A. What is called femoral head necrosis?
Femoral head necrosis, known as aseptic necrosis of the femoral head or ischemic necrosis of the femoral head, is a lesion caused by poor local blood flow to the femoral head for a variety of reasons, resulting in further ischemia, necrosis of bone cells, fracture of bone trabeculae, and collapse of the femoral head. Since 1888, when the disease was first recognized by the world medical community, osteonecrosis of the femoral head has been transformed from an uncommon disease to a common and frequent disease. Especially since the introduction of hormones and their widespread use, the incidence of femoral head necrosis has gradually increased. In addition, the increase in the number of accidents after the change of transportation and the change of people’s life style have made the number of patients with this disease increase dramatically. According to incomplete statistics, there are currently 30 million people with osteonecrosis of the femoral head worldwide, and about 4 million in China. The latest survey shows that there is no significant gender difference in the occurrence of osteonecrosis of the femoral head, and the disease can occur at any age, while the incidence of the disease increases significantly in people with a history of hormone application, hip trauma, alcoholism, and related diseases.
Femoral head necrosis can occur at any age, but it is most common between the ages of 31 and 60, with no gender difference. It starts with vague pain and dull pain in the hip joint or its surrounding joints, which is aggravated by activities.
Second, what are the causes of femoral head necrosis?
Traumatic:As a result of hip trauma, fracture of femoral head or femoral neck, hip fracture or dislocation, or injury of vascular branch without both fracture and dislocation, can cause local ischemia of femoral head, which further develops into necrosis.
Non-traumatic: (1) long-term or massive application of glucocorticoids accounted for 43% (2) alcohol intoxication (3) decompression sickness, diving, flight personnel in high-pressure situations, increased dissolved nitrogen in the blood and tissues, when the environmental pressure is reduced, the excess nitrogen that has been dissolved needs to be gradually discharged through the lungs, if the pressure is reduced too quickly, nitrogen can not be discharged in time, that is, free out in the body, the formation of bubbles, resulting in gas embolism, gas Embolism in the blood vessels, blood flow is blocked, and the local blood supply to the femoral head becomes poor, resulting in ischemic necrosis.
Others: hypertension, diabetes, atherosclerosis, obesity, gout, radiation therapy, after burns, can also cause necrosis of the femoral head.
Third, the pathogenesis of femoral head necrosis
The pathogenesis of traumatic femoral head necrosis is the ischemia caused by the sudden blockage of the internal and external bone arteries. Extraosseous vascular injury is due to damage to the blood supply vessels supplying the supporting band arteries or the vessels within the circular ligament when the joint capsule or the circular ligament is injured. Intraosseous vascular injury is when the fracture directly damages and interrupts the intraosseous vessels.
The pathogenesis of nontraumatic femoral head necrosis is complex, and a review of the anatomical features of the femoral head and neck is performed before discussing the pathogenesis.
In the diagram, the blue area around the head and neck of the femur is the joint cavity, which is filled with joint fluid that plays a role in lubrication and nutrition. The femoral head and neck are surrounded by hard bone cortex, with a large head and a thin neck. The femoral head and neck are filled with dense spongy bone trabeculae, which basically form a confined space. In addition, the weight-bearing area of the femoral head will be deformed and produce a temporary increase in the pressure in the medullary cavity during weight-bearing, and microfractures can occur in the normal femoral head. Necrosis is usually considered to be the joint consequence of multiple actions. The common causes for the onset of necrosis can be summarized as follows.
(A) lesions related to blood vessels
1, vascular lesions: can be divided into extraosseous and intraosseous vascular obstruction. Blockage can occur in: arteries, veins or capillary beds, because the head of femoral necrosis in diabetes and alcoholics, usually accompanied by hyperlipidemia, hypertension and coronary artery atherosclerosis, so outside Chandler et al. called the head of femoral necrosis “hip coronary artery disease,” Saito et al. due to the deposition of immune complex antibodies. Saito et al. suggested that obstructive vasculitis is caused by a metamorphic reaction to the deposition of immune complex antibodies in the vessel wall. Radiation arteritis and intraosseous obstructive vasculitis are also associated with necrosis.
