1 Femoral head necrosis Cause:
Femoral head necrosis is local poor blood supply. Circulation disorder occurs in the arterial blood supplying the femoral head, which leads to insufficient blood required in femoral head , further necrosis, reduced bone density, and prone to femoral head A disease that causes collapse. The earliest related report of osteonecrosis was published by Alexander Munro in 1738. It was not until 1957 that a foreign scholar reported the first case of hormone-related osteonecrosis. Currently, femoral head necrosis may occur at any age, with the average age being less than 50 years old, and most cases involve bilateral necrosis [4]. In recent years, hormone drugs have been clinically used in the treatment of various acute and chronic diseases, such as systemic lupus erythematosus , rheumatoid arthritis , spinal cord injury , etc. However, high-dose or long-term use of hormones Drugs can cause a series of serious complications, such as femoral head necrosis, Cushing's syndrome, induce or aggravate infections, etc. [5]. According to the epidemiological study, there are 8.12 million patients with non-traumatic femoral head necrosis. Men are significantly more affected than women. The prevalence in the north is higher than in the south. The prevalence in urban residents is higher than in rural areas. The widespread use of hormones in clinical practice is bound to exist. Regarding its potential dangers, some scholars have shown that steroid-induced femoral head necrosis and have occupied the first place in non-traumatic femoral head necrosis [6]. The main causes of non-traumatic femoral head necrosis in China are the use of corticosteroids, long-term alcohol abuse, decompression sickness, and hemoglobinopathies; smoking, pregnancy, and radiation therapy also increase the risk of femoral head necrosis [7].
2 The pathogenesis of femoral head necrosis:
Most doctors have different opinions on the pathogenesis of femoral head necrosis, and it is still unclear so far. Some people think that femoral head necrosis is caused by genetic susceptibility to metabolic factors and local factors of blood supply (including blood vessels). Injury, increased intraosseous pressure and mechanical stress), some studies have reported that femoral head necrosis caused by long-term use of steroid drugs is closely related to the duration and dose of the drug. The main reason is that hormones can easily cause fat embolism and make the blood in a hypercoagulable state , causing vasculitis . Hormone-induced osteoporosis causes the strength of bones to decrease and their load-bearing strength to disappear, so collapse is prone to occur [ 8]. The mechanisms currently recognized by scholars include osteoporosis, increased intraosseous pressure, and intravascular coagulation. Due to long-term use of hormones, patients develop osteoporosis and are prone to microfractures of trabecular bone due to pressure. Due to more accumulated damage, the mechanical resistance decreases, resulting in collapse, and the bone marrow cells and blood vessels are compressed and the femoral head occurs due to ischemia. Necrosis. The use of hormones can increase the volume of intramedullary fat, leading to microvascular fat embolism and fat deposition in osteocytes. Bone marrow cells are occupied by a large number of adipocytes. The adipocytes fuse into fragments, resulting in the death of bone marrow-derived cells and an increase in intramedullary space pressure. Tissue hypoxia, edema, and blood leakage aggravate microcirculation disorder , reduce the blood supply to the femoral head, and eventually lead to femoral head necrosis. Taking a large amount of hormones for a long time causes a large amount of hormones to accumulate in the human body, causing the blood in the patient's body to become sticky, causing high coagulation and low fibrinolysis, and the local coagulation activity increases, forming microthrombi local vascular occlusion, leading to Femoral head necrosis in the dominated area [9].
3 Femoral head necrosis bone tissue Pathology changes:
Femoral head necrosis animal model preparation is divided into early, middle and late stages from a pathological perspective (see Table 1). In traumatic femoral head necrosis, arterial and venous blood supply is blocked in the early stage, and obvious changes can be seen in magnetic resonance imaging and [10].
