Adult osteonecrosis
Introduction
Introduction to adult osteonecrosis In general, osteonecrosis can be divided into two categories: infectious or non-infective. The former belongs to the results and manifestations of inflammatory lesions, which are not included in this section. Non-infectious osteonecrosis, also known as aseptic osteonecrosis, is widely recognized. basic knowledge The proportion of illness: 0.003% Susceptible people: no specific population Mode of infection: non-infectious Complications: hip dislocation hip joint tuberculosis
Cause
Cause of adult osteonecrosis
(1) Causes of the disease
Osteonecrosis is not a single disease, but a common sign caused by a variety of factors. The reasons are now described as follows.
Traumatic factors (35%):
Traumatic osteonecrosis is an ischemic necrosis that occurs as a result of trauma causing damage to a major blood supply to a certain part of the bone. Typical cases are sub-fractures of the femoral neck or dislocation of the hip, due to the joint support band that supplies blood to the femoral head. Injury of the arteries leads to avascular necrosis of the femoral head. In addition, fractures of the talus and lunate bone, dislocation, and fractures of the scaphoid and lumbar bones can also cause ischemic necrosis due to damage to the blood supply. The reason is relatively clear, is caused by blood supply disorders of the large vascular system, collectively referred to as traumatic ischemic osteonecrosis.
Other factors (30%):
Idiopathic osteonecrosis, also known as primary osteonecrosis, is still in the exploratory stage, but the following two factors are known to be closely related: (1) Decompression factors: well known, in the surrounding environment Changes in air pressure can endanger human health. For example, divers engaged in underwater operations, as well as operators in other high-pressure environments and professional practitioners in high-altitude flights, can experience osteonecrosis due to vascular blood supply disorders during rapid decompression. This condition is called decompression osteonecrosis. (2) hormonal factors: a large number of clinical cases show that long-term use of more than the physiological requirements of adrenal corticosteroids, easy to cause femoral head necrosis, in addition, radiation, alcoholism, pancreatitis, sickle cell anemia, Gaucher disease, liver disease , polycythemia, diabetes, obesity, hyperuricemia, etc. can also induce the disease, it is unclear how all these factors cause or induce osteonecrosis, but it is speculated that most of them are related to hormones.
Why do these two factors cause osteonecrosis? It may be related to the microvascular anatomy of the subchondral bone, because the blood vessels in the subchondral bone are end vessels, which are perpendicular to the cartilage surface when approaching the subchondral bone. And expand the vascular sinus here, and then turn 180° back into the veins in the bone below it. These extravasculars are surrounded by hard bone shells, making it less prone to collateral circulation, especially in adults; Here, foreign particles circulating in the blood vessels, such as fat droplets, gas, etc., can be stopped, causing obstruction of blood vessels and causing bone and bone marrow necrosis. According to this anatomical feature, decompression osteonecrosis is due to Nitrogen bubbles accumulate in bone marrow or blood vessels during decompression; abnormal sugar glycols of Gaucher disease can accumulate in blood vessels, causing vascular obstruction; abnormal red blood cells of sickle cell anemia accumulate in blood vessels, causing local thrombosis, a considerable part Patients with idiopathic osteonecrosis have hyperuricemia, may be due to uric acid crystallization and vascular obstruction, long-term use of more than the physiological requirements of adrenal corticosteroids and alcohol In patients with poisoning, fatty liver and hyperlipidemia can be produced. In addition, animal experiments have also shown that in this case, fat embolism confined to the subchondral bone can be produced, although the factors related to primary or idiopathic osteonecrosis are Not identical, but their X-ray findings and pathological changes are very similar, so we can think that their common pathogenic basis depends on the anatomy of local microvessels.
Unknown factor (15%):
There are still many cases in the clinic that still have no obvious incentives to determine. There is no history of drinking, no clear history of trauma and a history of long-term use of hormonal drugs. Of course, various factors that are unclear, including trauma in childhood, It is also difficult to clarify the overload load, etc. The clinical proportion of such cases is not less than 15%.
In short, in recent years, there have been clinical studies showing that there are many factors in such patients, so the cause of the disease may be the result of multi-factor combination.
(two) pathogenesis
Under normal conditions, the metabolic process of bone tissue is very active, with new bone formation and bone resorption, and is shaped to adapt to the needs of mechanical changes or changes in internal biochemistry, the mechanical and chemical stimulation of living bone tissue. The response is a change in the shape, volume and structure of the bone by altering the rate of bone formation or bone resorption.
The repair process of bone belongs to another complicated process of change. Regardless of the cause of death of the bone, the repair response is basically the same. The only difference between the repair of the dead bone and the reaction of the living bone is that when the dead bone is repaired, The repair material is not from the dead bone itself, but from adjacent living bone, connective tissue and blood-borne osteoblasts.
Clinical observation and animal experiments have shown that when bone tissue is necrotic, its pathological changes can be divided into the following two stages.
1. The first stage of the elimination phase, which is characterized by local necrosis of bone tissue and intramedullary cells. The capillaries and bone marrow matrix are gradually dissolved, transferred and absorbed, and finally the dead bones disappear, but this is not easy in large bones. carry out.
