Classification, symptoms and treatment of osteochondropathy. aseptic necrosis of the femoral head (angbk)

Osteochondropathy is a group of diseases of bones and joints, occurring mainly in childhood and adolescence and manifested by aseptic necrosis of subchondral parts of the skeleton subject to increased stress (most often spongy substance, apophyses and epiphyses tubular bones).

Among the entire pathology of the organs of the musculoskeletal system, osteochondropathy accounts for about 2.7%, while aseptic necrosis bone and cartilage tissue hip joint develops in 34% of cases, the radiocarpal joint and wrist - in 14.9%, the knee joint - in 8.5%, the elbow - in 14.9%. Joint damage upper limbs observed in 57.5% of patients, lower extremities- in 42.5% of cases. The age of patients with aseptic necrosis ranges from 3-5 to 13-20 years.

Classification

Osteochondropathy is conventionally divided into four groups:

1. Osteochondropathy of the epiphyses of tubular bones - the humerus (Hass disease), the sternal end of the clavicle, metacarpal bones and phalanges of the fingers (Thiemann's disease), head femur(Legg-Calve-Perthes disease), heads II-III metatarsal bones(Kehler II disease).

2. Osteochondropathy of short spongy bones - vertebral bodies (Calve's disease), lunate bone of the hand (Kinböck's disease), sesamoid bone of the I metatarsophalangeal joint, navicular bone of the foot (Kohler's disease I).

3. Osteochondropathy of the apophyses (apophysitis) - juvenile apophysitis of the vertebrae (Scheuermann's disease - May), apophysitis pelvic bones, tuberosity of the tibia (Osgood-Schlatter disease), patella (Larsen-Johanson disease), pubic bone, tubercle calcaneus(Haglund-Shinz disease), metatarsal apophysitis (Islen disease).

4. Partial wedge-shaped necrosis of the articular ends of the bones (dissecting osteochondrosis) of the head of the humerus, the distal epiphysis of the humerus, the medial condyle of the distal epiphysis of the femur (Koenig's disease), the body of the talus (Haglund-Sever's disease).

Etiology and pathogenesis

The causes and mechanisms of development of osteochondropathy have not been finally established. However, there are a number of factors that play an important role in the development of the disease. Thus, a congenital or family predisposition to the development of the disease has been proven. Often, osteochondropathy occurs in children with dyshormonal disorders, in particular, those suffering from adiposogenital dystrophy. Confirmation important role endocrine system in the pathogenesis of osteochondropathy is the high frequency of this form of pathology in patients with acromegaly and hypothyroidism. There is also a connection between osteochondropathy and infectious diseases.

There are five stages in the development of osteochondropathy:
I - aseptic necrosis as a result of vascular disorders;
II - compression fracture;
III - fragmentation, characterized by the development connective tissue in areas that have undergone necrosis;
IV - productive with intensive recovery processes(reparative);
V - recovery (reconstruction bone tissue).

A certain value in the pathogenesis of osteochondropathy is played by vascular disorders, among which it is necessary to highlight the neuro-reflex angiospasm caused by trauma or prolonged microtraumatization terminal branches vessels. The development of osteochondropathy is also facilitated by prolonged pressure loads on spongy bones, which leads to impaired microcirculation and obliteration of blood vessels, followed by the development of avascular necrosis. In the case of early elimination of the etiological factor, osteoclast proliferation is possible, followed by complete or incomplete restoration of the bone structure.

Aseptic bone necrosis was first identified in children and adolescents with differential diagnosis with widespread at that time osteoarticular tuberculosis. This disease differs from the osteoarticular form of tuberculosis in a much more favorable course. Its first name is osteochondropathy (literally, “disease of bone and cartilage”). However, it does not provide information about the etiology and pathogenesis pathological changes. In world literature, this term has not been used for a long time. The term "aseptic osteonecrosis" indicates both the nature of the pathological changes (necrosis) and the non-infectious origin of the necrosis, in contrast to, for example, osteonecrosis in osteomyelitis.

The role of circulatory disorders in the development of aseptic necrosis is evidenced by the absence of radiopharmaceutical penetration into the necrotic area of the bone in the early stage of the disease during bone scintigraphy and its signal enhancement after contrasting with MRI. Undoubtedly, the importance of circulatory disorders in the development of aseptic necrosis after fractures and dislocations, accompanied by vascular ruptures, as well as in hemoglobinopathies, which lead to erythrocyte aggregation and increased blood viscosity, or in decompression sickness. Aseptic necrosis in Gaucher's disease and hypercortisolism is explained by a violation of microcirculation due to an increase in intraosseous pressure. This is due to the growth in the bone marrow spaces of histiocytes in Gaucher disease and due to an increase in the volume of fatty tissue. bone marrow with hypercortisolism. Osteonecrosis is often combined with hyperlipidemia. In case of violations fat metabolism Fat embolism is considered possible due to destabilization and agglomeration of plasma lipoproteins or ruptures of adipose marrow and extraosseous adipose tissue. However, explicit etiological factor is not always detected in aseptic necrosis.