4 Femoral head necrosis Imaging
Imaging examination methods are essential when establishing animal models. The success of animal modeling can be evaluated through imaging examinations. The current examination methods mainly include X-ray films, CT and MRI [11-12] (see Table 2).Clinically, Ficat staging is used for femoral head necrosis, which is mainly divided into 4 stages: Stage 1 has clinical symptoms, magnetic resonance visible signal intensity changes, bone marrow edema ; stage 2 X-ray films have reduced bone density, cystic degeneration , osteosclerosis and other symptoms, but the shape of the femoral head is normal; in stage 3, the femoral head can be collapsed, but the joint space remains normal; in stage 4, the joint space can be narrowed and the acetabulum has abnormal changes. In the early stage, the morphology of the internal tissue cells of the femoral head has not changed significantly, so X-ray films are of little significance in the early diagnosis of avascular necrosis of the femoral head . In the late stage, X-ray films can show that the femoral head loses its original spherical structure due to collapse and undergoes degeneration. symptoms of arthritis [12]. CT examination can show subtle damage to cancellous bone and cortical bone. It can clarify the anatomical relationships and abnormalities of anatomical structures or overlapping areas. It can display the internal structure of lesions more accurately than ordinary X-ray films. The density resolution of CT is better than that of X-ray films, and it can distinguish soft tissues of different properties to a certain extent. In micro-CT analysis, it has obvious advantages in measuring bone mineral density, which is also the basis for predicting fracture risk. Micro-CT can measure the three-dimensional structure of bone in any direction, and has the advantages of continuity and integrity. It can also observe changes in bone quality comprehensively, three-dimensionally, and in real time, and evaluate bone volume fraction, trabecular space, etc. Therefore, micro-CT has the advantages of continuity and integrity. The three-dimensional reconstruction analysis method is more comprehensive than the traditional method [15].
5 Femoral head necrosis animal model selection
After establishing the animal model, we hope to more completely simulate the pathological and physiological changes of human femoral head avascular necrosis from early to late stages, and the necrotic area is similar to the location of human femoral head avascular necrosis. At present, Mainly using some relatively mature modeling methods, there is a lack of an ideal animal model to highly simulate the clinical process of avascular necrosis of the femoral head, so it needs to be continuously improved and improved. Currently, four-legged animals commonly used as modeling animals include dogs, rabbits, rats, and pigs; bipedal animals include chickens and emu[16].
The construction of experimental animal models should be based on the clinical status quo in order to produce satisfactory experimental data. First, the physiological structure and histological characteristics of the experimental animals should be selected to reliably reflect human diseases, and they should have good evolutionary kinship with humans. characteristics and similarities, the progression of the disease in humans also needs to be reflected in animal models. In the late animal model, the femoral head will collapse and deform, that is, osteonecrosis of the femoral head should occur in the articular cartilage area. The size of the femoral head must also be ensured. The structure should be related to biomechanics . Generally, most of the animals used are four-limbed animals, so the weight-bearing conditions of the limbs must be considered when building the model. Wang Haiyang et al. [17] used vertical osteotomy in the middle of the femoral neck and screw internal fixation, and selected imaging X-ray films to prepare a canine unilateral femoral neck fracture internal fixation model. Gong Jianbao et al. [18] used a minimally invasive cryogenic freezing device ( argon-helium knife ) to establish a model of avascular necrosis of the canine femoral head through precise positioning of magnetic resonance. This method has the advantages of small incision, easy control of the necrotic part, and the death of the animal. The characteristics of reduced risk, high success rate of modeling, strong repeatability, and convenience for standardized research provide experience for the medical development of treatment methods for femoral head necrosis. Gu Jiangjiang et al. [19] used alcohol to burn green-footed No-Maj to prepare a femoral head necrosis model. They used a hollow electric drill to drill holes in the femoral head, and filled the holes with alcohol cotton balls to ensure full contact between the cancellous bone and alcohol. X-rays taken after 1 month of observation showed collapse of the joint surface. Qu Chuntao et al. [20] used 3 cycles of liquid nitrogen freezing and then radiofrequency heating to prepare an animal model of emu femoral head necrosis. Except for 2 animals that died and 4 animals were infected, edema was seen in the remaining femurs after 6 weeks. After 12 weeks, Bone morphology and joint space changes were obvious, and at 16 weeks, some emu developed femoral head collapse and late stages of osteonecrosis.
Bipeds are characterized by similar weight-bearing methods to humans. This animal was mainly selected to study the biomechanical factors in the course of avascular necrosis of the femoral head.The emu femoral head necrosis model is the best animal femoral head necrosis model. Although emu sources are scarce, difficult to obtain, and difficult to feed, the emu is a bipedal weight-bearing animal. The height, body mass, and stress on the femoral head Both animals are similar to humans. The stress distribution of the femoral head is similar to the measurement data of the human hip joint; and the force is along the direction of the femoral shaft, which is similar to humans. The hip joint biology of bipeds and quadrupeds The difference in mechanics is the key factor that causes the collapse of different femoral heads [21]. Compared with other animals, the green-footed chicken used in the experiment is easy to obtain, easy to raise, and has low mortality. The femoral head is larger, which is convenient for surgery and postoperative observation. It is a bipedal animal and has to stand in a standing position for a long time. The mechanical stress on the bone is similar to the biomechanics of the human body, which can better simulate the performance of femoral head necrosis and repair under load-bearing conditions. Rabbits are the most commonly used animal model for steroid-induced femoral head necrosis. Although they have the advantages of low cost and easy maintenance, and the femoral head is larger than that of rats, it is easy to observe and collect materials. However, the modeling period is long and the model is difficult to complete. The rate is not high [22].
