes and mechanisms of the disease from macroscopic perceptual understanding and research into biochemical and other, pathological microscopic changes in the exploration.
First, the etiology of femoral head necrosis
The root cause of femoral head necrosis is the damage to the blood flow of the femoral head. According to the pathogenesis can be divided into two categories: one is traumatic femoral head necrosis, which is caused by the sudden interruption of blood flow to the femoral head, such as femoral neck fracture, hip dislocation, hip trauma, etc. can directly or indirectly damage the blood flow to the femoral head, resulting in ischemic necrosis of the femoral head; the other category is non-traumatic femoral head necrosis, which is more common. There are many factors that cause non-traumatic femoral head necrosis, some of which are clearly related to femoral head necrosis, while others are vague, with only case reports, and some with unclear etiology are called idiopathic femoral head necrosis. Common pathogenic factors include: massive application of hormones, long-term alcoholism, kidney transplantation, chronic liver disease, diving disease, sickle cell anemia, pancreatitis, hyperlipidemia, gout, radiation disease, arteriosclerosis and other vascular stenosis disorders, collagen diseases, etc.
1, hip trauma femoral neck fracture, sprain, fall, hip dislocation can occur femoral head necrosis. Take femoral neck fracture as an example: the time of its occurrence is generally considered to be within 3 years after the fracture of the vast majority, and at present, according to the clinical diagnosis mainly based on x-ray photo performance, the earliest can be 1.5 months after the injury that is, 98% occurred within 5 years. Hip injury (including hip dislocation, femoral neck fracture, rotor fracture, etc.) directly affects the local blood supply, especially the femoral head, and leads to femoral head necrosis. Ischemic necrosis caused by traumatic hip dislocation is related to the age at the time of injury, the time of effective reset (not more than 24h), the severity of hip injury, the combination of acetabular fracture, delayed diagnosis, or premature weight holding, etc.
2, hormonal drugs Hormones as risk factors for femoral head necrosis were first reported in 1957 [1]. Oral, intravenous injection, enema, or oral, intravenous input combined application of hydrocortisone or dexamethasone can cause osteonecrosis. Femoral head necrosis is associated with the timing and dosage of corticosteroid use, and studies have shown that hormone use is higher in patients with femoral head necrosis than in those without necrosis. However, the duration and dosage of hormone use varies greatly from patient to patient, and Koo et al [2] showed that in 22 MRI-confirmed cases of stage I femoral head necrosis, the duration of hormone use ranged from 1 month to 16 months, and the cumulative amount of hormone use (prednisone) ranged from as little as 1800 mg to as much as 15505 mg. The ability of hormones to cause femoral head necrosis is also related to a number of risk factors in the host, such as Research shows that SLE patients and organ transplant patients are more likely to develop femoral head necrosis.
3, alcohol consumption is another important factor that causes femoral head necrosis, which was first reported in 1922. The incidence of femoral head necrosis in a group of alcoholic patients was 5.3%. Studies have shown that the risk of femoral head necrosis increases with the increase of daily alcohol consumption, and the risk of femoral head necrosis increases 3 times, 10 times and 18 times with alcohol consumption <400ml/week, 400-1000ml/week and >1000ml/week, respectively.
4, bone and joint diseases related to femoral head necrosis include: slipped epiphysis, Ehlers-Danlos disease, Legg-Calve-Perthes disease, hereditary osteogenesis imperfecta, congenital dysplasia and dislocation of the acetabulum. These diseases can lead to femoral head necrosis due to abnormal stress distribution in the femoral head and destruction of articular cartilage due to asymmetry of the head and socket. Osteodystrophy is caused by poor long-term diet, insufficient calcium and phosphorus intake, which cannot meet the metabolism and growth of bone tissue, resulting in circulatory disorders and necrosis of the femoral head due to insufficient blood supply.
