Osteopathic correction of the foot. Osteopathy of the calcaneus

Osteochondropathy develops in patients of childhood and adolescence, more often affects the bones of the lower extremities, is characterized by a benign chronic course and a relatively favorable outcome. There are no confirmed data on the prevalence of osteochondropathy in the medical literature.

Classification of osteochondropathy

In traumatology, four groups of osteochondropathy are distinguished:

Osteochondropathy of the metaphyses and epiphyses of long tubular bones. This group of osteochondropathy includes osteochondropathy of the sternal end of the clavicle, phalanges of the fingers, hip joint, proximal metaphysis of the tibia, heads of the II and III metatarsal bones.
Osteochondropathy of short spongy bones. This group of osteochondropathy includes osteochondropathy of the vertebral bodies, the lunate bone of the hand, the navicular bone of the foot, and the sesamoid bone of the I metatarsophalangeal joint.
Osteochondropathy of the apophyses. This group of osteochondropathy includes osteochondropathy of the pubic bone, apophyseal discs of the vertebrae, calcaneal tuberosity and tibial tuberosity.
Wedge-shaped (partial) osteochondropathy affecting the articular surfaces of the elbow, knee and other joints.

The course of osteochondropathy

The first stage of osteochondropathy. Bone necrosis. Continues up to several months. The patient is concerned about mild or moderate pain in the affected area, accompanied by dysfunction of the limb. Palpation is painful. Regional lymph nodes are usually not enlarged. X-ray changes during this period may be absent.

The second stage of osteochondropathy. "Compression fracture". It lasts from 2-3 to 6 or more months. The bone "sags", the damaged bone beams are wedged into each other. On radiographs, a homogeneous darkening of the affected parts of the bone and the disappearance of its structural pattern are revealed. With the defeat of the epiphysis, its height decreases, the expansion of the joint space is revealed.

The third stage of osteochondropathy. Fragmentation. Lasts from 6 months to 2-3 years. At this stage, the necrotic areas of the bone are resorbed and replaced by granulation tissue and osteoclasts. Accompanied by a decrease in bone height. On radiographs, a decrease in the height of the bone, fragmentation of the affected parts of the bone with a random alternation of dark and light areas are revealed.

The fourth stage of osteochondropathy. Recovery. It lasts from several months to 1.5 years. There is a restoration of the form and, somewhat later, the structure of the bone.

The full cycle of osteochondropathy takes 2-4 years. Without treatment, the bone is restored with a more or less pronounced residual deformity, which further leads to the development of deforming arthrosis.

Perthes disease

The full name is Legg-Calve-Perthes disease. Osteochondropathy of the hip joint. Affects the head of the femur. It often develops in boys aged 4-9 years. The occurrence of osteochondropathy may be preceded (not necessarily) by an injury to the hip joint.

Perthes disease begins with mild lameness, which is later joined by pain in the area of injury, often extending to the area of the knee joint. Gradually, the symptoms of osteochondropathy increase, movements in the joint become limited. On examination, mild atrophy of the muscles of the thigh and lower leg, limitation of internal rotation and abduction of the thigh is revealed. Possible soreness with a load on the greater trochanter. Often, a shortening of the affected limb by 1-2 cm is determined, due to subluxation of the hip upward.

Osteochondropathy lasts 4-4.5 years and ends with the restoration of the structure of the femoral head. Without treatment, the head becomes mushroom-shaped. Since the shape of the head does not correspond to the shape of the acetabulum, deforming arthrosis develops over time. For diagnostic purposes, ultrasound and MRI of the hip joint are performed.

In order to ensure the restoration of the shape of the head, it is necessary to completely unload the affected joint. Treatment of osteochondropathy is carried out in a hospital with bed rest for 2-3 years. Perhaps the imposition of skeletal traction. The patient is prescribed physiovitamino- and climatotherapy. Regular exercise therapy is of great importance. to maintain range of motion in the joint. In case of violation of the shape of the femoral head, osteoplastic operations are performed.

Ostgood-Schlatter disease

Osteochondropathy of the tibial tuberosity. The disease develops at the age of 12-15 years, boys are more often ill. Gradually there is swelling in the affected area. Patients complain of pain aggravated by kneeling and walking up stairs. The function of the joint is not disturbed or only slightly impaired.

Treatment of osteochondropathy is conservative, carried out on an outpatient basis. The patient is prescribed limiting the load on the limb (with severe pain, a plaster splint is applied for 6-8 weeks), physiotherapy (electrophoresis with phosphorus and calcium, paraffin applications), vitamin therapy.

Osteochondropathy proceeds favorably and ends with recovery within 1-1.5 years.