2. The second phase of the repair phase begins with the proliferation of stromal cells and capillary endothelial cells adjacent to the undifferentiated bone, followed by the proliferation of capillaries and undifferentiated interstitial cells to the trabecular space between the trabecular bones. Infiltration, gradually replaces necrotic bone marrow, and the posterior interstitial cells differentiate into osteoblasts on the surface of necrotic trabeculae, forming new reticular primitive bone on the trabecular bone, and then forming lamellar bone, wrapping the dead bone trabeculae. The bone mass is increased in the local unit volume. At this time, the local bone density is increased on the X-ray film. After that, the necrotic bone trabeculae wrapped by the new bone is gradually absorbed and replaced by the new living bone. Mostly the lamellar bone, and finally the repaired trabecular bone is further shaped, and the new reticular primitive bone is replaced by lamellar bone. This process is not balanced, the necrotic bone is different, and the repair process It is also different. When the margin has been in the repairing trabecular bone shaping stage, the central part may still be in the initial stage, that is, the undifferentiated stromal cells and capillary endothelial cells proliferate.
The process of such proliferation and absorption is that the latter is larger than the former, and thus the joint degeneration of the cartilage is eventually formed.
Due to the different causes of osteonecrosis, the speed, extent and extent of these reactive changes can vary widely. For example, after renal transplantation, interstitial and capillary endothelial cells are still intact due to osteonecrosis due to extensive use of adrenal corticosteroids. Hyperplasia, and spread to the bone marrow space of the necrotic trabecular bone, but can be differentiated into osteoblasts, so there is very little new bone formation on the surface of the trabecular bone in the necrotic area, and some other causes of special hair Osteonecrosis, often with a large number of cell proliferation, and differentiation into osteoblasts, quickly formed a large number of new bone.
It is clear that the repair of osteonecrosis caused by traumatic ischemia is more complete. When the repaired tissue crosses the fracture line, the proliferation, spread and new bone formation of the cells are relatively rapid and develop.
The repair process of the cortical bone is more difficult, the bone is absorbed in a large amount, but there is little new bone formation, so that there is a large amount of bone loss in the subchondral area. In this case, if the dead bone is not absorbed, the mechanical strength can be maintained. It has not changed for several years; once it is absorbed in a large amount, it is easy to produce subchondral fracture due to stress, which is why the crescent-shaped transparent area is displayed on the X-ray film.
Prevention
Adult osteonecrosis prevention
1 For the femoral neck fracture, strong internal fixation is used. At the same time, the bone graft with vascular bone flap is used to promote the healing of the femoral neck, increase the blood supply to the head, prevent osteonecrosis, and should be followed up regularly after surgery. Calcium to prevent ischemic development of the femoral head.
2 Because the relevant diseases must be applied with hormones, it is necessary to master the principle of short-term and appropriate amount, and cooperate with dilatation of vascular drugs, vitamin D, calcium, etc., do not listen to the doctor's advice and abuse hormone drugs.
Complication
Adult osteonecrosis complications Complications hip dislocation hip joint tuberculosis
With lameness and increased pain, hip function is gradually limited, and the hip joint can be stiff and disabling in the late stage.
Symptom
Adult osteonecrosis symptoms common symptoms traumatic osteoporosis osteosclerosis
Chronic medical history, such as history of trauma, excessive application of hormones and excessive drinking history, early local pain symptoms, from mild to heavy, late dysfunction can also occur, limb malformation, so that the function is completely lost.
According to X-ray findings and bone biopsy results, Hungerford and Zizic divided the femoral head necrosis caused by alcoholism into the following four phases:
1. Phase 1: X-ray plain film is normal, and a bone biopsy is required to make a diagnosis.
2. Phase 2: X-ray plain film was positive, showing atypical signs of idiopathic femoral head necrosis, but the articular cartilage bone plate was normal.
3. Phase 3: showed a specific change, showing the anterior and posterior cruciate bone of the femoral head, sclerotic osteoporosis, infarct or translucent lines under the cartilage, and the femoral head lost its normal spherical shape.
4. Stage 4: X-ray plain film shows late changes, at this time the femoral head is obviously deformed, and the joint space is narrow or disappears.
Examine
Adult osteonecrosis
In recent years, with the extensive development of CT and MRI imaging techniques, not only can clearer images be obtained than conventional X-ray films, but lesions can be detected early. The authors found that the positive ones can be seen earlier than the X-ray films. ~3 months, can be selected early, and compared with X-ray film.
Diagnosis
Diagnosis and diagnosis of adult osteonecrosis
The diagnosis of this disease is mainly based on chronic medical history, clinical manifestations and imaging examinations, especially the latter, which is not only conducive to the diagnosis and differential diagnosis of the disease, but also to the determination and staging of the disease, the choice of treatment methods and the prognosis. Importantly, according to the X-ray film, the osteonecrosis of adults can be staged, but the causes are different, and the opinions of the experts are not uniform.
Osteonecrosis needs to be differentiated from various injuries, especially common diseases in the predilection site. For example, cases involving femoral head necrosis often require hip joint tuberculosis, hip suppurative inflammation, rheumatoid arthritis, rheumatism, Hip tumors and hip diseases of various ages are differentially diagnosed; scaphoid necrosis of the wrist, lumber osteonecrosis and talus necrosis of the ankle and foot are all required to be differentiated from localized onset.