Some scholars have proposed the theory of extraosseous arterial obstruction based on the finding of an interruption of the superior supporting zone artery from the internal rotor femoral artery by superselective angiographic analysis. However, other scholars have suggested that the angiographic interruption is not necessarily a vascular obstruction, but more likely an artifactual venous return obstruction caused by distal blood stasis: Starklint in 1995 found intraosseous venous obstruction rather than arterial system obstruction by special staining of hip resection specimens, and intravenous accumulation of new or old fibrous masses (and perivascular centripetal fibrosis) was seen. This finding may explain the increased intraosseous pressure in femoral necrosis, the slow blood flow throughout the venous system and the reduced partial pressure of oxygen in the intramedullary portion of the bone seen on intramedullary angiography. The high incidence of necrosis of pregnancy is usually considered to be related to the enlarged uterus affecting pelvic venous drainage
2. Vascular embolism and intravascular coagulation. The causes of embolism are fat embolism, sickle cell or nitrogen gas bubble embolism: fatty liver is the main source of fat embolism caused by fat embolism, and fat embolism hydrolysis produces free fatty acids, which can damage the endothelial cells of blood vessels and increase obstruction. Nitrogen gas bubble embolism is seen in decompression sickness. Deformed red blood cells in sickle cell anemia can increase blood viscosity and vascular obstruction in intramedullary capillaries and veins. As an intermediate link, the intravascular coagulation process can be activated by various risk factors (intraosseous fat embolism, endotoxin, allergic reactions, proteolytic enzymes, and tissue factors). For example, the release of lipolytic enzymes from pancreatitis that hydrolyze bone marrow fat to produce free fatty acids with toxic effects on endothelial cells can cause intravascular coagulation. Vascular embolism will be recanalized by natural thrombolysis afterwards, but repeated episodes of fibrosis will inevitably occur to block the vessels.
(B) Increased pressure in the joint cavity
Fluid accumulation in the joint cavity such as trauma, inflammation, arthritis, and bleeding within the joint capsule in hemophilia can increase the pressure in the joint cavity and compress the blood vessels through the base of the joint capsule affecting the blood supply to the femoral head.
(iii) Increased pressure in the bone marrow cavity
Since the femoral head is a confined space, any increase in volume caused by any cause within this space will increase the pressure within the marrow cavity, compressing the blood vessels and causing necrosis. Hormones can cause hypertrophy and accumulation of bone marrow adipocytes, resulting in increased intramedullary pressure, which compresses the microvascular structures in the bone and leads to impaired circulation. Similarly bone marrow fat can absorb large amounts of nitrogen to increase its size, sickle cell anemia can increase the size of fat cells, and increased fat within bone cells can also increase in size to compress veins and impede return flow. Bone marrow hyperplasia caused by anemia can also increase the pressure in the medullary cavity. In Gaucher’s disease, the lack of b-glucosidase prevents the breakdown of glucocerebrosides in the bone marrow reticuloendothelial cells, which increasingly accumulate in the endothelial cells causing increased intraosseous pressure. Repeated bleeding in the marrow cavity in hemophilia can also increase the intramedullary pressure. Bone marrow metastasis from inflammation and tumors can also increase intramedullary pressure and cause necrosis
(iv) Decreased mechanical strength of bone structure
The elevated parathyroid hormone level after renal dialysis increases the rate of bone structure renewal in subchondral bone, and the new disorganized bone matrix is unable to bear normal weight-bearing, resulting in microfractures that increase the intramedullary pressure. Excessive osteoporosis can also tend to increase the number of microfractures causing increased pressure. Alcohol abuse can promote the development of osteoporosis and reduce the mechanical strength of bone. In addition, alcohol and hormones themselves have toxic effects on the bone.
(v) Lesions of the femoral head
Slipped epiphysis can be seen in patients with hypothyroidism, growth hormone use, and radiation therapy. When slipped epiphysis of the femoral head occurs, the epiphysis is displaced upward and the epiphysis is externally rotated, which distorts the lateral epiphyseal artery and affects the blood supply to the epiphysis. In congenital hip dislocation with abduction and internal rotation, the iliopsoas muscle and joint edges compress the internal rotor femoral artery affecting the blood supply to the femoral head.