Kohler-II disease

Osteochondropathy of the heads of the II or III metatarsal bones. Most often affects girls, develops at the age of 10-15 years. Kohler's disease begins gradually. Periodic pain occurs in the affected area, lameness develops, which disappears when the pain disappears. On examination, a slight edema is revealed, sometimes - hyperemia of the skin on the back of the foot. Subsequently, a shortening of the II or III finger develops, accompanied by a sharp limitation of movements. Palpation and axial load are sharply painful.

In comparison with the previous form, this osteochondropathy does not pose a significant threat to the subsequent dysfunction of the limb and the development of disability. Outpatient treatment is indicated with maximum unloading of the affected foot section. Patients are given a special plaster boot, vitamins and physiotherapy are prescribed.

Koehler-I disease

Osteochondropathy of the navicular bone of the foot. It develops less often than the previous forms. Most often affects boys aged 3-7 years. Initially, for no apparent reason, pain in the foot appears, lameness develops. Then the skin of the back of the foot turns red and swells.

Treatment of osteochondropathy is outpatient. The patient is limited in the load on the limb, with severe pain, a special plaster boot is applied, and physiotherapy is prescribed. After recovery, it is recommended to wear shoes with arch support.

Shinz's disease

Osteochondropathy of the calcaneal tuber. Shinz's disease develops rarely, as a rule, it affects children aged 7-14 years. Accompanied by pain and swelling.

Treatment of osteochondropathy is outpatient, includes load restriction, calcium electrophoresis and thermal procedures.

Sherman Mau disease

Osteochondropathy of the vertebral apophyses. Common pathology. Scheuermann-Mau disease occurs in adolescence, more often in boys. Accompanied by kyphosis of the middle and lower thoracic spine (round back). Pain may be mild or absent altogether. Sometimes the only reason for contacting an orthopedist is a cosmetic defect.

Diagnosis of this type of osteochondropathy is carried out using radiography and CT of the spine. Additionally, to study the state of the spinal cord and ligamentous apparatus of the spinal column, an MRI of the spine is performed.

Osteochondropathy affects several vertebrae and is accompanied by their severe deformation, which remains for life. To maintain the normal shape of the vertebrae, the patient must be provided with rest. Most of the day, the patient should be in bed in the supine position (in case of severe pain syndrome, immobilization is performed using the back plaster bed). Patients are prescribed massage of the muscles of the abdomen and back, therapeutic exercises. With timely, proper treatment, the prognosis is favorable.

Calve's disease

Osteochondropathy of the vertebral body. Calve's disease develops at the age of 4-7 years. The child, for no apparent reason, begins to complain of pain and a feeling of fatigue in the back. On examination, local tenderness and protrusion of the spinous process of the affected vertebra are revealed. On radiographs, a significant (up to ¼ of the norm) decrease in the height of the vertebra is determined. Usually one vertebra in the thoracic region is affected.

Treatment of this osteochondropathy is carried out only in a hospital. Rest, therapeutic exercises, physiotherapy are shown. The structure and shape of the vertebra is restored within 2-3 years.

Partial osteochondropathy of articular surfaces

It usually develops between the ages of 10 and 25 and is more common in men. About 85% of partial osteochondropathy develops in the area of the knee joint.

As a rule, the area of necrosis appears on the convex articular surface. Subsequently, the damaged area can separate from the articular surface and turn into a “joint mouse” (freely lying intra-articular body). Diagnosis is by ultrasound or MRI of the knee joint.

At the first stages of the development of osteochondropathy, conservative treatment is carried out: rest, physiotherapy, immobilization, etc. With the formation of an “articular mouse” and frequent blockades of the joint, surgical removal of the free intraarticular body is indicated.

Osteochondropathy - treatment in Moscow

Source: www.krasotaimedicina.ru

Osteochondropathy

Brief description of the disease

Osteochondropathy is a disease of children and adolescents, in which a degenerative-dystrophic process develops in the bones.

With osteochondropathy, the calcaneus, femur, apophyses of the vertebral bodies, and tuberosity of the tibia are most often affected.

Reasons for the appearance

To date, the causes of the onset of the disease have not been fully studied, but there are several decisive factors:

congenital or family predisposition;
hormonal factors - the disease develops in patients with pathology of the function of the endocrine glands;
metabolic disorders of essential substances. Osteochondropathy often causes a violation of the absorption of calcium, vitamins;
traumatic factors. Osteochondropathy occurs after excessive physical exertion, incl. increased muscle contractions, frequent injuries. Initially, these types of loads lead to progressive compression, and then to narrowing of the small vessels of spongy bones, especially in areas of greatest pressure.

