Femoral epiphysis osteochondrosis
Introduction
Introduction to femoral skull tibial rickets Femoral condyle osteochondrosis is a secondary articular osteochondrosis. The main cause is osteophyte embolism caused by certain factors, resulting in necrosis of all or part of the ossification center of the epiphysis, and may be associated with endochondral bone disorder. Femoral condyle osteochondrosis is also known as avascular necrosis of the femoral head in children, or Legg-Calvè-Perthes disease, which was described by three scholars in 1910, referred to as Perther disease, which is caused by a blood vessel disorder in the femoral head. The femoral skull has different degrees of necrosis. After the lesion heals, the femoral head is often flattened, so it is also called flat hip. basic knowledge The proportion of illness: 0.002% Susceptible people: good for children Mode of infection: non-infectious Complications: osteoarthritis
Cause
Femoral skull osteochondrosis
(1) Causes of the disease
The causes of the disease are diverse, but the real cause is not clear and may be related to the following factors:
Femoral head blood supply defects (23%):
A study by Trurta et al found that children aged 4 to 8 years had only one blood vessel supplying the blood of the femoral head, the external iliac artery. The blood supply from the main iliac artery was often blocked by the tarsal plate, and the external iliac artery was highly susceptible to the external circumflex muscle. The group's oppression interrupted the blood supply. After the age of 8 years, the round ligament vessels also participated in the blood supply of the femoral head, so the incidence of the disease was reduced. In addition, the variation of the vascular anastomosis of the femoral head inside the child, especially the boy, was very large, even Absence is also a cause of femoral head ischemia.
High intra-articular pressure (20%):
Any factors that can cause increased pressure in the hip joint cavity, such as blood in the joint cavity after trauma, infection and temporary synovitis, can cause the blood vessels supplying the femoral condyle to be compressed and cause the disease. Ma Chengxuan et al. Intra-osseous pressure at the upper end of the femur in 17 patients, the intra-osseous pressure of the affected side was significantly higher than that of the healthy side, and the venous angiography revealed that the internal and external venous stenosis was not developed and the development rate of the internal and external veins of the circumflex femur was significantly lower than that of the healthy side. Increased pressure in the hip joint cavity causes the venous return of the upper femur to cause this disease.
Trauma factor (14%):
Because the disease occurs mostly in boys, and the hip joint is a weight-bearing joint with more activities, some scholars have proposed the trauma theory that the disease is caused by repeated repeated repeated damage to the upper end of the femur.
Environmental factors (8%):
Including perinatal and post-natal living conditions, some scholars have reported that the incidence of breech-born children is four times that of normal-born children. Parents are older at birth, children after the third child, and children living in poverty are easy. Hair disease.
Endocrine factors (7%):
Tiroza Tanara measured serum growth factor A (SMA) levels in 47 children and found that the level of serum in normal children was significantly lower. The main function of SMA was to stimulate cartilage growth. Therefore, it is considered that SMA level is a disease. Promote factors.
Genetic factors (10%):
Perthes disease has a certain family history, and the chances of the disease are increased in the patient's brothers and in the first and second grade relatives, but no genetic evidence has been found in the study.
In recent years, coagulation dysfunction is considered to be a potential cause of the disease. Gregosiewicz et al. detected plasma levels of 12 antitrypsin in children with Perthes disease significantly higher than the control group, suggesting that fibrinolysis is reduced and the risk of endovascular embolization is increased. May cause this disease, Glueck found that anti-thrombin III (AT2III), protein C (PC), protein S (PS) and other active abnormalities and anti-active protein C (APCR) positive in children with Perthes disease The hypothesis of Perthes' disease etiology suggests that thrombophilia (PC, PS deficiency and APCR positive, etc.) and low fibrinolysis (t2PA, PA I and high lipoprotein, etc.) are closely related to the pathogenesis of Perthes disease.
The relationship between Perthes disease and endocrine, especially thyroxine disorder, shows that although children with Perthes disease have normal thyroid function, free thyroxine and free triiodothyronine are significantly increased, and the degree of femoral head involvement is directly proportional to plasma free thyroxine levels. However, whether these changes are the cause or the cause of the disease remains unclear, and some scholars have proposed the theory of growth retardation. Kealey measured serum interleukin A (SMA) levels in children with Perthes disease significantly lower than normal children, and indirectly supported developmental delay. Doctrines, other scholars suspect that Perthes disease is genetically related, Wansbrrugh (1959) first reported that the disease has a genetic predisposition, Renwick (1972) pointed out that Perthes disease parents had 0.3%, brothers and sisters 3.8%, collateral relatives There were 0.3% with the same disease, and Catterall (1970) noticed that Perthes disease was related to physical factors, but no obvious genetic evidence was found.