In recent years the literature has placed more emphasis on the association of thrombophilia (increased tendency of thrombosis) and hypofibrinolysis (diminished ability to dissolve thrombi). We have also noted that in some patients with femoral head necrosis, the acetabulum often shows necrotic density changes on plain radiographs, and perhaps it may be more appropriate to view femoral head necrosis as a hip disease. Both protein s and protein c are vitamin K-dependent plasma proteins, and they and coagulation factor 5 can be involved in inhibiting the blood clotting process. Protein s activates protein c, and when activated, protein c causes enzymatic cleavage of activated coagulation factors 5 and 8, inhibiting blood clotting. Lack of protein s and protein c, as well as structural abnormalities of coagulation factor 5 and resistance to activated protein c, can affect the inhibition of blood coagulation and produce a hypercoagulable state (thrombophilia). Lesions of the fibrinolytic system in the body affect the release of fibrinogen activator activity in tissues and increase lipoprotein A levels, producing a hypercoagulable state, increased aggregation of red blood cells, and ultra-high viscosity leading to reduced blood flow and ischemia. Hyperfibrinogenemia is seen in patients with hyperlipoproteinemia (types II and IV) who smoke, have diabetes mellitus, or use oral contraceptives.
According to a large-scale epidemiological survey in Japan, post-corticosteroid treatment and alcohol abuse were found to be the two most important risk factors, associated with about 90% of patients. Of these patients, 5-25% were associated with hormone use and almost 100% had bilateral onset. Most of the necrosis that occurs in alcoholics have a relatively long, 11-fold increase in the incidence of necrosis with a history of weekly alcohol consumption exceeding 400 ml. Both alcohol and hormones have toxic effects on osteoblasts, and both can cause fat to be deposited in the liver and become a source of fat emboli. Hormones can also cause hypertrophy of fat cells in the bone marrow, conversion of red marrow to yellow marrow and inhibition of vascular regeneration. So in short, the pathogenesis of femoral head necrosis is extremely complex, it is impossible to use a single doctrine to explain, can be seen as the result of a combination of factors.
Fourth, the natural repair process of femoral head necrosis
The vast majority of human tissues will not return to normal after the injury, and can only be repaired with granulation and fibrous scar tissue, severe burns and open incisions can only grow scars. However, bone tissue, unlike other tissues, has a strong ability to repair and regenerate, and bones can be joined together when broken, and bones can grow back where they are defective. Now take a fresh fracture as an example to illustrate the process of bone growth and repair: after the fracture, bleeding occurs at the fracture site, forming a hematoma, then a granulation, then a cartilage scab, and finally a hard bone scab, or bone tissue. This bone tissue has a disturbed arrangement of trabeculae, and the bone structure is completely restored to normal by shaping it over a longer period of time. It is an accepted fact that the bone repair process is exactly the same regardless of the cause of necrosis, whether it is a fracture, a drilling, or osteomyelitis-induced osteonecrosis.
Because of the special anatomy of the femoral head, what happens after femoral head necrosis is usually ineffective bone repair, and it took a long time for humans to recognize the natural repair process of ineffective bone repair in femoral head necrosis. In 1920, Phemister suggested that this increase in density was due to an external increase in density caused by a decrease in the density of the surrounding bone. In 1958, Bonfiglio and Bardenstein found that new bone was attached to the surface of necrotic trabeculae in the sclerotic area of the femoral head. The necrotic trabeculae were widened by the attachment of new bone on the surface, and the increase in bone density was proportional to the width of the trabeculae. They highlighted that sclerosis was both a result of necrosis and a clear sign of vascular regeneration and repair in the necrotic area. This is a famous experiment, and Kenzora believes that the diagnosis of osteocyte survival by light microscopy is not reliable, because osteocytes can remain intact for a considerable period of time after death, and therefore the determination of osteocyte physiology should be more sensitive and reliable than histomorphology. The most sensitive and reliable indicator of a cell’s survival is its ability to synthesize ribonucleic acid (RNA), and loss of synthesis indicates that the cell is dead. Since the radioactive isotope H3CVcytidine is the precursor of RNA synthesis, autoradiography can be performed with H3CVcytidine, and if bone cells cannot be labeled with this isotope, they are dead. Using this method, it was demonstrated that most cells lost their synthesis capacity at 2 hours of ischemia and all cells in the femoral head except cartilage were dead at 12-24 hours.