Causes of aseptic necrosis:

trauma (fractures and dislocations);
hypercortisolism;
hemoglobinopathies;
decompression sickness;
alcoholism;
pancreatitis;
collagenosis (damage to small vessels);
Gaucher disease;
kidney transplant;
gout and hyperuricemia;
radiation therapy;
disorders of fat metabolism;
diabetes.

The occurrence of necrosis is explained by ischemia of the affected area of the bone. It has been shown that already in the first 12-14 hours after the cessation of blood supply, hematopoietic cells die, bone tissue cells can remain viable for up to 2 days, and adipose bone marrow cells - from 2 to 5 days. However, not all cases of aseptic necrosis can be explained by the cessation of blood circulation and, as a result, the development of bone tissue necrosis. Often undetectable in aseptic necrosis obvious reasons. It is not clear in what form this violation of the blood supply occurs. Morphologically vascular bed usually not changed. Without questioning the importance of the hemodynamic factor, one cannot exclude the role of other factors in the development of aseptic necrosis, including increased load. With disorders of fat metabolism, the development of aseptic necrosis can be facilitated by static overload due to weight gain. An example would be women with postpartum obesity who initially develop aseptic necrosis of the heads of the femurs, and after they begin to use crutches while walking, aseptic necrosis of the heads of the femurs humerus. This can be explained by the transfer of the load on the hands. Perhaps the cause of aseptic necrosis is a mismatch between the blood supply to a given area of bone tissue and the load being performed.

The epiphyses of tubular bones and some cancellous bones affected by aseptic necrosis are in relatively unfavorable conditions of blood supply. Most of their surface is covered with articular cartilage, and only a small part remains on the share of surfaces through which vessels can penetrate into the bone. In addition, in the growing skeleton, the blood supply to the epiphyses is relatively isolated from the rest. vasculature bones, which limits the possibility collateral blood flow. Under these conditions, the probability of blood supply to the epiphysis or small bone increases with a single artery with no collateral blood supply. Aseptic necrosis develops, as a rule, in the heads of the bones, and not in the articular cavities. The most vulnerable is the head of the femur. Aseptic necrosis may have multiple localizations. In such cases, all known systemic causes should be ruled out.

Necrosis arising in the metadiaphysis long bones, it is customary to call bone marrow infarcts, although spongy substance is also involved in the process. They have much more favorable course, are limited to the medullary cavity, do not affect the cortical layer and are usually detected incidentally already in remote period after the development of a heart attack. The common origin of aseptic necrosis and bone marrow infarcts is confirmed by cases of their combination in the same area.

In children and adolescents:

femoral head;
head of the II or III metatarsal bone (second Alban-Keller disease);
navicular bone of the foot (first Alban-Keller disease);
epiphyses of the phalanges of the fingers.

In adults:

femoral head;
head of the humerus;
talus block;
lunate bone (Kinböck's disease).

Aseptic necrosis excludes variants of ossification of some bones, such as the calcaneus, as well as some diseases that were initially mistaken for aseptic necrosis. Among them is Scheuermann-Mau's disease, which was considered as necrosis of the annular apophyses of the vertebral bodies. Such necrosis was obtained under extremely non-physiological conditions of the experiment (creation of a sharp kyphosis by suturing the tail of rats under the skin of the abdomen) and has not been confirmed by anyone in humans. Currently, the prevailing opinion is about the dysplastic nature of this disease with a disorder of enchondral ossification of the growth cartilage plates of the vertebral bodies, uneven growth of the latter and the occurrence of local protrusions into the vertebral bodies (Schmorl's nodes). Osgood-Schlatter disease occurs as a result of microtraumatic injuries that occur in adolescents involved in sports (separations of small cartilage fragments from the tuberosity apophysis, ruptures of the fibers of this tendon itself, chronic tendinitis and bursitis).

Calve's disease is characterized by a uniform flattening of the vertebral body, and in most cases an eosinophilic granuloma is detected in it.

Pathomorphologically, in aseptic necrosis, several zones are distinguished. The zone of actual necrosis is characterized by the death of all cells, including adipose tissue. Theoretically, it should become hypointense on T1-weighted MRI images, but it may retain a normal signal for the bone marrow for a long time or be manifested by other changes in the signal. There are indications of the possibility long-term preservation lipid depot and after cell death.

When partial lesion bones, there are reactive changes outside the zone of necrosis. On its periphery there is a zone of ischemia, in which the cells of fatty bone marrow can be preserved as less sensitive to hypoxia. In place of the ischemic zone, a reactive zone is formed over time, delimiting the necrotic area from the living bone. Necrosis causes inflammatory response with the formation of granulation tissue on the border with the necrotic zone, which absorbs the necrotic bone. Even further to the periphery, adipose marrow cells transform into fibroblasts or osteoblasts, which produce atypical fibrous bone in sheets on the surface of necrotic bone trabeculae. Behind this zone is a zone of hyperemia of intact bone.