Dogs are quadrupeds. Although dogs are chosen for modeling, their biomechanical load-bearing areas are not consistent with humans and cannot completely simulate the characteristics of human femoral head necrosis. However, their anatomy and tissue structure are very similar to humans, and their body size is suitable. , the source is easy to obtain, so it is the most widely used in preparation [23]. It can be used for various head-saving surgical treatments of avascular necrosis of the femoral head, providing a more ideal model for later treatment after successful modeling [24].
6 Selection of preparation methods for animal models of femoral head necrosis
There are many methods for preparing animal models, which are mainly divided into traumatic and non-traumatic. Traumatic methods include surgical trauma modeling, surgical blood supply occlusion method, chemical injury modeling method, Absolute ethanol modeling, liquid nitrogen freezing modeling, etc.; non-invasive methods mainly include simple hormone modeling, hormone combined with lipopolysaccharide , hormone combined with horse serum and other methods [25-26].
Trauma is a common cause of femoral head necrosis. Some scholars hope to study femoral head necrosis through surgical trauma modeling. Surgical modeling mainly blocks the blood supply to the femoral head. The blood supply to the femoral head mainly comes from the medial and lateral femoral circumflex artery, the round ligament artery of the femoral head, and the nutrient artery of the femoral shaft [27]. The medial circumflex femoral artery originates from the profunda femoral artery more than the femoral triangle, and a few originates from the femoral artery. After the medial circumflex femoral artery emerges from the profunda femoral artery, it goes medially and divides into two branches at the medial edge of the iliopsoas muscle . It is thicker and runs behind the two muscles of pectineus and iliopsoas muscle. The collateral branches supply nearby muscles. The final branch runs deep from the quadratus femoris muscle to the trochanteric fossa, crosses the obturator externus muscle, and supplies the base of the femoral neck. , continues as the lateral ascending carotid artery. Most of the lateral circumflex femoral artery also originates from the profunda femoral artery. Compared with the medial circumflex femoral artery, it originates from below the profunda femoral artery, has a slightly thicker diameter, and runs laterally. It starts from the muscle between sartorius and rectus femoris. It passes through the gap and then divides into ascending and descending branches. The ascending branch runs laterally deep into the vastus lateralis muscle. Finally, there are some small branches on the lateral surface of the base of the femoral neck, which together with the branches of the medial femoral circumflex artery form the extracapsular arterial ring. . The branches from the extracapsular arterial ring distribute to the capsular branch of the hip joint capsule, then enter the bone to nourish the femoral shaft, and go up along the femoral neck to nourish the ascending carotid artery of the femoral head and femoral neck. The small part that originates from the obturator artery and comes from the medial femoral circumflex artery is called the round ligament artery of the femoral head and the medial femoral epiphyseal artery. Simulate clinical femoral head venous stasis caused by femoral neck fractures and dislocation , osteonecrosis caused by damage and interruption of arterial blood supply, and structural changes in the femoral head.
6.1 Femoral head ligament ligation Femoral neck fracture will affect the blood supply of the hip joint, causing damage to the surrounding blood vessels, thus affecting the blood supply to the femoral head. Generally, fractures will be accompanied by displacement, changes in hemodynamics and , and eventually femoral head necrosis.In addition, oozing or bleeding in the hip joint further increases the pressure in the joint capsule, causing blood loss in the internal structure of the femoral head, increasing muscle tissue permeability, causing edema to occur locally, and ultimately leading to avascular necrosis of the femoral head [28] . Wang Junfeng [29] used femoral head ligament ligation to observe the morphological changes of the rabbit femoral head structure. The surgical team made a vertical incision in the rabbit's lower abdomen, opened the skin layer by layer, pushed it away from the muscle space, and opened the hip joint capsule. The femur was externally rotated by hand, the femoral head ligament was ligated, and the femoral head dislocation caused by external rotation was reduced and then the joint capsule was sutured, and each layer of muscle and fascia was sutured; the control group only opened the joint capsule , find the femoral head ligament, directly close and suture the joint capsule without ligating it, and suture it layer by layer. Four weeks after surgery, the expression of bone morphogenetic protein 7 in hypertrophic chondrocytes under the cartilage was significantly enhanced when examined under a light microscope. This shows that after ligation, the blood in the articular surface around the femoral head ligament is blocked and changed; the cartilage articular surface The growth and proliferation of chondrocytes and subchondral cells were inhibited, and even necrosis occurred; the expression of bone morphogenetic protein 7 was enhanced, indicating that it plays an active repair role in chondrocytes. An animal model was successfully prepared by ligation, which is helpful for clinical research on the treatment of traumatic avascular necrosis of the femoral head.