In the conclusion of the article, Kenzora states that the inability of cells to take up the isotope deuterated cytosine was used to confirm the necrosis of the femoral head in adult rabbits. Proliferating capillaries and undifferentiated mesenchymal cells in the bone marrow of the living bone near the osteotomy rapidly filled the marrow spaces of the dead femoral head. The mesenchymal cells gradually took on osteoblastic characteristics as they proliferated toward the surface of the dead bone trabeculae. Finally, they differentiate into functional osteoblasts that cover the surface of the necrotic trabeculae. New bone forms on the surface of the dead bone and expands to fill the trabecular space, resulting in increased bone content per unit volume and increased radiographic density of the femoral head. The core of dead bone in the center of the trabeculae is later resorbed and replaced by living bone. The new trabeculae are thicker than the original ones and are living plate-like bone. The biological response of the subchondral dead dense bone occurs later because of the location far from the starting point of repair. Unlike the rough trabeculae, the primary response here is bone resorption rather than bone formation. The pace of new bone formation does not keep up with the pace of bone resorption resulting in subchondral bone loss. Capillary penetration and tissue resorption progresses all the way to the cartilage, causing a proliferative response of chondrocytes and changes within the cartilage matrix similar to those seen in osteoarthritis. In addition, destructive synovial opacities form, growing on the cartilage surface and destroying the articular cartilage. The mismatch of the joint, the loss of cartilage is similar to the degenerative osteoarthritis of the femoral head causing similar changes in the acetabular cartilage with subsequent complete destruction of the joint.
In simple understanding, different anatomical parts of the rabbit femoral head necrosis repair process have different manifestations: 1 cancellous bone, after necrosis repair new bone is formed on the surface of and between the necrotic trabeculae, which increases bone density per unit volume, and later the necrotic trabeculae are gradually revived. 2 osseous articular surfaces, that is, the subchondral bone dense mass gradually resorbs and disappears. 3 cartilage and joints are gradually destroyed. The bone repair ability of human is far inferior to that of rabbits, and the repair of necrotic cancellous bone in many people cannot be completed for life, and in a few people it takes 10 years to complete, with obvious femoral head deformation and osteoarthritis. Even if a person can reach the repair capacity of a rabbit, he or she cannot avoid joint destruction. It is necessary to exceed the repair capacity of rabbits in order to cure femoral head necrosis.
The appearance of hypodense areas in the necrotic femoral head in humans has been explained by atrophy of the trabeculae or resorption during the repair process, but recent studies by PlenkHJr et al. of the Vienna Institute of Tissue and Embryology on necrotic resected femoral heads have shown that there are three types of repair in human femoral head necrosis: 1 limitedrepair, in which a sclerotic rim is formed next to the vascularized zone. 2 destructiverepair, which causes significant bone resorption and fragmentation of the femoral head, and 3 reconstructiverepair, which reduces the extent of necrosis and slows or stops the progression of the disease for a certain period of time. The results of this study can better explain the appearance of sclerotic margins and hypodense versus dense areas on plain radiographs after necrosis. In the past, many people mistook the bone resorption produced by destructive bone repair for osteoporosis, which delayed the diagnosis of necrosis. In another article, he also pointed out that all three types of repair are ineffective and that reconstructive bone repair also inevitably decreases the mechanical strength of the femoral head, causing it to collapse. It is generally accepted that femoral head necrosis is incurable once the lesion has progressed to the point where changes appear on plain radiographs.
The three challenges in the repair of human femoral head necrosis are the collapse of the femoral head as the repair process progresses, the resorption of the osseous articular surface (subchondral bone dense mass), and the destruction of the articular cartilage. Why does femoral head necrosis collapse? Although the bone cells have died after femoral head necrosis, the inorganic salts of the bone matrix remain unchanged and basically retain the original mechanical strength unchanged. With the development of the repair process, the mechanical strength and elastic modulus of the femoral head gradually decreases, and the mechanical strength is only about half of the original one. In addition, microfractures will appear in the femoral head of normal people, and these microfractures will slowly heal, but once necrosis occurs, these microfractures cannot heal, and time often decreases the loading capacity, and eventually subchondral fractures will inevitably appear, and the femoral head will collapse. In other words, the faster this ineffective repair, the faster the collapse, so the collapse of young people, faster than the elderly, the collapse will be accelerated after the use of blood-activating drugs. The process of femoral head necrosis repair is summarized in the table below.