Osteonecrosis does not receive direct imaging on radiographs and is detected due to secondary reactive change in the surrounding bone tissue.

The increased density of the necrotic zone is explained by its exclusion from metabolism, as a result of which it retains its original density, thereby standing out against the osteopenic background, which is due to increased resorption of the surrounding living bone tissue in the zone of hyperemia.
The necrotic area is delimited from the unchanged bone tissue by the reactive zone (if not the entire bone is affected, but only part of it).

However, in order for these secondary changes reached sufficient severity and were displayed on radiographs, several months should pass. The diagnosis can be established much earlier according to scintigraphy (the “cold” zone in the affected part of the bone) and MRI.

The considered processes lead to a weakening of the strength bone structures. As a result of continued mechanical loading, an impression fracture occurs, which is first manifested by contour deformation. articular surface.

Since the articular cartilage receives its nourishment from the articular synovial fluid, ischemia does not damage it: unlike arthrosis, the normal width of the joint space is maintained for a long time. Children even develop hyperplasia articular cartilage with widening of the joint space.

Subsequently, the affected bone or part of the bone undergoes flattening in the direction most pressure, usually along the axis of the limb, and delimited from living bone tissue. Occasionally, one or more fragments of necrotic bone are torn away, becoming free intra-articular bodies. Delimitation of necrotic bone is characterized by the development of granulation tissue on the border with a zone of necrosis and osteosclerosis along the periphery. This is displayed on the radiograph as a double border around the periphery of the area of osteonecrosis. On radiographs, an inner rim of enlightenment and an outer rim of compaction are noted, in some cases only an osteosclerotic rim is observed. On T2-weighted MRI images, the inner border has an increased signal intensity, and the outer border has a low signal intensity. On T1-weighted images, both zones look like a single border with a low signal. It should be taken into account that such a fringe in MRI may occur due to the effect of chemical shift (especially with GRE pulse sequences).

The considered sequence of events is typical for aseptic necrosis of the femoral head and is observed with certain variants in other localizations of osteonecrosis.

For more early stages The course of aseptic bone necrosis goes through the same stages (necrosis, impression fracture, flattening) regardless of the patient's age. In the future, the course of aseptic necrosis differs in the immature and in the mature skeleton. In children, aseptic necrosis ends with the restoration of bone tissue. This is possible with revascularization of the affected area of the bone, which occurs in the process of ingrowth of connective tissue into it. Apparently, the regenerative potency of the cartilage at this age also plays a role, which undergoes hyperplasia and also grows into the affected area. At the end of the disease, the bone remains deformed, but its structure is restored completely or almost completely. Such a course of aseptic necrosis in children served as the basis for distinguishing a number of stages, reflecting the ingrowth of cartilage and connective tissue into necrotic bone and reparative processes in the classical Axhausen scheme. In adults, the regenerative ability of cartilage is lost or sharply weakened: bone tissue is not restored, and the process of resorption of necrotic bone drags on for years, culminating in severe arthrosis with a defect in the affected bone. That is why in adults there cannot be that staging of the development of aseptic necrosis, which is reflected in the Axhausen scheme.

A special form of damage to the subchondral bones is limited aseptic necrosis, which occupies part of the articular surface. The degree of distribution of aseptic necrosis is different - from a total lesion of the subchondral bone, small bone of the wrist or tarsus to changes limited to small areas. At the same time, limited aseptic necrosis is distinguished by a certain peculiarity and is considered as special form. On the other hand, Koenig's osteochondrosis dissecans, previously considered as limited aseptic necrosis, has a traumatic origin.

There are 3 groups of aseptic necrosis:

widespread aseptic necrosis in the immature skeleton;
widespread aseptic necrosis in the mature skeleton;
limited aseptic necrosis.

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Osteochondropathy is an aseptic (non-infectious) necrosis of bone tissue resulting from a violation local circulation and metabolism.

There are more than ten types of osteochondropathy, each of which has its own symptoms, course and resolution.

In most cases, osteochondropathy develops in children and adolescents under 17 years of age. Most often they are diagnosed in boys.

Those parts of the musculoskeletal system that experience the greatest load are most susceptible to disease: the wrist, knee, hip joint and wrist.

The disease is quite rare. Among all orthopedic diseases it is only 2.5-3%. However, in Lately the proportion of patients with this disease has increased significantly.

This is associated with the intensive development of sports among children and adolescents and, as a result, an increase in the load on the musculoskeletal system.

Disease types

Depending on the place of development of the necrotic process, 4 types of osteochondropathy are distinguished.

Necrosis of the epiphyses of tubular bones:

heads of II and III metatarsal bones;
phalanges of fingers;
head of the femur;
varus deformity of the leg.

Necrosis of short spongy bones:

lunate bone;
sesamoid bone of the I metatarsophalangeal joint;
scaphoid;
vertebral body.