Symptoms of osteochondropathy

Osteochondropathy of the calcaneus (Haglund-Shinz disease) develops most often in girls 12-16 years old, characterized by gradually increasing or acute pain in the calcaneal tubercle that occurs after exercise. At the place of attachment of the Achilles tendon, swelling is noted above the calcaneal tubercle. Patients begin to walk, leaning on a toe, and playing sports, jumping become physically impossible.

Osteochondropathy of the spine (Scheyerman-Mau disease) develops most often in young men aged 11-18 years. The first stage is characterized by increased thoracic kyphosis (curvature of the spine in its upper section), the second - back pain (especially with prolonged walking, sitting), fatigue and weakness of the spinal muscles, an increase in thoracic kyphosis. At the third stage of osteochondropathy of the spine, a complete fusion of the apophyses with the vertebrae is observed. Over time, osteochondrosis develops with increasing pain.

Osteochondropathy of the femur (Legg-Calve-Perthes disease) develops in most cases in boys 4-12 years old. At the beginning of the disease, there are no complaints, after which pains appear in the hip joint, radiating to the knee. There are pains after exercise and disappear after rest, so children do not always complain about them. The movements of the hip joint are gradually limited, muscle atrophy develops, and the thigh on the affected side loses weight.

Osteochondropathy of the tibial tuberosity (Schlatter's disease) develops in boys aged 12-16, especially in those involved in ballet, sports dancing, and sports. The patient complains of pain under the patella, swelling. With tension of the quadriceps femoral muscle, when squatting, climbing stairs, the pain intensifies.

Diagnosis of the disease

To determine osteochondropathy of the calcaneus, they are based on clinical data and the results of an x-ray examination (fragmentation, compaction of the apophysis, "roughness" on the calcaneal tubercle is noted). A differential diagnosis of osteochondropathy with a heel spur (in older patients), achilles bursitis is also carried out.

Diagnosis of osteochondropathy of the spine occurs on the basis of examination data (increased thoracic kyphosis) and X-ray examination (the pictures show that the shape of the vertebrae has changed - they become wedge-shaped).

Osteochondropathy of the femur is also determined by x-rays. Five stages of changes in the femoral head have been identified.

Osteochondropathy of the tibial tuberosity is established according to the clinical picture and is specified after an X-ray examination.

Treatment of osteochondropathy

Therapy for osteochondropathy of the calcaneus consists in prescribing non-steroidal anti-inflammatory drugs (if severe pain is bothering), physiotherapy procedures, and reducing physical exertion. To relieve the load on the calcaneus, special arch support insoles are used.

Osteochondropathy of the spine is treated with massage, swimming, underwater stretching, physiotherapy exercises. In some cases, with a strong violation of posture, an operation is prescribed.

Treatment of osteochondropathy of the femur can be operational and conservative. Various osteoplastic operations are prescribed depending on the stage of the disease. Conservative treatment of osteochondropathy consists in bed rest (the patient cannot sit), foot massage, and physiotherapy. Practice skeletal stretching for both hips.

For the treatment of osteochondropathy of the tibial tuberosity, physiotherapeutic procedures and warmth are prescribed. If the pain is severe, apply a plaster cast. Sometimes they resort to surgery - they remove a fragment of tuberosity. Loads on the quadriceps femoral muscle are excluded.

Disease prevention

For the prevention of osteochondropathy of the calcaneus, it is recommended to wear loose shoes.

Prevention of osteochondropathy of the spine consists in physiotherapy exercises to create a muscular corset. Intense physical activity should be limited. Wearing a corset in this disease is ineffective.

A good prevention of osteochondropathy of the femur is massage, swimming.

To prevent osteochondropathy of the tibial tuber, athletes during training are recommended to sew foam rubber pillows 2-4 cm thick into the form.

Source: www.neboleem.net

Osteochondropathy in childhood and adolescence

Osteochondropathy is a group of diseases that occur in childhood and adolescence due to malnutrition (malnutrition) of bone tissue. In the area of the bone, the blood supply is disturbed and areas of its necrosis appear.

The disease often occurs in the epiphyses and apophyses of the tubular bones of the arms, legs and vertebrae. The epiphysis is a site of growth of bone tissue. Apophysis - a protrusion of bones near the growth zone, to which muscles and ligaments are attached. Usually it is the end part of a long tubular bone. The disease is chronic and often develops in the lower extremities, which are under greater stress. Most osteochondropathy have a hereditary background.

Legg-Calve-Perthes disease or chondropathy of the femoral head is also called juvenile osteochondrosis of the femoral head. Boys aged 4 to 12 get sick more often. Usually, an injury to the hip joint occurs first, then the blood supply to the femoral head is disrupted.