At present, the natural course of osteonecrosis and the speed of collapse development are not well understood by human beings, and it is usually believed that the course of femoral osteonecrosis develops faster. Femoral head collapse usually occurs within two years of the onset of pain, and 50% of patients have to undergo surgery within 3 years of establishing the diagnosis. We found that many patients had mild collapse within 4-6 months of the onset of symptoms.
V. Clinical manifestations of femoral head necrosis
The first conscious symptom of femoral head necrosis is pain, which is around the hip joint, inner thigh, anterior side or knee. In the early stage, the pain is vague, dull and intermittent, and the pain is aggravated by more activities, and can be relieved or reduced by rest. However, there are some cases of persistent pain, whether it is from exertion or rest, or even from lying in bed. Moreover, the pain gradually increases. At this time, although there is no obvious abnormal morphological change on the X-ray, the hip joint has different degrees of functional limitation. For example, the patient’s hip joint on the affected side is limited in abduction and rotation, and cannot squat in place. At the advanced stage of femoral head necrosis, the femoral head collapses, fractures and deforms, and some of them may cause hip dislocation, and the pain at this time is directly related to hip joint activities and weight bearing. The pain is caused by bony friction in the joint when moving, but the pain is not obvious when there is no friction between the head and socket at rest. Therefore, the pain is aggravated by walking and activity, while the pain is stopped or reduced by movement. In short, the early stage is mainly pain, accompanied by functional limitations; late stage is mainly functional impairment, accompanied by pain.
Six, how to determine the early femoral head necrosis disease
Femoral head necrosis, the earliest symptom is hip joint soreness, sleepiness, sometimes intermittent pain. This is the main symptom of the disease. There are many causes of hip pain, trauma, hip dislocation, degenerative disease, inflammation, tumor, lumbar spine disorders and medical and dermatological diseases, etc., which can cause pain in the hip joint. Femoral head necrosis is only one of the many diseases that cause hip pain, and as an independent disease, femoral head necrosis has its own special characteristics.
Self-examination to determine whether you have osteonecrosis of the femur is carried out from the following aspects.
(1) Hip pain radiating to the groin area or to the posterior, lateral or medial side of the hip or knee.
(2) Stiffness, weakness and limited movement of the hip joint, inflexibility in lifting the leg, early appearance of symptoms such as planking or outward skimming of the leg as well as difficulty in squatting.
(3) Limping: the affected limb does not dare to put weight on it when walking, like walking on tiptoe.
(4) After the fracture, dislocation or sprain of hip joint heals, intermittent or persistent pain in the hip appears gradually or suddenly. The pain is aggravated after walking activities, sometimes it is rest pain, and the pain is mostly pins and needles-like or sore, and the above-mentioned reaction occurs.
(5) Long-term or short-term heavy use of hormones or frequent alcoholics develop hip pain, mostly vague and dull, often located in the groin, obvious during activity and relieved after rest.
(6) Cold and damp: when the weather is cold, the hip joint is sore and sleepy, the pain is aggravated and the function is limited.
(7) Inflammation: When you have a cold and fever, blood sedimentation is accelerated, white blood cells are elevated, and the pain in the affected hip is aggravated.
Those who have the above conditions may have femoral head necrosis and need to be diagnosed in hospital.