Osteochondropathy of the apophyses:

calcaneal tuberosity;
tuberosity tibia;
vertebral rings.

Partial necrosis of the surfaces of the joints:

condyles of the thigh;
capitate eminence of the humerus.

Causes and risk factors

Violation occurs due to dysfunction of the local blood supply to the bone tissue. As a result of the fact that blood cannot deliver to micronutrients to tissues, they die, that is, bone necrosis is formed. Then the dead areas disintegrate.

Circulatory disorder is the main, but not the only reason for the development of necrosis.

For example, there is still no consensus about the occurrence, which affects the vertebral body. It is believed that necrosis develops under the influence of eosinophilic granuloma. At least no circulatory disturbance is observed.

Despite the fact that the causes of many osteochondropathy are not completely clear, doctors distinguish whole line risk factors for the formation of necrosis:

belonging to the male sex;
overweight;
hereditary predisposition;
metabolic disorders;
neurotrophic disorders;
taking corticosteroids;
children's and youthful age;
malnutrition or excessive dieting;
endocrine pathology;
trauma;
connective tissue disorders.

How more people has risk factors, the higher the likelihood of the onset of the disease.

Symptoms and treatment of the disease

Each type of osteochondropathy has its own clinical manifestations, so it requires more detailed description. Since many types of this disease are represented isolated cases Let's take a look at the most common ones.

Non-infectious. It is characterized by a curvature of the neck and head of the femur, which leads to the development of coxarthrosis.

It usually occurs in males at the age of 5-10 years. This pathology is characterized by gait disturbance, lameness, and pain in the hip joint. Muscle atrophy appears, movement in the joint is limited.

IN calm state joint pain subsides or disappears altogether. Treatment of the disease includes rest, as well as stimulation of bone tissue restoration processes with physiotherapy and medications. IN rare cases perform surgery.

Necrosis of the epiphysis of the navicular bone of the foot

It is he who becomes the reason for going to the doctor. This type of osteochondropathy is accompanied by deformation of several vertebrae at once. To mitigate the consequences, the patient is prescribed complete rest.

Treatment includes gymnastic exercises, massage of the muscles of the back and abdomen. With timely detection of pathology, its outcome is favorable.

Osteochondropathy of the calcaneal tuber

Quite a rare pathology, which is detected, as a rule, at the age of 7-14 years. It is characterized by swelling and pain in the heel area.

Treatment includes thermal procedures, calcium electrophoresis and limiting the load on the leg.

Necrosis of the semilunar bone

The main symptoms include swelling on the back of the hand and pain in wrist joint. Pain increase with disease progression and movement.

As a treatment, immobilization is used - immobilization of the joint with the help of a plastic or plaster splint. Also, the patient is credited with mud therapy, novocaine blockades, paraffin therapy. In some cases, surgery is performed.

Partial osteochondropathy

These include Panner's disease, and others. In most cases, osteochondropathy develops in the knee joint.

They most often affect men under 25 years of age. First on convex surface the joint develops necrosis, and then the affected area is separated from the healthy one and turns into a “joint mouse”.

All this is accompanied painful sensations in the knee joint, limitation of movement and swelling.

At the initial stage of the development of pathology, it is shown conservative treatment: physiotherapy, paraffin therapy, immobilization, complete rest.

If "" is formed and frequent blockades of the joint occur, they surgical intervention during which necrotic tissue is removed.

Don't put your hands down

At first glance, the diagnosis of osteochondropathy sounds like a sentence. However, do not be afraid of this disease. First, meets it is very rare.

Secondly, most types of aseptic necrosis have a favorable resolution. Of course, over time, complications such as arthrosis or osteochondrosis may occur, but they do not pose a great danger to human life.

The main thing that is required to combat this pathology is colossal patience.

The disease develops very slowly, and it can take years for the dead bone tissue to be replaced by new ones. But if you stick proper treatment and lead healthy lifestyle life, the disease will definitely recede.

This pathological process, characterized by necrosis of the bone area of that part of the skeleton that undergoes significant stress. Primary A. n.k. (osteochondropathy) are observed during the growth of the body, i.e., in childhood and adolescence. They are based on subchondral avascular necrosis of the bone and bone marrow. There is no cartilage damage, so ankylosis never occurs. Osteochondropathies proceed relatively benignly with the restoration of bone tissue and favorable outcome. They should be distinguished from secondary A. n.k. at rheumatic diseases when there is a simultaneous or sequential lesion of the cartilage (due to the growth of the pannus or degenerative changes followed by destruction). For example, with aseptic necrosis of the femoral head, protrusion of the acetabulum of the innominate bone often occurs, which is not observed in osteochondropathy. There are osteochondropathy of the femoral head (Legg-Calve-Perthes disease), heads of the metatarsal bones, usually the second and third (Kohler II disease), navicular bone of the foot (Kohler I disease), lunate bone of the hand (Kienböck disease), phalanges of the fingers (disease Tiemann), navicular bone of the hand (Praiser's disease), vertebral body (Calve's disease), sesamoid bone of the first metatarsophalangeal joint, tuberosity of the tibia (Osgood-Schlatter disease), tuberosity of the calcaneus (Haglund-Schinz disease), body of the talus (Haglund's disease) ), vertebral apophyses (Scheuermann-Mau disease) patella(Larsen-Johansson disease), partial (wedge-shaped) osteochondropathy of the articular ends of the distal epiphyses of the humerus and femur (Koenig's disease). Rheumatic diseases (rheumatoid arthritis, SLE, systemic scleroderma, osteoarthritis) are usually observed aseptic necrosis of the femoral heads, much less often - heads of the humerus, ulna and radius bones, even rarer bones of the leg and wrist.