Initially, necrosis of the bone tissue of the femoral head occurs. This can be seen on an x-ray. In the second stage of the disease, the head of the femur is flattened, under the influence of a large load. The next stage is called the fragmentation stage. In this case, the resorption of zones of necrotic bone tissue occurs. If left untreated, the fourth stage occurs - osteosclerosis. The femoral head is restored, but its normal shape is changed. The final stage, with insufficient treatment, is deforming arthrosis of the hip joint with a violation of its function.

At the beginning of the disease, there are practically no complaints. Then there are pains in the hip joint, which are given to the knee. Often pain occurs after exertion and disappears after rest and at night. The child may not pay attention to the pain and not complain. Gradually there is a restriction of movements in the hip joint. During this period, you can notice the weight loss of the thigh on the affected side, caused by muscle atrophy. X-rays are taken to establish the diagnosis. Radiologically, five stages of the disease are distinguished, corresponding to changes in the femoral head.

Treatment of chondropathy of the femur. Treatment can be operative and conservative. Conservative treatment includes mandatory bed rest. The patient is forbidden even to sit, in order to eliminate the load on the femoral head. Apply skeletal traction for both thighs. Appointed daily massage of the lower extremities, physiotherapy. Surgical treatment consists in performing various osteoplastic operations. Types of surgical interventions depend on the stage of the disease.

This is a chondropathy of the bones of the foot. There are Keller's disease I and Keller's disease II.

Keller's disease I is a chondropathy of the navicular bone of the foot. The disease develops in childhood from 4 to 12 years. The patient develops pain and swelling of the upper (dorsal) surface of the foot above the navicular bone. The pain gets worse while walking. The child is lame. To clarify the diagnosis, x-rays of the bones of the foot are performed. A change in the shape of the navicular bone, its fragmentation is detected.

Treatment consists in unloading the foot. A plaster bandage is applied for 4-6 weeks. After removing the cast, physiotherapy exercises, physiotherapy procedures are prescribed, which are combined with a decrease in the load on the foot. For 1-2 years, the child must wear orthopedic shoes.

Keller II disease is a chondropathy of the metatarsal heads. Most often, the second metatarsal bone is affected. The patient has pain in the affected area. Pain increases sharply when walking, especially barefoot on uneven surfaces and in shoes with soft soles. Finger shortening may occur. When probing, a sharp soreness of the bases of the fingers is detected. The heads of the metatarsal bones increase in size. The diagnosis and stage of the disease are specified using x-rays.

Treatment of Keller II disease is conservative. The foot is unloaded. To do this, a plaster boot is applied for one month. Then the child must wear orthopedic shoes, as there is a high risk of developing flat feet. Massage, physiotherapeutic procedures, therapeutic exercises are used. The disease lasts 2-3 years. In the absence of a good effect from conservative therapy and the development of severe deforming arthrosis of the joint, surgical treatment is prescribed.

This is a chondropathy of the semilunar bone of the hand. It is manifested by the development of aseptic necrosis in this bone. The disease develops in men 25-40 years old after major injuries or prolonged microtraumatization of the hand, when working with a large physical load on the hands. The patient has discomfort in the hand, constant pain, which is aggravated by exertion, movements. There is swelling at the base of the hand. Gradually, limitation of mobility in the wrist joint develops. The restriction of joint mobility, in turn, causes a decrease in the work of the muscles of the forearm and their atrophy. The diagnosis is clarified with the help of X-ray examination.

Treatment of Kienböck's disease. The load on the bone is limited. To do this, a plaster cast is applied for 2-3 months. After removing the plaster, massage, physiotherapy, physiotherapy exercises are prescribed. With the development of severe deforming arthrosis, surgical treatment is used.

Schlatter's disease or Ostgood-Schlatter's disease.

Schlatter's disease occurs in boys from 12 to 16 years old, especially in those involved in sports, sports dancing, and ballet. Under increased load, chondropathy of the tibial tuberosity develops. The tuberosity of the tibia is located on its anterior surface, below the patella. The quadriceps femoris muscle is attached to the tuberosity of the tibia.

In young men, the process of ossification of the tibial tuberosity is not yet completed, and it is separated from the tibia proper by a cartilaginous zone. With a constant load on the tuberosity, the blood supply is disturbed, the areas of the tuberosity undergo necrosis, then recovery. By the age of 18, the tuberosity fuses with the tibia and recovery occurs. The patient complains of pain below the patella, swelling. The pain increases with tension of the quadriceps femoris muscle, when climbing stairs, squatting.

The diagnosis is confirmed radiographically. Treatment consists in eliminating the load on the quadriceps femoris muscle. Heat, physiotherapy procedures are prescribed. With severe pain, a plaster cast is applied. Occasionally it is necessary to use surgical methods, which consist in the surgical removal of a fragment of the tibial tuberosity.