6.2 Alcohol modeling mainly involves local injection of anhydrous ethanol into the femoral head, causing avascular necrosis of the femoral head, and then necrotic bone resorption, decreased trabecular strength, hip joint continued biological pressure hinders osteonecrosis The repair effect of the bone trabeculae causes a further decrease in the mechanical strength of the trabecular bone, making the animal model prone to progression to collapse of the femoral head. This type of animal model is often used to study treatments for avascular necrosis of the femoral head. Since Axhausen reported in 1922 that patients with ethanol poisoning were susceptible to osteonecrosis, people have been exploring the relationship between alcohol and the onset of femoral head necrosis, and studying its mechanism, pathological process, etc. Among the causative factors of non-traumatic femoral head necrosis, femoral head necrosis caused by alcohol is the second largest factor after hormone-related factors. Cases of femoral head necrosis caused by long-term drinking are very common in clinical practice and are more likely to occur at parties. Many young and middle-aged people have symptoms and imaging changes on both sides of the femoral head once the disease develops. The disease develops to stages 3 to 4, with deformation and collapse of the surface structure of the femoral head and irreversible osteoarthritis. The patients can take care of themselves. Loss of ability can only be treated with artificial hip replacement surgery. Yang Yun et al. [30] used ethanol to prepare the alcoholic femoral head necrosis rat model. Except for 6 rats that died during the experiment, the rest were in good condition. After 4 months of observation, the femoral head cartilage appeared dark in color and lost its original moisture. The elastic fibers of some blood vessels decreased, the elastic fibers proliferated, and the number of microthrombi increased. After 6 months, the surface structure of the femoral head was damaged or even fell off, and the bone quality decreased. There was no obvious deformation, collapse, or acetabular wear change of the femoral head. Rats bear weight on their limbs, and their hind limbs bear less weight. Therefore, placing food and water at a high place will increase the weight-bearing capacity of both lower limbs when rats eat water. This method will be more similar to human biomechanical characteristics. Therefore, studying the pathogenesis of alcohol-induced femoral head necrosis requires considering the impact of multiple factors on the experimental process, and drawing on biomechanical principles during the modeling process to make the development of necrosis similar to the pathological phenomena of human femoral head. This will be the future The main development direction of animal model research on femoral head necrosis [31].
6.3 Liquid nitrogen freezing method is a relatively widely used modeling method. This method has a short modeling cycle, high success rate, and good repeatability.Fully expose the surgical site through the posterolateral incision of the hip joint, cut off the round ligament in the femoral head, and use three layers of sterile gauze to protect the surrounding tissue to prevent damage, then soak liquid nitrogen in the femoral head, freeze it and rewarm it several times , after this operation freezes the femoral head locally with liquid nitrogen, the temperature of the surrounding tissue cells in the bone drops rapidly and shock occurs, causing spasm in some blood vessels within the femoral head, capillary endothelial cell water loss, cell shrinkage, and micro-thrombi. In addition, freezing can cause the permeability of capillaries to increase, resulting in increased blood viscosity and slow blood flow. Modeling uses liquid nitrogen cryogenic freezing and several cycles of rewarming, which can destroy some cells in the bone, intraosseous cell structure proteins and cytoskeleton protein, further blocking the DNA replication , allowing the active ingredients inside the femoral head to appear Necrosis. Zhou Zhengli [32] used liquid nitrogen to prepare a rabbit femoral head necrosis model under sterile conditions. Using the bilateral greater trochanters as a connecting line, an arc-shaped transverse skin incision was made, and the superficial and deep fascia were peeled off to fully expose them. Muscle tissue, cut off the round ligament of the femoral head, put the femoral head in a state of total dislocation, expose the articular surface of the femoral head, fix the rubber funnel, and freeze the femoral head with liquid nitrogen. It was only 4 weeks after the operation that the joint surface became incomplete and began to peel off. 6 months after the operation There was a defect on the periphery, and the femoral head showed obvious collapse after 8 weeks of observation. This method is currently the most effective and most successful of these modeling methods to cause femoral head necrosis; and the use of liquid nitrogen freezing can better simulate bone repair in the necrotic area during the pathophysiological process of human femoral head necrosis, and the experiment is feasible. It is highly reproducible and can control the freezing range and time. It is a convenient and controllable standardized animal model.