Diagnostic criteria experts suggest that the diagnostic criteria proposed by the Japan Institute of Osteonecrosis (JIC) and Mont be integrated to develop our diagnostic criteria. I. Main criteria 1. Clinical symptoms, signs and history: arthralgia mainly in the groin and hip and thigh areas, limited internal rotation of the hip joint, history of hip trauma, history of corticosteroid application, history of alcoholism. 2. X-ray changes: collapse of the femoral head, not accompanied by narrowing of the joint space; sclerotic zone of demarcation within the femoral head; subchondral bone with transverse X-ray zone (crescent sign, subchondral fracture). 3. Nuclear scan shows cold areas in the hot zone within the femoral head. 4. T1-weighted phase of MRI of the femoral head shows banded low signal (banded type) or T2-weighted phase with bilinear sign. 5. Bone biopsy shows more than 50% osteocyte vacuolation fossa in the trabeculae and involvement of multiple adjacent trabeculae with bone marrow necrosis. Secondary criteria 1. X-ray shows femoral head collapse with narrowing of the joint space, cystic degeneration or speckled sclerosis in the femoral head, and flattening of the outer upper part of the femoral head. 2. Nuclear bone scan shows a cold or hot zone. 3. MRI shows a band type with homogeneous or heterogeneous low signal intensity without T1 phase. Meeting two or more major criteria will confirm the diagnosis. Complying with one major criterion, or the number of positive secondary criteria ≥ 4 (including at least one kind of positive radiographic changes), the diagnosis is possible.
Seven, the staging of femoral head necrosis
(I) Stage I of femoral head necrosis (ultrastructural variant stage).
X-rays show disorganized and fractured bone trabecular structures in the bearing system of the femoral head, with the appearance of hairy edges of the femoral head, clinically with or without limited mild pain.
Femoral head necrosis stage II (sensitized stage).
X-rays show small cystic lesion shadows inside the femoral head, with uneven density in the ring area around the cystic lesion area. The bone trabecular structure is disturbed, sparse or blurred. Small collapses may also appear, and the area of collapse may be 10-30%. The clinical condition is accompanied by significant pain and slight restriction of movement.
Femoral head necrosis stage III (necrosis stage)
X-rays show morphological changes of the femoral head, including incomplete, worm-like or flattened edges, partial loss of bone trabeculae, uneven bone density, widening or narrowing of the acetabulum and femoral head gap, and formation of redundant bone.
Femoral head necrosis stage IV (disabling stage)
The morphology and structure of the femoral head are obviously changed, with large irregular collapse or flattening, and the structure of the bone trabeculae is mutated. The gap between the acetabulum and the femoral head disappears, etc. Clinical manifestations include pain, functional impairment, stiffness and inability to walk, dislocation or subluxation, and limitation of functional activities of the involved knee joint. Since osteonecrosis often involves both sides, most patients end up with joint deformity and secondary osteoarthritic changes. Although there are numerous treatment methods available, none of them are sure of their efficacy, making treatment quite tricky. However, it has been proven that the earlier the treatment, the better the results. Because ischemic necrosis of the femoral head is common and difficult to deal with, treatment is used as an example.
(II), Ficat staging
Stage 0: no pain, normal plain film, abnormal bone scan and MRI.
Stage I: pain, normal plain film, abnormal bone scan and MRI.
Stage II (excessive stage): pain, cystic degeneration or/and sclerosis on plain film, abnormal bone scan and MRI, no subchondral fracture.
Stage III has pain, with collapse of the femoral head on plain radiographs and abnormalities on bone scan and MRI, with crescentic sign (subchondral collapse) or/and subchondral step-like collapse of the bone.
In stage IV, there is pain, acetabular lesions are seen on plain film, joint space narrowing and osteoarthritis are seen, and abnormalities are seen on bone scan and MRI.
(iii) Steinberg stage, i.e. University of Pennsylvania stage
Stage 0: normal plain film, bone scan and MRI
Stage I: normal plain film, abnormal bone scan or/and MRI
AC mild femoral head lesion <15% in extent
BC moderate 15-30%
CC severe:>30%
Stage II: transillumination and sclerotic changes in the femoral head
A mild:<15%
B Moderate:15-30%
C severe:>30%
Stage III: subchondral collapse (crescent sign), no flattening of the femoral head
A mild:<15% of articular surface length
BC moderate:15-30% of articular surface length
C Severe:>30% of articular surface length
Stage IV:Femoral head flattened
A mild:<15% articular surface or collapse <2-mm
B Moderate:15-30% articular surface or collapse 2-4-mm
C Severe:>30% articular surface or collapse >4-mm
Stage V:Joint stenosis or acetabular lesion
A Mild:
B Moderate
C Severe
VI stage of severe degenerative changes
(D), international staging of femoral head necrosis (bone circulation society ARCO stage)
Stage 0: biopsy results consistent with necrosis, the rest of the examination is normal
Stage 1: Positive bone scan or/and MRI
A magnetic resonance femoral head lesion extent <15%.