Osteochondropathy of the vertebral bodies

Calve's disease is a chondropathy of the vertebral body. Most often, the lower thoracic or upper lumbar vertebrae are affected. Boys from 7 to 14 years old are ill. The patient has pain in the area of the affected vertebra or in the thoracic and lumbar spine. On examination, you can find a protruding spinous process of the diseased vertebra. When probing the spinous process, the pain intensifies. On the radiograph, a sharp decrease in the height of this vertebra and its expansion are found.

Treatment of Calve's disease is conservative. Bed rest is prescribed in a special laying on the bed to reduce the load on the vertebra. Physiotherapy is used, which consists of a set of exercises to strengthen the muscles of the back to create a muscular corset. After that, the patient must wear a special corset for several years. Surgical treatment is prescribed in the absence of the effect of conservative therapy and progressive spinal deformity.

Kümmel's disease or Kümmel-Verneuil's disease is a traumatic aseptic (microbial-free) inflammation of the vertebral body (spondylitis). The cause of this disease is an injury to the vertebra, which leads to the development of areas of necrosis in the vertebral body. The patient has pain in the area of the injured vertebra, which disappears after 10-14 days. This is followed by a period of false well-being, sometimes lasting up to several years. Then again there are pains in the area of the injured vertebra. The patient may not remember the previous trauma. Pain appears first in the spine, then given to the intercostal space. X-ray examination reveals a wedge-shaped vertebra.

Treatment consists in unloading the spine. For this, bed rest is prescribed for 1 month. The bed should be hard. A roller is placed under the thoracic region. Then physiotherapy treatment and physiotherapy exercises are prescribed.

Scheuermann's disease, Schmorl's disease, chondropathic kyphosis, juvenile kyphosis, apophysitis of the vertebral bodies (inflammation of the attachment sites of muscles to the vertebra) or chondropathy of the apophyses of the thoracic vertebrae are different names for the same disease. With this disease, 7-10 thoracic vertebrae are most often affected. The disease occurs in boys from 11 to 18 years old. The patient complains of back pain, fatigue of the back muscles during normal exercise. On examination, an increase in thoracic kyphosis (bending of the spine in the thoracic region with a posterior bulge) is found. X-rays show a change in the shape of the vertebrae. Normal vertebrae in the thoracic region look like bricks, with smooth edges. In Scheuermann-Mau disease, the vertebrae in the lower thoracic region become wedge-shaped.

Treatment consists in the appointment of physiotherapy exercises, massage, underwater traction, swimming. Occasionally, with a pronounced violation of posture, surgical treatment is used.

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Disease pathogenesis

reparation (restoration);

Causes of pathology

Diagnostic methods

Source: osteocure.ru

Osteochondropathy of the heads of the metatarsal bones

More often, females aged 12 to 18 years (70-80%) get sick. Sometimes the lesion is bilateral. In 10% of cases, several metatarsal bones are affected. There are familial forms of the disease.

Etiopathogenesis. The cause of the disease is considered to be malnutrition of the bone as a result of: acute and chronic injuries, wearing irrational shoes; activities associated with overloads on the lower limbs; static transverse and longitudinal flat feet. The pathogenetic picture of the disease, as with other localizations of osteochondropathy, repeats all the characteristic stages of this disease.

Clinical picture. The disease begins gradually, gradually, extremely rarely - acutely. At the level of the corresponding head of the metatarsal bone, pain appears during exercise, and then at rest. The pain gets worse over time and lameness appears. Walking barefoot, in soft shoes, on uneven ground becomes unbearable. A swelling appears on the dorsum of the foot at the level of the affected head, which spreads proximally along the course of the metatarsal bone. Palpation of the head is very painful, it is enlarged and deformed. There is a gradual shortening of the finger adjacent to the head and deformation of the metatarsophalangeal joint, with limited range of motion in it. A sharp pain is determined when pressed along the axis of the finger and when the forefoot is compressed in the transverse direction. After about 2 years, the pain disappears, but there is a possibility of their resumption due to the development of deforming arthrosis of the affected metatarsophalangeal joint. When creating situations of the above etiological nature, pain may occur.

X-ray: at the first stage of aseptic necrosis, a slight compaction of the bone tissue structure of the affected metatarsal head is determined. The second stage is characterized by a flattening of the articular surface of the head and an increase in the density of its bone tissue.