Etiology and pathogenesis. According to most researchers, the main cause of osteochondropathy is trauma in combination with impaired local circulation, leading to ischemia of the corresponding parts of the bone. In the emergence of A. n.k. vascular changes also play an important role in rheumatic diseases. It is believed that in this case, intraosseous vessels of an immune, in particular immunocomplex, nature are damaged (i.e., one of the manifestations of vasculitis occurs). Of certain importance are such facts as thrombosis or fat embolism of the vessels of the epiphyses of bones. The negative role of glucocorticosteroids used in the treatment was exaggerated, since A. n.k. often occurred in patients who had never taken them. A. n.k. observed in decompression sickness, alcoholism, radiation, hemoglobinopathies ( sickle cell anemia). Among osteochondropathy, Legg-Calve-Perthes, Osgood-Schlatter, Scheuermann-Mau diseases are most common, less often Koehler, Koenig, Kienböck diseases.

Osteochondropathy of the femoral head (primary aseptic subchondral necrosis, Legg-Calve-Perthes disease).

The disease occurs mainly in children aged 5-12 years, less often at an earlier or later date.

clinical picture. The disease has several stages, characterized by anatomical and radiological changes. In the first stage ( initial stage necrosis) histologically observed pattern of focal necrosis of the bone and bone marrow. There are no changes on radiographs during this period. In the second stage (the stage of a compression fracture), which develops several months after the onset of the disease, compression of the dead bone area is detected due to fractures of the bone beams and restructuring of the surrounding bone tissue. The epiphysis of the femur is reduced and deformed. On radiographs, this is manifested by compaction of the shadow of the bone and an increase in the joint space. In the third stage (stage of resorption), resorption of the necrotic bone occurs. On the X-ray, the shadow of the head appears to be divided into several isolated structureless fragments. After 1.5-3 years, the transition of the disease to the fourth stage (reparation stage) is noted. The newly formed bone tissue replaces the necrotic areas of the bone. The process takes 1-2 years. Sequester-like shadows disappear on radiographs. And in the last fifth stage, the structure and shape of the femoral head are restored. With incomplete repair, conditions are created for the development of secondary arthrosis.

Aseptic necrosis of the femoral head in rheumatic diseases on early stages has a similar radiological picture, in addition, there are characteristics coxitis: osteoporosis, narrowing of the joint space, cystic lucency and bone erosion (especially with rheumatoid arthritis).

The lesion is often bilateral. A feature of the process is a very slow and incomplete reparation or (more often) its absence.

clinical picture. Usually, after an injury or an awkward movement, intermittent local pain(at first on motion), lameness at times. Pain often radiates to groin, hip, knee joint. There is pain during rotation and abduction of the hip, lameness increases, the function of the limb is gradually impaired (in late stages much). The affected limb is shortened by several centimeters. A positive Trendelenburg symptom is noted: when standing on the affected leg, the femoral-gluteal fold of the unaffected side falls below the similar fold of the opposite side. Often, pain bothers the patient 1-2 years before the first radiological changes appear. There is often some inconsistency clinical picture and radiological changes: at an early stage there may be sharp pains and significant gait disturbance, and as it develops compression fractures leading to severe deformity of the femoral head, pain temporarily decreases, while there is a significant limitation of abduction and rotation of the hip.

Diagnosis. The main thing in the diagnosis is the characteristic x-ray picture. However, at the first stage, the disease is not diagnosed radiographically. Currently, the possibilities of nuclear magnetic resonance for the diagnosis of aseptic necrosis at an early stage are being studied. In rheumatic diseases A. n.k. always are. complications, and therefore their diagnosis after the establishment of the underlying disease is not difficult.

Differential Diagnosis Carried out with tuberculous coxitis. With the latter, there are also pains, flexion contractures and signs of destruction of the femoral head on radiographs, there is a significant increase in the hip joint, the formation of subcutaneous abscesses and fistulas with serous-purulent discharge (odorless). The presence of neuropathic arthropathy (see) is suggested in cases where there are significant radiological changes joint without pain.