B MR femoral head lesion extent 15-30%.
C magnetic resonance femoral head lesion extent >30%.
Stage 2: patchy uneven density of femoral head, sclerosis with cyst formation, no manifestation of collapse on plain film and CT, positive MRI and bone scan, no change in acetabulum.
A magnetic resonance femoral head lesion extent <15%.
B MR femoral head lesion extent 15-30%.
C magnetic resonance femoral head lesion extent >30%.
Stage 3: Crescentic sign on the frontal and lateral photographs
A Crescent length – <15% of the joint surface length or <2mm collapse
B crescent length – 15-30% of articular surface length or collapse 2-4mm
C Crescent length – >30% of the joint surface length or collapse >4-mm
Stage 4: Collapse and flattening of the articular surface, narrowing of the joint space, necrotic changes in the acetabulum, cystic changes, cysts and bone spurs.
ARCO staging is as follows.
In fact, the greater the extent of femoral head necrosis lesions, the worse the prognosis. A disadvantage of Ficat staging is that there are no quantitative criteria, and there is no connection between the size and extent of lesions and staging. ARCO staging puts subchondral fracture and femoral head collapse in one stage, and puts mild joint space stenosis and severe osteoarthrosis in the same stage, which we found in our daily work. There is a relatively large difference in the treatment outcome of subchondral fractures and femoral head collapse, and the treatment outcome of mild and severe osteoarthritis is also different. We think the Steinberg (University of Pennsylvania) staging is more reasonable and use it to judge our treatment outcome. Below is the table of femoral head necrosis staging.
Eight, the treatment of femoral head necrosis
1.Why should femoral head necrosis be treated early?
Femoral head necrosis is a progressive disease, such as no special treatment, 70% to 80% of patients in the x-ray and clinical manifestations of disease progression. The natural course of femoral head necrosis includes two aspects, namely, progressive collapse of the femoral head and secondary osteoarthritis of the hip joint. If it progresses to severe osteoarthritis, only artificial total hip replacement can be performed. Since the disease mostly occurs in young adults, the aim of treatment is to preserve the femoral head as much as possible before collapse and delay the time of artificial joint replacement, in addition to improving clinical symptoms. On the contrary, if you are afraid of surgery and take various kinds of blood-activating and pain-relieving drugs, or take some special drugs orally, you will miss the time of surgery, and when the femoral head develops into the collapsed stage or osteoarthritis stage, it will be more difficult to treat. If the patient does not receive timely and regular treatment, the best time for treatment will be missed, plus the collapse of the femoral head caused by weight bearing (such as walking, climbing, carrying things, etc.) and the formation of osteoarthritis, the final result is that the patient will be disabled.
2.Conservative treatment
(1) Avoid weight-bearing: you can first rely on canes, axillary canes and other supports to strictly limit weight-bearing, which can restore blood supply to ischemic tissues and protect them from pressure to control lesion development, prevent collapse, and promote self-healing of ischemic necrosis of the femoral head. However, it is generally believed that weight-bearing restriction cannot save the development of femoral head necrosis. This method is mainly applied to elderly patients who are not suitable for surgical treatment, poor general condition, progressive ischemic necrosis and patients with poor prognosis. The possibility of self-healing is related to the size of the lesion and the distance from the joint surface: if the lesion is small or far from the joint surface, it can mostly heal by itself; if the lesion is adjacent to the joint surface or if the lesion is large in scope, the possibility of self-healing is extremely small even without weight-bearing.
(2) Pharmacological treatment: For the etiological theory of fat metabolism disorder and intravascular coagulation, the application of lipid-lowering drugs and anticoagulants for the treatment of hormonal femoral head necrosis provides a new idea for drug prevention and early treatment. Studies have confirmed that high-dose application of hormones along with earth kinase and aspirin can slow down the process of hormonal osteonecrosis and have a role in preventing hormonal osteonecrosis. The application of drugs for the treatment of femoral head necrosis is less reported. In short, the effect of drug treatment is not yet certain, but it is still an important research direction because of its non-invasive nature.