The degree of deformity of the metatarsal head ranges from a slight straightening of the articular surface to a significant decrease in the height of the head. During this period, the expansion of the joint space of the adjacent metatarsophalangeal joint is clearly defined. The third stage - the stage of resorption of necrotic bone tissue - radiographically manifests itself in the form of fragmentation of the head of the metatarsal bone. The shape, size and density of the fragments are different. Their contours are uneven, jagged or emphatically clear. The joint space remains widened. The fourth stage is the restoration of a uniform pattern of the structure of the deformed head and the disappearance of signs of fragmentation. Its structure is formed by rough thickened bone beams. The contour of the head acquires a saucer-like shape with a recess in the center and with edges protruding to the sides. As a result of this flattening of the head, shortening of the metatarsal bone occurs. The joint space narrows and has an uneven width. The fifth stage is the development of deforming arthrosis of the metatarsophalangeal joint.

Differential diagnosis is carried out with a consequence of a fracture of the head of the metatarsal bone, an inflammatory process in it (tuberculosis, infectious arthritis), marching fractures (Deichlander's disease).

Treatment is conservative. In the first and second stages of the disease - immobilization: a plaster boot is applied for 1 month. In later stages, an orthopedic insole is used with careful laying out of the transverse (especially carefully) and longitudinal arches of the foot with the simultaneous appointment of appropriate orthopedic shoes. Exclude activities associated with overloads on the feet. Assign a relaxing massage, unloading therapeutic exercises.

Physiotherapy treatment: ultrasound with Trilon B, solux, foot baths and overnight compresses (wine or with glycerin, medical bile), electrophoresis with novocaine and potassium iodide, mud or paraffin-ozocerite applications. In the third or fourth stages, radon, hydrogen sulfide, naftalan baths are prescribed.

Surgical treatment is rarely used: with the failure of conservative treatment in order to remove bone growths on the deformed head of the metatarsal bone, which increase pain and interfere with the use of shoes. With stiffness of the metatarsophalangeal joint, the base of the main phalanx of the corresponding finger is resected.

The prognosis is favorable. If left untreated, the course is long (over 3 years), and the developed deforming arthrosis of the metatarsophalangeal joints leads to dysfunction of the forefoot and is the cause of pain.

Prevention. Exclude activities associated with overloads on the feet, conduct timely treatment of static deformities of the feet.

Source: www.blackpantera.ru

Osteochondropathy of the knee joint. Causes, symptoms, diagnosis and treatment

Osteochondropathy of the knee is most common in childhood and adolescence. A common cause of the disease is a high mechanical load on the knee joint and injuries resulting from vigorous activity. Early diagnosis and treatment of the disease can achieve high results and minimize the recurrence of the disease in the future.

Varieties of osteochondropathy of the knee joint

Osteochondropathy of the knee includes several diseases in the knee area. Each of them has its own symptoms and affects a specific area of the knee. Specifically, in the area of the knee joint, 3 types of the disease can be found:

Koenig's disease (Konig) - osteochondropathy of the patellofemoral joint and the surface of the knee joint.
Osgood-Schlatter disease is a disease of the tibial tuberosity.
Sinding-Larsen-Johansson disease (Sinding-Larsen-Johansson) - osteochondropathy of the upper or lower patella.

Let's take a closer look at each disease separately.

Koenig's disease

Koenig's disease or osteochondritis dissecans is characterized by neurosis of the bone surface with the formation of a bone and cartilage fragment on it. With the complication of the disease, its further penetration into the joint cavity occurs.

Although the first description of the disease was made in 1870, the term osteochondritis dissecans was first proposed by Franz Koenig in 1887.

On average, osteochondritis dissecans occurs in 30 cases out of 100,000 people. The average age of patients suffering from Koenig's disease ranges from 10 to 20 years. It should be noted that boys are affected 3 times more often than girls. In almost 30% of cases, bilateral damage to the knee joints is possible.

Unlike Koenig's disease, which is an intra-articular lesion, Osgood-Schlatter and Sinding-Larsen-Joganson diseases are considered by physicians as apophyses.

Osgood-Schlatter disease

Osgood-Schlatter disease is characterized by lesions of the tibial tuberosity. The average age of patients is from 8 to 15 years, and in girls the maximum age threshold does not exceed 13 years. As with Koenig's disease, the majority of patients are boys. This is primarily due to their greater activity.

The single cause of the disease is unknown, but there are a number of factors that can lead to the defeat of the tuberosity of the tibia. These can be both structural changes in the patella, as well as necrosis and disruption of the endocrine glands. Now the most accepted theory is repeated microtrauma of the tibia.

Sinding-Larsen-Joganson disease

Sinding-Larsen-Joganson disease or osteochondropathy of the patella is accompanied by pain in the knee joint and is detected by X-ray fragmentation of the upper or lower kneecap. Pathology most often occurs in patients aged 10 to 15 years.