(two) pathogenesis
The pathological process of avascular necrosis of the femoral head, including osteonecrosis, followed by bone resorption and new bone formation, as well as remodeling of the femoral head, can be divided into four stages.
1. In the early stage, synovitis is swollen joint capsule, synovial congestion and edema and joint fluid exudation, but no inflammatory cells in synovial fluid. This period lasts for 1 to 3 weeks.
2. The anterior and lateral femoral head of the femoral head was involved at the earliest stage, or the whole epiphysis was necrotic due to ischemia. At this time, the bone structure remained normal, but the bone lacuna was empty, and the bone marrow cavity was filled with amorphous debris and the bone was small. The beam is broken into pieces or compressed into pieces. Due to the ischemic necrosis of the femoral head, the internalized endochondral bone of the epiphysis is temporarily inhibited, and the surface layer of the articular surface is continuously grown by synovial nutrition. X-ray On the slice, the femoral condyle is small and the joint space is widened. The necrotic trabecular bone is broken due to fragmentation, compression and new bone deposit on the surface of the necrotic trabecular bone, which increases the density, while the dry end is loose and decalcified. Decalcification of the end is caused by localized hyperemia. It is a soft tissue invasion of blood vessels and absorbs the tissue reaction of necrotic bone. There is no obvious change in the general morphology and femoral head contour in this period, and the necrosis period is longer, after 6 to 12 months, clinical It is generally asymptomatic. Salter claims that this stage is a clinical quiescent period. It is a potential avascular necrosis of the femoral head. If blood supply can be restored at this time, it is expected that no serious deformity will remain.
3. Fragmentation or regeneration period Due to the stimulation of dead bone, the connective tissue composed of capillaries and monocytes invades the necrotic area, absorbs necrotic trabecular bone fragments, and forms fibrous tissue in the medullary cavity, and osteoclasts increase. It is active and involved in the absorption of necrotic trabeculae. At the same time, abundant osteoblast activity is enhanced, and normal osteoids are formed between the necrotic trabecular bone and on the surface. These vascular tissues are derived from the round ligament. The periosteum and metaphysis, the metaphyseal vessels or the epiphyseal plate or the tissue surrounding the epiphyseal plate, the trabecular bone formed by the newly born osteoid is relatively slender, and later converted into lamellar bone, cartilage around the necrotic area There is still no obvious change, but the basal layer cartilage can not get the nutrition of the synovial fluid because it is far away from the joint surface, and it can lose its activity. At this stage, the new bone quality is low, and it is gradually shaped into normal bone or according to the stress-bearing condition. Changing the shape, Salter called it "bioplastic", the process lasted about 2 to 3 years.
4. Healing period Because the newly formed trabecular bone is an immature lamellar bone, which is slender and fragile, it is easy to compress with the unabsorbed necrotic trabeculae. The compression zone is mostly confined to the anterior lateral part of the femoral head, and the frog On the X-ray film, the cup-shaped defect appears. On the X-ray film, the cup-shaped defect overlaps with the intact bone, which shows cystic changes. For example, the entire nucleus is involved, and there are many degrees of deformation, similar to mushrooms. The mushroom shape, the final femoral head is significantly enlarged, from a circular femoral head (coxa magna) in the center of the acetabulum, into a flat femoral head (coxa plana).
Salter emphasizes that the deformation of the femoral head and neck is due to the subchondral fracture in the necrotic phase, which initiates the absorption of necrotic bone and the original interwoven bones. At the same time, synovial reaction and muscle spasm can occur, followed by adductor muscle and iliopsoas contracture. The lateral dislocation of the bone to the lateral side is limited, and the hip joint activity is limited. For example, the stress concentration area of the femoral head is subjected to excessive stress, which causes the femoral head to be flat or saddle-shaped deformed, further causing the femoral head to subluxate to the front and the outer side, and the femoral head continues. Ischemia not only causes ischemic necrosis of the epiphysis, but also causes ischemic necrosis of the epiphyseal plate to cause premature closure of the epiphyseal plate, which will affect the longitudinal growth of the lower extremity, especially the growth of the femoral neck, while the growth of the femur and greater trochanter is not disturbed. As a result, the femoral neck becomes shorter, and the greater trochanter can exceed the level of the tip of the femoral head. Although this deformity is different from the hip varus, it is like a hip varus in dysfunction, which is not conducive to the activity of the abductor muscle. Hip gait, called functional hip varus, in summary, the pathogenesis of avascular necrosis of the femoral head in children can be summarized.