Treatment. The main thing in the treatment of secondary A. n.k. should be considered active therapy the underlying disease, preventing the occurrence of conditions for the development of aseptic necrosis (coxitis, immunocomplex vasculitis). After establishing the diagnosis, it is necessary to free the affected limb from physical activity(walking with a cane or crutches). Assign drugs that improve the processes of microcirculation (complamin, prodectin, etc.). Good results obtained by prescribing repeated courses of calcitrina (thyrocalcitonin) - hormonal drug obtained from thyroid glands animals. It prevents resorption and stimulates the deposition of calcium and phosphorus in bone tissue. Before starting treatment, a test is carried out (intradermal injection of 1 unit of calcitrina in 0.1 ml of solvent). With good tolerance, the drug is prescribed at a dose of 3-5 IU intramuscularly, daily for 1-1.5 months or every other day for 2-3 months. Repeated courses are possible not earlier than in 2 months. At the same time, calcium preparations (calcium gluconate - 3-4 g per day), sodium fluoride (coreberon, etc.) 0.025 g 3 times a day and vitamin D2 (ergocalciferol) 1000-5000 IU per day are prescribed for a long time (for years). Appoint anabolic drugs(retabolil, nerobolil) repeated courses. Definite analgesic effect provide physiotherapy (electro- and phonophoresis, laser therapy, microwave therapy). The use of anticoagulants and antiplatelet agents in the treatment of these patients was discussed, but they did not find wide application. Exercise therapy is carried out only in conditions of reducing the load on the affected joint. From surgical methods in the early stages, osteotomy is used, in the later stages - endoprosthesis replacement, arthroplasty.

Aseptic necrosis of the tibial tuberosity (Osgood-Schlatter disease)

The disease is predominantly of adolescence (usually up to 18 years); often bilateral. Patients are concerned about pain in the tibial tuberosity, especially when walking; on palpation, a painful swelling in this area is determined. On the radiograph in the lateral projection in the area of the tuberosity of the tibia, areas of enlightenment are visible, alternating with areas of darkening, sometimes complete fragmentation of the tuberosity is noted. The disease lasts 0.5-1.5 years, usually ends in complete recovery.

Treatment. At pain syndrome- rest, in the subsequent limitation of loads, physiotherapy.

Osteochondropathy of the spine (Scheuermann-May disease)

Aseptic necrosis of the apophyses of the vertebral bodies.

clinical picture. The disease starts at adolescence. Initially, there is a slight pain in the spine, often of a diffuse nature, aggravated after exertion and disappearing after a night's rest; gradually develops arcuate curvature of the spine (kyphosis). Often there is a rough crunch in the spine when the body is tilted forward. In the future, radicular pains join.

Diagnosis. The correct diagnosis allows us to make a characteristic X-ray picture of the spine, especially in the lateral projection: the vertebral bodies are wedge-shaped, their anterior sections are located below the posterior ones; unlike Calve's disease, several vertebrae are affected. Differential diagnosis is carried out with osteomyelitis, tuberculosis of the spine.

Treatment. The main role is given to exercise therapy and orthopedic activities. When radicular syndrome treatment is usually stationary (traction, massage of the back muscles, physiotherapy). With an unfavorable course, osteochondrosis develops.

Aseptic necrosis The epiphysis of the femur (Koenig's disease). In these cases, the distal epiphysis of the femur is more often affected.

clinical picture. At first, pains (non-permanent) in one, less often in both knee joints; then the pains become constant, aggravated by walking. Often there is a secondary synovitis. In the future, there are periods of "blockade" of the joint - with an incorrect movement, a sharp pain appears, the knee joint remains in a fixed position at an angle. On the radiograph in the region of the femoral condyle, at first there is a focus of enlightenment, then a shadow of the bone fragment is detected.

Differential Diagnosis Carried out with damage to the meniscus, tuberculous osteitis.

Treatment In the early stage, conservative (rest and reduction of the load on the joint, physiotherapy), after separation of the bone fragment - surgical.

Aseptic necrosis of heads, metatarsals (Kohler's disease II, usually 2nd or 3rd)

Girls are more likely to get sick during puberty. At the same time, wearing uncomfortable shoes, flat feet, and professional factors: work while standing with a forward bend, which creates additional load on the metatarsal heads. The right foot is most commonly affected.

clinical picture. Pain in the foot, swelling, sharp pain on palpation at the level of the corresponding metatarsal head are noted. Radiologically, the same evolution of the process is observed as in Legg-Calve-Perthes disease.

Differential Diagnosis Carried out with tuberculosis, chronic osteomyelitis.

Treatment Conservative (at an early stage, a plaster boot, then wearing orthopedic shoes, physiotherapy).

Aseptic necrosis of the navicular bone of the foot (Kohler's disease)

It is rare, usually in boys.

clinical picture. Patients have pain and swelling in the area of the medial surface of the rear of the foot, often lameness. On the radiograph, the shadow of the navicular bone becomes homogeneous at first, then sequestration occurs; subsequently deformity of the bone develops.

Treatment Symptomatic.