Pathological process in diseases of Osgood-Schlatter and Sinding-Larsen-Joganson

The causes of osteochondropathy of the patella are not fully known, but it has been found that they are similar to the causes of Osgood-Schlatter disease. Increased function of the quadriceps muscle can lead to rupture and separation of the bone tissue from the patella, which leads to necrosis.

It should be noted that all of the above diseases most often occur in male adolescents involved in sports. Sinding-Larsen-Joganson and Osgood-Schlatter diseases are observed mainly in adolescence during puberty.

In addition to the above varieties of osteochondropathy, there is osteochondropathy of the calcaneus in children. Its symptoms and treatments are very similar to other types of the disease.

Clinical picture

It should be noted that osteochondropathy of the knee joint in the initial stages is characterized by the absence of obvious symptoms. The primary manifestations of all three types of diseases are accompanied by pain. At the first stages of development of osteochondropathy, pain syndrome is observed with intense physical exertion on the knee. At the same time, at rest, pain is completely absent.

Over time, the pain becomes more noticeable and localized. In Koenig's disease, pain is most often manifested in the region of the medial condyle. Constant pain in the anterior region of the knee is characteristic of Sinding-Larsen-Joganson disease.

Pain localization. Osgood-Schlatter disease (left) and Sinding-Larsen-Joganson disease (right).

If you do not take action in time, then knee pain can become permanent. Over time, patients develop lameness and limited movement of the knee joint. Complications of osteochondropathy can lead to progression of quadriceps hypertrophy. The characteristic features of Sinding-Larsen-Joganson and Osgood-Schlatter diseases include the appearance of pain at the time of contraction of the quadriceps muscle.

When examining a patient with Koenig's disease, an increase in the affected joint is observed due to the development of synovitis. An increase in the volume of the joint can also be observed with tibial tuberosity and osteochondropathy of the patella. But in this case, the cause of swelling is due to local changes, such as hyperemia, and the development of bursitis.

Diagnostics

There are several ways to diagnose osteochondropathy of the knee joint. Depending on the symptoms of the disease and the complexity of the disease, the following types of diagnostics are divided:

ultrasound. Ultrasound examination makes it possible to diagnose osteochondropathy of the knee joint with a high probability. Since the doctor has the opportunity to assess the state of x-ray structures. However, this diagnostic method can be effective only if a highly qualified specialist is available.

Scintigraphy. An equally effective method for diagnosing osteochondropathy, which allows you to diagnose the disease at different stages. But this method in pediatrics is used extremely rarely.

Magnetic resonance imaging. This diagnostic method is most informative in Koenig's disease. It allows you to identify the disease at the initial stages, and to assess the current state of the knee joints. When diagnosing tibial tuberosity and osteochondropathy of the patella, magnetic resonance imaging makes it easy to identify the anatomy and pathology of diseases.

Differential diagnosis. This type of diagnosis is most relevant for detecting the disease in the initial stages.

Arthroscopy. It is used to diagnose Koenig's disease, and is highly effective at almost all stages of the disease. The main feature of arthroscopy is that it allows you to accurately assess the condition of the knee joint, which is very important when choosing tactics for further treatment. Arthroscopy also allows you to combine diagnostic and therapeutic measures.

In the treatment of osteochondropathy of the knee joint, there are conservative and surgical methods. Which method is more appropriate to use depends on the stage at which the disease proceeds and the presence of complications.

A feature of conservative treatment is to reduce the load on the knee by fixing it. With the disappearance of the symptoms of the disease over time, you can slightly increase the load on the joint. If there is no positive dynamics in the period of 3 months, in this case, surgical methods of treatment are used.

Surgical methods of treatment are carried out using arthroscopic equipment, and include the following procedures: removal of the cartilaginous body followed by chondroplasty, as well as microfracturing and osteoperforation.

The treatment of Sinding-Larsen-Joganson and Osgood-Schlatter diseases is similar to each other and is almost always limited to conservative methods. The main goal of conservative treatment is to reduce activity in the knee as much as possible and to eliminate all movements that cause pain in the joint. Analgesics and anti-inflammatory drugs are used to relieve pain.

Surgical treatment of the above diseases can be attributed to the patient in case of constant exacerbations of the disease, and separation of apotheosis. In rare cases, surgical methods are used to remove a detached bone fragment and for cosmetic purposes.

The prognosis directly depends on the stage of osteochondropathy of the knee joint. In adolescent patients, with timely detection and treatment of the disease, a complete recovery is observed. In the later stages of the book's disease, gonarthrosis may develop.

With a disease of tibial tuberosity and osteochondropathy of the patella, a complete recovery of the knee joint occurs within one year. In some cases, discomfort in the knee area can be observed in the period from 1 to 3 years. In general, the younger the patient, the easier and faster the treatment proceeds.