5, metabolic diseases can cause necrosis of the femoral head metabolic diseases are: Cushing’s syndrome, Gaucher’s disease, hyperlipidemia, abnormal glucose metabolism, pancreatitis, etc.. Such as hyperlipidemia, the lipid component of the blood is too high, the blood viscosity increases, the flow rate slows down, thus forming small emboli and blocking small arteries and veins, leading to osteonecrosis.
6, blood disease hemoglobinopathy is a group of diseases caused by genetic defects in the hemoglobin molecule due to abnormal structure of Hb molecules or peptide chain synthesis disorders. These diseases are closely related to femoral head necrosis. The ischemic necrosis of the femoral head caused by various hemoglobinopathies shows similar performance, presenting diffuse or limited osteoporosis, cartilage exfoliation-like changes of the femoral head, typical ischemic necrosis of the femoral head and collapse of the femoral head. There are reports showing that hemophilia is related to femoral head necrosis, but it is only a case report.
7, decompression sickness decompression sickness is due to the sudden reduction of air pressure in the environment and the syndrome, femoral head necrosis is one of the symptoms of decompression sickness. These patients (such as divers, caisson workers, flight crew, etc.) due to changes in environmental pressure, decompression is not appropriate, that is, the decompression rate is too fast, the magnitude is too large, the gas that has been dissolved in the body before decompression (mainly inert gas nitrogen) out of the dissolved state, the formation of bubbles and embolism vascular or compression of tissue caused by osteonecrosis. The incidence of osteonecrosis in patients with experience working in a decompression environment is related to factors such as the length of time they have been in the work environment, the number of times they have been there, the severity, and whether they have entered at intervals.
Many other factors have been reported to be associated with osteonecrosis of the femoral head, although the number of cases of each is small. These are referred to as probable etiologies, meaning that they may be associated with a process of subsequent osteonecrosis or increased incidence in a particular disease, but have not been proven.
Second, the pathogenesis of osteonecrosis of the femoral head
1, femoral head necrosis prone to anatomical factors first, the hip joint is heavily loaded, the pressure between the head and socket is bound to increase, long-term maintenance of this greater pressure, not only easy to cause structural damage, and will largely affect the local blood circulation. Moreover, the angle of 132 degrees is formed between the femoral stem and the neck of the femoral head, and the gravity of the trunk is not perpendicular to the line of force when it moves from the acetabulum through the femoral head and neck to the femoral stem, forming a shear force. Therefore, the physiological pressure on the head and neck is much greater than that on other joints.
Secondly, the range of motion of the hip joint is second only to that of the shoulder joint, and it is capable of completing various axial movements including extension, adduction, abduction, rotation, etc. There are more chances of injury. In addition to the weight-bearing and anatomical characteristics of the hip joint, the degree of injury is also relatively heavy.
The most important anatomical factor that makes femoral head necrosis easy to occur is the blood supply characteristics of the femoral head. The blood supply of the femoral head mainly relies on the lateral supporting band and the medial supporting band arteries emanating from the extracapsular arterial ring, and the amount of anastomotic branches of the vessels is small and weak. In addition, the vascular diameter within the round ligament of the femoral head is highly variable, and its role in supplying blood to the femoral head cannot be determined yet. Therefore, when one vessel is blocked and the other cannot compensate in time, it will cause the blood supply to the femoral head to be impaired. In particular, it has been shown that the lateral supporting zone vessels are the most important source of blood supply to the femoral head, while the medial supporting zone vessels only nourish a small portion of the femoral head and neck. For example, a fracture of the femoral neck across the entry point of the lateral support zone vessels can lead to severe impairment of blood supply and consequently osteonecrosis.
2, the development process and staging of femoral head necrosis when the blood supply to the femoral head is blocked, the bone around the necrotic area thickens to form a sclerotic zone. If the necrotic area is located in the weight-bearing area, the subchondral bone will fracture. The repair process of the necrotic zone is usually incomplete and can destroy the integrity of the subchondral bone, while repeated microfractures and continuous weight-bearing prevent complete fracture healing. When the fracture progresses to the site of union of the subchondral bone and the sclerotic generation, the femoral head collapses over time. The deformation of the femoral head leads to cartilage wear and tear and eventually the development of osteoarthritis.