6.4 Hormone modeling The imbalance between osteogenic differentiation and adipogenic differentiation is the main cause of steroid-induced femoral head necrosis. Some studies have found that steroid hormones can reduce the expression of type I collagen and osteocalcin mRNA. The bone marrow is invaded by lipid metabolism disorder , which accelerates the death of osteoprogenitor cells and slows the repair of damage [33]. Long-term use of large doses of hormone drugs will cause increased blood lipids and slow blood flow, which may easily lead to the formation of fat embolism throughout the body. Local blood stasis may occur in the blood source supplying the femoral head. The formation of necrotic fat cells in the femoral head will cause the death of bone marrow hematopoietic cells, and ultimately Leading to femoral head necrosis. Long-term high-dose use of hormones can cause lipid metabolism disorders in patients, increased blood viscosity, fat accumulation in bone cells, and fatty degeneration . These reasons slow down the blood flow, reduce the amount of blood leading to bone cells, and even cause blood coagulation, The medullary cavity is under pressure, and the tiny blood vessels in the femoral head are blocked, eventually leading to ischemic osteonecrosis . The use of glucocorticoids will directly reduce protein synthesis, hinder the body's absorption of calcium, cause a large amount of calcium loss, significantly reduce bone quality, and cause osteoporosis. On the other hand, the speed of adult osteoblasts repairing the body is roughly the same as that of osteoclasts . Large doses of glucocorticoids slow down the repair speed of osteoblasts, reduce bone turnover, reduce bone quality, and easily lead to The weight-bearing part of the femoral head collapses or even becomes necrotic [34]. After taking glucocorticoids, osteoblasts and osteocytes are most vulnerable to damage. The apoptosis of osteocytes will reduce bone density and disorder bone trabeculae. At this time, the femoral head will fracture due to trauma, and finally the femoral head will become ischemic. Necrosis forms. Tong Peng et al. [35] used , prednisolone acetate, combined with horse serum to establish an animal model based on the animal model method constructed by modern research. During the experiment, the characteristics of human biomechanics were taken into consideration, and the suspension method was used to give the rabbits water to keep the lower limbs upright. As a result, 8 rabbits were successfully modeled, but the cartilage structure changed and the cartilage collapsed seriously.
In summary, there are certain disadvantages in establishing a femoral head necrosis model through surgery. The surgical wound is large, the animal tissue is damaged, the mortality rate is high, and the pathological changes are different from human pathological processes. For femoral head necrosis prepared by ethanol, the success rate of modeling is low. Whether the amount of ethanol and the modeling process can accurately act on the femoral head will make it difficult to progress to the later stage.It is difficult to grasp the degree of damage to other tissues during the liquid nitrogen freezing modeling operation, and the freezing range cannot be determined. In addition, the animal has a strong recovery ability, and it is still unknown whether the model can be successfully created; its causative factors are not related to human femoral head necrosis, and it is not very likely. Suitable for research on the causes, mechanisms and characteristics of femoral head necrosis. Compared with others, hormone preparation is less invasive and easy to operate, and is more suitable for studying the pathological process of femoral head necrosis. Moreover, hormone combined with horse serum and hormone combined with lipopolysaccharide have a higher success rate in modeling [36].
In recent years, the rate of femoral head necrosis due to the use of hormones has increased. Therefore, it is essential to explore an animal model that is close to the pathological changes of human femoral head necrosis to provide effective clinical treatments. Since hormones have similar mechanisms of action in animals and humans [37], people began to use hormones to prepare animal models. There are currently many methods for modeling animal models of steroid-induced femoral head necrosis, such as using hormones alone, hormones combined with horse serum, hormones combined with endotoxin, etc. The dosage and method of administering drugs to animals in experiments are different.