(3) Electrical stimulation: It has osteogenic effect and can promote fracture healing. Electrical stimulation can be used as an independent treatment for osteonecrosis or as an adjunct to surgery.
(4)Hyperbaric oxygen therapy
(5)Interventional treatment
(6)Stem cell therapy
(7) Chinese medicine treatment
(8)Other treatment methods: such as radiotherapy, etc., not much reported, the effect needs to be further determined.
3.Surgical treatment
(1)Treatment of preserved femoral head, applicable to early femoral head necrosis.
(1) Borehole decompression (central decompression): it can reduce intraosseous pressure, promote venous reflux, release trophoblastic vascular spasm, and enable neovascularization to grow into the ischemic area along the bone hole. It is mainly used for patients without joint surface collapse in the early stage, and is the simplest surgical method to treat osteonecrosis.
Osteotomy: Osteotomy includes autologous cancellous bone graft, autologous cortical bone graft, allogeneic bone graft, cartilage graft, which can be combined with other treatment methods such as central decompression, electrical stimulation and osteotomy. Among them, autologous cancellous bone and cortical bone graft are more frequently used. Autologous cancellous bone has good osteogenesis induction and can promote the repair of necrotic femoral head, while cortical bone plays a supporting role for articular cartilage and subchondral bone in the necrotic area during the repair of femoral head. Bone grafting methods include bone grafting after central decompression, slotting bone grafting at the craniocervical junction, opening a window in the articular cartilage of the femoral head, lifting cartilage bone grafting and then resetting the cartilage. Bone grafting can be used for ficat stage II, early stage III patients and patients who have failed central decompression. The recent efficacy of this method is more certain, but the long-term efficacy is still controversial. However, it is worthwhile to accelerate the repair of the femoral head with the help of bone graft and shorten the time of bed rest, and the combination of growth factors, electrical stimulation and other methods to promote bone healing can improve its efficacy.
Bone graft with blood supply: There are more methods of bone graft with blood supply, which can come from iliac bone, greater trochanter or fibula, and can be with myofibular or vascular tip. The clinical results are reported in the literature, but the x-ray improvement is not ideal, and a significant proportion of patients still need arthroplasty in the long-term follow-up.
④Osteotomy: By changing the corresponding position relationship between the femoral head and the femoral stem, it can increase the weight-bearing area of the femoral head, reduce the pressure on the femoral head, and move the necrotic lesion of the femoral head out of the weight-bearing area, thus reducing the local stress. At the same time, osteotomy makes the medullary cavity open, which can reduce the intraosseous pressure and improve the blood circulation of the femoral head.
(5) Compression allograft bone grafting
(2)Arthroplasty
①Femoral head surface replacement: surface replacement was proposed by Judet, a French doctor, in the 1950s as a predecessor and an early design of hip arthroplasty. By replacing a small portion of the proximal femoral head and neck with a special prosthesis, only the necrotic cartilage is removed, preserving most of the femoral head and femoral neck bone, which will not affect subsequent total hip replacement surgery in case of failure. It is suitable for younger patients with extensive pre-collapse lesions or a collapsed femoral head but no acetabular involvement. The recent (3-year) success rate of surface replacement is between 84% and 88%. Hungerfold et al. (1998) reported 33 cases of femoral head surface replacement with excellent rates of 91% and 61% at 5 and 10 or 5 years, respectively. Nelson et al. reported 21 cases of femoral head surface replacement with a mean follow-up of 6 or 2 years and an excellent rate of 86%. Beaule et al. reported 37 cases of Horton and Cook (2001) reported another group of cases with 5- and 10-year survival rates of 79% to 91% and 56% to 67%, respectively. Recently, Siguier et al. (2001) reported a group treated with partial femoral head surface replacement, in which only dead bone was removed during surgery and a specially designed cemented prosthesis was used for filling and fixation.
②Metal cup arthroplasty
③Total hip arthroplasty: applied to patients with collapsed femoral head necrosis.