Prevention
Femoral skull osteochondrosis prevention
The cause of this disease is not very clear, and there are no effective preventive measures. It is worth mentioning that because this disease is often accompanied by sequelae, children with Perthes disease can detect early signs of various sequelae and treat them in time. Perhaps it can prevent the occurrence of its sequelae, scientifically exercise, prepare well before the practice, do not run excessively, jump, squat, step by step, avoid damage.
Complication
Femoral condyle osteochondrosis complications Complications osteoarthritis
As the disease continues to progress, the pain becomes persistent, the sick child's sputum is obvious, the gluteal muscles and the thigh muscles are disused atrophy, the Qu's test is positive, and the hip flexion is inverted, causing the affected limb to become relatively short. The formation of the flat hip, the absolute length of the limb is also shorter than the healthy side, leading to early osteoarthritis in adulthood
A significant number of patients with Perthes disease have sequelae, including:
1 large rotor moves up;
2 limb shortening;
3 double head deformity;
4 Osteoarthritis, osteoarthritis is a long-term sequela of this disease, the first three malformations will promote its early occurrence to varying degrees.
5 hip subluxation.
Symptom
Femoral condyle osteochondrosis symptoms Common symptoms Inability to revascular disorders Dead osteochondral dysplasia and... Endochondral ossification
1. Clinical manifestations The onset of the disease is concealed, and the course of disease is long-lasting, with the main symptoms of hip pain and paralysis.
(1) Early: There may be no obvious symptoms, or only the limbs are weak, and there will be painless lameness after long distance walking. The painful parts may have groin, inner thigh and knee.
(2) Femoral head necrosis: significant hip pain, accompanied by tendon and limb shortening, tendon with adductor and iliopsoas, and gluteal and thigh muscle atrophy, hip mobility Restricted, especially outreach, the internal rotation activity is limited.
(3) Late stage: symptoms such as pain are relieved, disappear, joint activity returns to normal, or leftovers and rotational activities are limited.
2. There are many types of avascular necrosis of the femoral head introduced in the classification literature, such as Catterall, Lioyd-Roberts, Salamon, Salter-Thompson and Herring. The purpose of the classification is to select the treatment method for understanding the extent of the lesion, no matter which. The classification methods are based on the X-ray film to determine the extent and extent of the involvement of the femoral head. In order to facilitate the understanding of many of the classification criteria, before the introduction of the specific classification method, the common points of these classifications are summarized: The involvement of the bone skull is less than half of it or only a small part is type I. If it is more than half, it is type II and type III. If it is tired, all of it is type IV, and the Salter-Thompson classification basis is different. They are classified according to the range of subchondral fractures of the femoral head necrosis (active phase). If the extent of the subchondral fracture line does not exceed half of the radius of the femoral head hemisphere, it is type A. If more than half is Type B, the former has a good prognosis, and the latter has a poor prognosis. The current clinical classifications are as follows:
(1) Catterall classification: Catterall is divided into 4 types according to the pathological changes, combined with the extent of femoral head involvement on X-ray films. It has guiding significance for clinical selection and prognosis, and has been widely accepted and applied by clinicians. .
Type I: The front of the femoral head is involved, but there is no collapse, no lesions appear on the epiphyseal plate and the metaphysis, and no obvious deformity remains after healing.
Type II: partial femoral head necrosis, the density of necrotic part is increased in the orthotopic X-ray film, and the normal bone tissue on the inner side and the outer side of the necrotic bone has a columnar appearance, which can prevent the collapse of necrotic bone, especially the lateral X-ray. On the film, a complete column of bone tissue appears on the outside of the femoral head, which has great significance for the estimation of prognosis. This type of metaphysis has lesions, but the epiphyseal plate is protected by normal bone tissue that is extended to the anterior tongue-like metaphysis. Without damage, new bone formation is active, and the height of the femoral head is not significantly reduced. Because the epiphyseal plate maintains its integrity, its plasticity potential is not affected. After the lesion is stopped, if there are still several years of growth, the prognosis is very high. good.