(1) Simple hormone induction: Liu Wei et al. [38] simply used low-dose hormones to prepare a rabbit femoral head necrosis model. They used upright feeding and drinking methods to increase the weight-bearing of the femoral head. According to histopathological examination, methylprednisolone sodium succinate was injected intramuscularly. , 4 weeks after administration, the size of adipocytes increased, the nuclei disappeared, some disintegrated and ruptured, and bone marrow stem cells decreased relatively. At 6 weeks, it can be seen that the number of empty bone lacunae in trabecular bone gradually increases. At 8 weeks, necrosis can be seen in part of the femoral head cartilage area, and necrosis and cartilage surface collapse can be seen. Although one rabbit died, the modeling method is relatively safe and can ensure the final number of samples in the experiment. This method has a high success rate, consistent pathological changes, low cost, easy operation, avoids the influence of unnecessary factors, and is conducive to clinical exploration and research on the pathogenesis of femoral head necrosis.
(2) Hormone combined with horse serum induction: Cao Liangquan et al. [39] used different doses of horse serum and hormones to prepare rabbits with femoral head necrosis. They were divided into 4 groups and observed using magnetic resonance imaging. Two of them died. Abnormal signals appeared in the high-dose group in the 2nd week, and showed patchy or small nodular high-intensity shadows in the 4th week. In the 6th week, 80% of the high-dose group showed osteonecrosis signals; the remaining groups showed osteonecrosis. The ratios were all low, and histopathologically, the degree of empty bone lacunae gradually increased in the high-dose dexamethasone combined with high-dose horse serum group, and some bone trabeculae were damaged and incomplete. Glucocorticoids have been implicated as the most common cause of nontraumatic osteonecrosis of the femoral head. This experiment adjusts the dosage and time of horse serum and hormone injections to avoid animal death due to excessive immune response caused by excessive injection and too short interval, and has a high success rate and similar safety; it is conducted using hematology The serum cholesterol and triacylglycerol levels of the model rabbits were evaluated and observed for 30 days. All groups increased, especially the serum cholesterol level of the high-dose group increased significantly.
(3) Hormone combined with lipopolysaccharide induction: The use of hormone combined with lipopolysaccharide modeling has the advantages of reducing modeling time, reducing the risk of animal death, and high modeling success rate. Therefore, it is mostly used for research on the pathological mechanism of femoral head necrosis. Yu Junlun et al. [40] used spiral CT scanning, Micro-CT scanning, and hematoxylin-eosin staining to observe imaging manifestations such as rabbit femoral head morphology and bone density, and observed the shape, distribution, and cortical bone thickness of trabeculae. The bone mineral density and other factors were measured, and changes in the internal structure and density of the femoral head were observed on the 5th, 10th, 15th, and 20th days after modeling. The remaining morphology did not change. Micro-CT showed that the trabecular bone was disordered, bone quality was reduced, and small micro-fractures of the femoral head could be seen. Pathological examination shows increased bone cell apoptosis, increased bone mass loss, loss of load-bearing strength, and barriers to bone repair. Tian Li et al. [15] used dexamethasone combined with lipopolysaccharide to prepare femoral head necrosis. They used spiral CT, micro-CT, and histomorphological examination to compare rabbits with femoral head necrosis and normal rabbits. Spiral CT showed that bone density was uneven and joints The face was blurred; micro-CT showed that the bone mineral content and trabecular bone density were reduced; histomorphology showed that hematopoietic cells in the medullary cavity were significantly reduced, and thrombosis could be seen in the tiny blood vessels of the subchondral bone.In the experiment, CT, micro-CT scanning and pathological examination were used to evaluate early avascular necrosis of the femoral head. The three methods complement each other and are related to each other. The diagnosis is clear and objective. CT scanning is convenient and fast, and can observe the different characteristics of the femoral head. The change in cross-sectional density determines whether the modeling is successful.
In summary, no animal model can have the same pathological mechanism as human disease. The preparation time, modeling success rate, and modeling cost of the animal model all have an impact on the experiment. Different animals have their own advantages in establishing different models. Although physical modeling can reduce modeling mortality and shorten the modeling period, it does not conform to the clinical pathological process of the disease; chemical modeling is easy to remain in the animal body. Chemical substances have a greater impact on later research [42]. The etiology of the animal model of steroid-induced femoral head necrosis is close to that of patients with clinical femoral head necrosis. It is one of the commonly used modeling methods. This method does not require surgery and is simple to operate. However, there are also some problems. There are many types of hormones. , the impact of each hormone on it, whether the target of action is consistent, and the dosage, frequency of use, time of action and whether the action site of the hormone can be concentrated on the femoral head still need further discussion and research. It is believed that with the development of society and the deepening of research, better animal models will be established. This is also the goal and direction of progress that domestic and foreign scholars will jointly pursue in the next few years.
Information source: Chinese Tissue Engineering Research, 2021, 25(29):4691-4696.