Staging of femoral head necrosis is important to guide the diagnosis and treatment, assess the disease progression and judge the prognosis, especially for guiding whether to preserve the femoral head.
The most commonly used staging is the Ficat and Arlet staging, which is based on the radiographic presentation and divides femoral head necrosis into 4 stages. 1992 Association of Bone Circulation (ARCO) [5] combined the Ficat staging, Steinberg staging and Japanese osteonecrosis research staging to determine a new system, which is more systematic and comprehensive based on imaging, pathological findings and extent of necrosis, and is considered by most scholars to be the most practical system. Scholars believe that it is the most practical system, which has high value in determining the diagnosis, treatment and prognosis of the disease.
3, the doctrine of femoral head necrosis mechanism through clinical and animal experimental research, people have put forward many doctrines on the mechanism of femoral head necrosis occurrence, but none of them are widely recognized. The common factor leading to femoral head necrosis is the interruption of blood supply, including vascular factors, intravascular factors and extravascular factors.
Hormonal and alcoholic femoral head necrosis have been intensively studied in animal experiments, and disorders of lipid metabolism have received attention. The abnormalities of lipid metabolism caused by hormones and alcohol include: fatty liver, fat cell swelling and necrosis, osteoblast fat filling, hyperlipidemia, bone marrow hepatocyte fat formation, bone marrow fat infiltration and fat embolism. For example, hyperlipidemia can lead to increased serum free fatty acids and prostaglandins, causing vasculitis and coagulation.
It has been suggested that osteonecrosis occurs as a result of the inability to remove procoagulants from the blood and tissues, and that coagulation occurs when the vascular endothelium is damaged by abnormal lipid metabolism due to a prolonged hypercoagulable state. Procoagulants include: free protein S, protein C, lipoprotein A, homocysteine, etc [6].
Blood stagnation and increased pressure in the bone due to impaired venous return has long been appreciated. Bone scan studies have shown that although arterial perfusion within the femoral head is normal, venous return is significantly impaired. This has also been demonstrated in animal studies. The resulting ischemia can cause femoral head necrosis. This is one of the theories behind the decompression of the medullary core.
Altered osteoblast function is also associated with osteonecrosis. Biopsies have confirmed that the differentiation of osteoblasts in the osteonecrotic area is normal, but their proliferation rate is reduced. Also ischemia can lead to death and apoptosis of osteoblasts.
The occurrence of osteonecrosis is not the result of a single factor, but the result of the combined action of multiple factors. kenzora and glimcher et al. proposed the theory of cellular stress accumulation, that when various injury factors act on the cells, the cells can not recover from these chronic stress effects, osteonecrosis will occur.
4, the genetic study of femoral head necrosis why some people will occur femoral head necrosis, while others will not, whether and genetic related to recent years has also received attention. For example, the study found that the 4a allele of femoral head necrosis patients appeared higher than the control group. 4a allele and endothelial cells with reduced synthesis of nitrous oxide synthase, suggesting that nitrous oxide has a role in combating the occurrence of osteonecrosis.
5, bone marrow edema bone marrow edema is a common manifestation of osteonecrosis, but is not a unique sign, and can also occur in osteomyelitis, osteoarthritis, and occult fractures. There is a syndrome (bone marrow edema syndrome) in the past is considered to be the pre osteonecrosis, has been determined to be a disease different from osteonecrosis. It is a transient, self-limiting disease, commonly seen in middle-aged men and women during pregnancy, often recovering on its own after several months of onset, without subchondral fractures, and should be distinguished from osteonecrosis of the femoral head.
In conclusion, the etiology and pathogenesis of osteonecrosis of the femoral head are still unknown and need to be studied in detail.