Type III: About 3/4 of the femoral head is necrotic, the normal bone tissue column on the lateral side of the femoral head disappears, the cystic change occurs in the metaphyseal end, the epiphyseal plate loses the protective effect of the metaphysis, and necrotic changes are also observed. X-ray films It shows severe collapse and the collapsed necrotic bone is larger, and the longer the process, the worse the prognosis (Figure 4).
Type IV: The entire femoral head is necrotic, the femoral head collapses, and often the normal contour cannot be restored. In this period, the epiphyseal plate is directly damaged. If the tarsal plate is severely damaged, the normal growth ability will be lost, which will severely inhibit the plasticity of the femoral head. The potential of the shape, therefore, regardless of any treatment, the final outcome is very poor, although, after appropriate treatment, can reduce the degree of deformity of the femoral head (Figure 5).
(2) Classification of the lateral column of the femoral head: a new classification method proposed by Hering in 1992. The femoral condyle was divided into the inner, middle and outer columnar regions on the standard pelvis X-slice. The width of the femoral head is 15% to 30%, the central area is about 50%, and the inner area is 20% to 35%. The authors also refer to these areas as lateral pillars, central pillars, and medial columns. (medial pillar), and then according to the degree of involvement of the lateral column, the disease is divided into 3 types, type A: the outer column is not affected, the prognosis is good, the femoral head is not flat; B type: the outer column is involved, the degree of compression collapse is low 50% of the normal lateral column, the prognosis is still good, the femoral head is not flat; C type: the lateral column is involved, its height is >50%, the prognosis is poor, the femoral head is flat, in short, the more the lateral column is involved, the worse the prognosis (Figure 6 )
The early diagnosis of this disease is very important, and timely diagnosis and treatment are closely related to the prognosis of children.
When children aged 5 to 10 years have unexplained hip pain, lameness, and symptoms do not improve for several weeks, the possibility of suffering from this disease should be considered. The earliest X-ray signs are joint capsule swelling and femoral head to the outside. For shifting, the bilateral X-ray films should be carefully compared and regularly reviewed. Once the density of the epiphysis changes, the diagnosis can be confirmed. For suspicious cases, radionuclide scanning can also be performed. After 99Tc intravenous gamma scintigraphy It can display the radioactive sparseness of the osteonecrosis area or the radioactive concentration of the bone regeneration area in the early stage. The intraosseous pressure measurement also contributes to the early diagnosis, but the clinical application is less.
Examine
Femoral skull tibial rickets
1. X-ray examination is the main method and basis for clinical diagnosis of avascular necrosis of the femoral head. Regularly cast double-hip joint orthotopic and frog X-ray films can dynamically observe the morphological changes of the femoral head during the whole process of the lesion, and each One stage of X-ray film can reflect pathological changes.
(1) Synovitis: X-ray film mainly shows soft tissue swelling around the joint, while the femoral head is slightly displaced to the outside, but generally does not exceed 2 to 3 mm. These non-characteristic changes can last for several weeks. Line tracking observation.
(2) The early stage of femoral condyle involvement: the X-ray film sign of the early stage of necrosis, mainly the nucleus of the nucleus is smaller than the normal one. The continuous observation for 6 months does not show growth, indicating that the endochondral bone is temporarily stopped, the joint space is widened, and the femur The upper edge of the neck presents a circular protrusion (Gage sign), and the orthotopic X-ray film shows that the femoral head is displaced to the outside by 2 to 5 mm, and then the thickness of some or more epiphyses is increased. The reason is:
1 Degenerative osteoporosis decalcification of the femoral neck adjacent to the epiphysis, resulting in increased femoral condyle density;
2 necrotic trabecular bone is compressed;
3 revascularization of early necrotic callus, new bone formation on the surface of necrotic trabecular bone, resulting in a real increase in density, the authors pointed out that "crescent sign" may be the first X-ray signs of osteonecrosis, On the frog slice, a well-defined strip density reduction zone appears in the anterior lateral cartilage of the femoral head. Salter believes that the "New Moon Sign" is an important subclinical fracture of the articular cartilage, which is not only the main cause of diagnosis. Based on, and helpful to speculate the extent of necrosis of the femoral head, determine the severity of the lesion and estimate the prognosis.
(3) Necrotic phase: X-ray features anterior and lateral necrosis of the femoral head. An uneven density-increasing image is observed on the orthotopic X-ray film. For example, the X-ray film of the projection frog is located, and the dense area is located at the anterolateral side of the femoral head. In this case, it is necessary to follow up for 1 year to determine whether it is partial necrosis or total necrosis. If the system is completely necrotic, the epiphysis often has a flat deformity, but the articular angiography shows that the femoral condyle still retains its circular outline.