Aseptic necrosis of the semilunar bone of the wrist (Kienböck's disease), usually the right

With the disease, professional loads play a role (mainly carpenters and locksmiths are ill).

clinical picture. Patients are worried about persistent pain. and swelling in the region of the lunate bone; movement in the wrist joint is limited due to pain. On the radiograph, thickening of the lunate bone is determined, then fragmentation, followed by a sharp deformation.

Differential Diagnosis Carried out with tuberculosis of the bones of the wrist.

Treatment Conservative (immobilization, physiotherapy).

a pathological process characterized by necrosis of a part of the bone of that part of the skeleton that undergoes significant stress. Primary A.n.c. (osteochondropathy) are observed during the growth of the body, i.e. in childhood and adolescence. They are based on subchondral avascular necrosis of the bone and bone marrow. There is no cartilage damage, so ankylosis never occurs. Osteochondropathies proceed relatively benignly with restoration of bone tissue and a favorable outcome. They should be distinguished from secondary A.n.k. in rheumatic diseases, when there is a simultaneous or sequential damage to the cartilage (due to the growth of the pannus or degenerative changes with subsequent destruction). For example, with aseptic necrosis of the femoral head, protrusion of the acetabulum of the innominate bone often occurs, which is not observed in osteochondropathy. There are osteochondropathy of the femoral head (Legg-Calve-Perthes disease), heads of the metatarsal bones, usually the second and third (Kohler II disease), navicular bone of the foot (Kohler I disease), lunate bone of the hand (Kienböck disease), phalanges of the fingers (disease Tiemann), navicular bone of the hand (Praiser's disease), vertebral body (Calve's disease), sesamoid bone of the first metatarsophalangeal joint, tuberosity of the tibia (Osgood-Schlatter disease), tuberosity of the calcaneus (Haglund-Schinz disease), body of the talus (Haglund's disease) ), apophyses of the vertebrae (Scheuermann-Mau disease) of the patella (Larsen-Johansson disease), partial (wedge-shaped) osteochondropathy of the articular ends of the distal epiphyses of the humerus and femur (Koenig's disease). In rheumatic diseases (rheumatoid arthritis, SLE, systemic scleroderma, osteoarthritis), aseptic necrosis of the femoral heads is usually observed, much less often - the heads of the humerus, ulna and radius bones, and even less often the bones of the lower leg and wrists.

Etiology and pathogenesis. According to most researchers, the main cause of osteochondropathy is trauma in combination with impaired local circulation, leading to ischemia of the corresponding parts of the bone. In the emergence of A.n.c. vascular changes also play an important role in rheumatic diseases. It is believed that in this case, intraosseous vessels of an immune, in particular immunocomplex, nature are damaged (i.e. one of the manifestations of vasculitis occurs). Of certain importance are such facts as thrombosis or fat embolism of the vessels of the epiphyses of bones. The negative role of glucocorticosteroids used in the treatment was exaggerated, since A.n.k. often occurred in patients who had never taken them. A.n.k. observed in decompression sickness, alcoholism, radiation, hemoglobinopathies (sickle cell anemia). Among osteochondropathy, Legg-Calve-Perthes, Osgood-Schlatter, Scheuermann-Mau diseases are most common, less often Koehler, Koenig, Kienböck diseases.

Osteochondropathy of the femoral head (primary aseptic subchondral necrosis, Legg-Calve-Perthes disease).

The disease occurs mainly in children aged 5-12 years, less often at an earlier or later date. clinical picture. The disease has several stages, characterized by anatomical and radiological changes. In the first stage (the initial stage of necrosis), a pattern of focal necrosis of the bone and bone marrow is histologically observed. There are no changes on radiographs during this period. In the second stage (the stage of a compression fracture), which develops several months after the onset of the disease, compression of the dead bone area is detected due to fractures of the bone beams and restructuring of the surrounding bone tissue. The epiphysis of the femur is reduced and deformed. On radiographs, this is manifested by compaction of the shadow of the bone and an increase in the joint space. In the third stage (stage of resorption), resorption of the necrotic bone occurs. On the X-ray, the shadow of the head appears to be divided into several isolated structureless fragments. After 1.5-3 years, the transition of the disease to the fourth stage (reparation stage) is noted. The newly formed bone tissue replaces the necrotic areas of the bone. The process takes 1-2 years. Sequester-like shadows disappear on radiographs. And in the last fifth stage, the structure and shape of the head are restored

femur. With incomplete repair, conditions are created for the development of secondary arthrosis. Aseptic necrosis of the femoral head in rheumatic diseases in the early stages has

a similar x-ray picture, in addition, there are characteristic signs of coxitis: osteoporosis, narrowing of the joint space, cystic enlightenment and bone erosion (especially with rheumatoid arthritis). The lesion is often bilateral. A feature of the process is a very slow and incomplete reparation or (more often) its absence.

clinical picture. Usually, after an injury or an awkward movement, intermittent local pains (at first when moving), sometimes lameness, are disturbing. The pain often radiates to the groin, thigh, knee joint. There is pain during rotation and abduction of the hip, lameness increases, the function of the limb is gradually impaired (significantly in the later stages). The affected limb is shortened by several centimeters. There is a positive Trendelenburg sign: when standing

on the affected leg, the femoral-gluteal fold of the unaffected side falls below the similar fold of the opposite side. Often, pain bothers the patient 1-2 years before the first radiological changes appear. Often there is some discrepancy between the clinical picture and radiological changes: at an early stage, there may be sharp pains and significant gait disturbance, and as compression fractures develop, leading to severe deformity of the femoral head, the pain temporarily decreases, while there is a significant limitation of hip abduction and rotation.