(4) Fragmentation period: X-ray films show the distribution of hardened and sparse areas, the hardened area is the result of compression of the necrotic trabeculae and the formation of new bone, while the sparse area is the vascularized osteogenesis that has not been ossified. The image of the tissue, the femoral neck became shorter and wider, the necrotic femoral head corresponding to the metaphysis showed lesions, the lighter showed osteoporosis, and the severe cystic changes may be due to the reintegration of the epiphyseal plate chondrocytes and vascular tissue invasion. Caused.
(5) Healing period or sequelae: The lesions in this period have been stabilized, and the osteoporotic area is filled by normal trabecular bone, so the density of ossification tends to be uniform, but the femoral condyle is obviously enlarged and deformed, and the X-ray film is visible. The bone is oval, flat or mushroom-shaped, and is displaced to the outside or subluxated. The acetabulum is also modernized and the medial joint space is widened.
2. Nuclide examination can not only determine the blood supply of bone tissue, but also reflect the metabolic state of bone cells. It is of great significance for early diagnosis, early determination of the extent of femoral head necrosis and differential diagnosis. Clinically, 99TC is used intravenously, and then The gamma scintigraphy was performed, and the early stage showed the radioactive sparseness or defect of the necrotic area. The local radioactive concentration was observed during the regeneration period. Crenshaw et al believed that the radionuclide sparseness of the affected side and the contralateral side such as the femoral head necrosis area was less than 50%. The lesion is equivalent to Catterall's type I or II, or Salter's type A, otherwise it is advanced, equivalent to Catterall's type III or IV, or Salter's type B. Compared with X-ray examination, the radionuclide examination can be advanced 6~ The necrotic range was determined at 9 months, and vascular regeneration in the necrotic area was shown 3 to 6 months earlier.
3. Arthrography is generally not used as a routine examination, but some authors believe that arthrography can detect the enlargement of the femoral head early, which is helpful to observe the general morphological changes of articular cartilage, and can clarify the cause of poor early femoral head coverage. Arthrography can more accurately show the degree of joint deformation, which has reference significance for the choice of treatment, but this is an interventional examination. Some children who cannot cooperate with the examination need to be given anesthesia. Therefore, arthrography should not be included in the examination. Check the project.
In recent years, with the application of magnetic resonance imaging technology, some hospitals have also carried out this examination on Perthes disease. Practice has proved that this test is of great value in diagnosing bone ischemic changes, and can be diagnosed early, and the ischemic area is low. The signal area clearly shows the cartilage area and thickness of the acetabular rim of the femoral head. The hip joint of the magnetic resonance imaging is similar to that seen by arthrography. It can clearly show whether the shape of the femoral head is normal. Magnetic resonance imaging is used to determine the ischemic lesion. It was examined before X-ray and there was no radioactive damage, but it is not universally applicable at present.
Diagnosis
Diagnosis and diagnosis of femoral sacral osteochondrosis
Differential diagnosis
(1) Hip tuberculosis:
Often difficult to distinguish, especially in the early stage more confusing, hip tuberculosis is a limitation, progressive, destructive, inflammatory lesions, can involve the femoral head, acetabulum and femoral neck, showing joint capsule swelling due to joint fluid effusion X The line signs can last for a long time. The femoral head osteochondrosis is a subchondral aseptic necrotic lesion with increased necrotic bone density, deformation and secondary hip osteoarthritis as the main X-ray findings. Joint effusion or abscess formation.
(B) transient (temporary) synovitis of the hip:
Both of them are similar in terms of age of onset and synovitis, but the course of disease is different. There is no abnormal X-ray manifestation of transient synovitis. In recent years, 99mTc scan can help: 99Tc photo of femoral epiphyseal osteochondrosis Into the reduction.
(c) cretinism:
Osteoclastosis in patients with cretinism can manifest as irregular calcification, but its appearance time and fusion time are delayed compared with normal children. The long diameter of the bone is shortened due to internal cartilage bone disorder. In addition, the sick child still has The situation of low intelligence can be distinguished.
(four) femoral epiphyseal spondylolisthesis:
The clinical symptoms of the two are similar, but the age of onset of epiphyseal spondylolisthesis is larger, and the hip internal rotation and restricted activity (Drehman sign) are characteristic.
(5) Other bacterial infectious diseases such as infectious arthritis, upper femur osteomyelitis, and Kaschin-Beck disease, which is more common in Northeast China.