Diagnosis. The characteristic x-ray picture is the main in the diagnosis. However, at the first stage, the disease is not diagnosed radiologically. Currently, the possibilities of nuclear magnetic resonance for the diagnosis of aseptic necrosis at an early stage are being studied. In rheumatic diseases A.n.k. are always complications, and therefore their diagnosis after the establishment of the underlying disease is not difficult.

Differential Diagnosis carried out with tuberculous coxitis. With the latter, there are also pains, flexion contractures and signs of destruction of the femoral head on radiographs, there is a significant increase in the hip joint, the formation of subcutaneous abscesses and fistulas with serous purulent discharge (odorless). The presence of neuropathic arthropathy (see) suggest in cases where there are significant x-ray changes in the joint in the absence of pain.

Treatment. The main thing in the treatment of secondary A.N.K. active therapy of the underlying disease should be considered, preventing the occurrence of conditions for the development of aseptic necrosis (coxitis, immunocomplex vasculitis). After establishing the diagnosis, it is necessary to free the affected limb from physical activity as much as possible (walking with a cane or crutches). Assign drugs that improve the processes of microcirculation (complamin, prodectin, etc.). Good results were obtained with the appointment of repeated courses of calcitrina (thyrocalcitonin) - a hormonal drug obtained from the thyroid glands of animals. It prevents resorption and stimulates the deposition of calcium and phosphorus in bone tissue. Before starting treatment, a test is carried out (intradermal injection of 1 unit of calcitrina in 0.1 ml of solvent). With good tolerance, the drug is prescribed at a dose of 3-5 IU intramuscularly, daily for 1-1.5 months or every other day for 2-3 months. Repeated courses are possible not earlier than in 2 months. At the same time, calcium preparations (calcium gluconate - 3-4 g per day), sodium fluoride (coreberon, etc.) 0.025 g 3 times a day and vitamin D2 (ergocalciferol) 1000-5000 IU per day are prescribed for a long time (for years). Anabolic drugs (retabolil, nerobolil) are prescribed in repeated courses. A certain analgesic effect is exerted by physiotherapy (electro- and phonophoresis, laser therapy, microwave therapy). The use of anticoagulants and antiplatelet agents in the treatment of these patients was discussed, but they were not widely used. Exercise therapy is carried out only in conditions of reducing the load on the affected joint. Of the surgical methods, osteotomy is used in the early stages, and endoprosthesis replacement and arthroplasty are used in the later stages.

Aseptic necrosis of the tibial tuberosity (Osgood-Schlatter disease)

disease predominantly of adolescence (usually up to 18 years); often bilateral. Patients are concerned about pain in the tibial tuberosity, especially when walking; on palpation, a painful swelling in this area is determined. On the radiograph in the lateral projection in the area of the tuberosity of the tibia, areas of enlightenment are visible, alternating with areas of darkening, sometimes complete fragmentation of the tuberosity is noted. The disease lasts 0.5-1.5 years, usually ends in complete recovery.

Treatment. With pain syndrome - rest, subsequently limiting loads, physiotherapy.

Osteochondropathy of the spine (Scheuermann-May disease)

aseptic necrosis of the apophyses of the vertebral bodies.

clinical picture. The disease begins in adolescence. Initially, there is a slight pain in the spine, often of a diffuse nature, aggravated after exertion and disappearing after a night's rest; gradually develops arcuate curvature of the spine (kyphosis). Often there is a rough crunch in the spine when the body is tilted forward. In the future, radicular pains join.

Diagnosis. The correct diagnosis allows us to make a characteristic X-ray picture of the spine, especially in the lateral projection: the vertebral bodies are wedge-shaped, their anterior sections are located below the posterior ones; unlike Calve's disease, several vertebrae are affected. Differential diagnosis is carried out with osteomyelitis, tuberculosis of the spine.

Treatment. The main role is given to exercise therapy and orthopedic measures. When a radicular syndrome occurs, treatment is usually stationary (traction, massage of the back muscles, physiotherapy). With an unfavorable course, osteochondrosis develops.

Aseptic necrosis epiphysis of the femur (Koenig's disease). In these cases, the distal epiphysis of the femur is more often affected.

clinical picture. At first, pains (non-permanent) in one, less often in both knee joints are disturbing; then the pains become constant, aggravated by walking. Often there is a secondary