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Osteochondropathy of the tuber and apophysis of the calcaneus

Osteochondropathy of the tuber and apophysis of the calcaneus was first described in 1907 by Haglund. This disease mainly occurs in girls 12-15 years old. The pathological process affects one or both limbs.

The disease is characterized by the occurrence of aseptic necrosis of spongy bone areas that are under the influence of increased mechanical stress.

Most often, osteochondropathy of the calcaneus occurs in children. Usually the disease proceeds benignly and practically does not affect the function of the joints and the general condition of the person.

Quite often, the disease goes away without treatment, as evidence of the disease, only deforming arthrosis remains.

Disease pathogenesis

The pathogenesis of the disease has not been fully elucidated. It is believed that osteochondropathy of the calcaneus is a consequence of local circulatory disorders, leading to a decrease in the supply of adjacent tissues, which is the starting point for the development of the disease.

There are five stages in the development of the disease:

aseptic necrosis (necrosis);
fracture and partial fragmentation;
resorption of dead bone tissue;
reparation (restoration);
inflammation or deforming osteoarthritis, if untreated.

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Causes of pathology

Researchers suggest that such pathogenic factors as microtrauma, increased load (running, jumping), tension in the tendons of the muscles attached to the calcaneal tuberosity, endocrine, vascular and neutrophic factors cause calcaneal osteochondropathy.

Diagnostic methods

A characteristic feature of the disease is that pain in the area of the calcaneal tuberosity occurs only when it is loaded or when pressed, there is no pain at rest.

This feature allows you to distinguish this disease from bursitis. periostitis, osteomyelitis, bone tuberculosis, malignant tumors.

Above the calcaneal tubercle there is swelling without redness and any other signs of inflammation.

Patients with osteochondropathy of the calcaneus are characterized by walking with the transfer of support to the forefoot, so walking with support on the heel becomes impossible due to the unbearable nature of the pain.

Most patients note the appearance of skin atrophy, moderate soft tissue edema, increased skin sensitivity on the plantar surface of the foot in the area of the calcaneus. Quite often, the muscles of the lower leg atrophy.

X-ray examination determines the presence of a lesion of the calcaneus apophysis, which is manifested by loosening of the bone structure and cortical substance under the apophysis.

For pathology, a characteristic feature is the presence of shadows of dead areas of the bone, displaced to the side, as well as the unevenness of the contour of the bone surface will be more pronounced than normal on a healthy leg.

What treatments are available?

Conservative treatment for this pathology is not always effective. But still, it is better to start with it.

In acute pain syndrome, rest is prescribed, immobilization is carried out with a plaster cast. For anesthesia, soft tissues in the heel area are chipped with novocaine.

Physiotherapeutic procedures are carried out: electrophoresis of novocaine with analgin, microwave therapy, ozocerite applications, compresses, baths.

Prescribe drugs such as pyrogenal, brufen, vitamins of group B.

With the ineffectiveness of conservative therapy, they resort to the operational intersection of the tibial and saphenous nerves with branches going to the heel.

This allows the patient to get rid of unbearable pain, and also makes it possible to load the tubercles of the heel bones when walking without fear.

Unfortunately, the operation entails a loss in the heel region of not only pain, but also skin sensitivity.

In the case of timely and correct treatment, the structure and shape of the calcaneus is completely restored.

If the disease is not detected in time or irrational treatment is used, the increase and deformation of the calcaneal tuberosity will remain forever, which will lead to difficulty in wearing ordinary shoes. This problem can be solved by wearing special orthopedic shoes.

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Due to many diseases of the feet, the foot can be damaged. On the video, shooting a surgical intervention in order to save the patient from pathology.

More often, females aged 12 to 18 years (70-80%) get sick. Sometimes the lesion is bilateral. In 10% of cases, several metatarsal bones are affected. There are familial forms of the disease.

Differential Diagnosis carried out with a consequence of a fracture of the head of the metatarsal bone, an inflammatory process in it (tuberculosis, infectious arthritis), marching fractures (Deichlander's disease).

Treatment conservative. In the first and second stages of the disease - immobilization: a plaster boot is applied for 1 month. In later stages, an orthopedic insole is used with careful laying out of the transverse (especially carefully) and longitudinal arches of the foot with the simultaneous appointment of appropriate orthopedic shoes. Exclude activities associated with overloads on the feet. Assign a relaxing massage, unloading therapeutic exercises.

Forecast- favorable. In the absence of treatment, the course is long (over 3 years), and the developed deforming arthrosis of the metatarsophalangeal joints leads to dysfunction of the forefoot and is the cause of pain.

Prevention. Exclude activities associated with overloads on the feet, conduct timely treatment of static deformities of the feet.

The doctrine of osteochondropathy arose thanks to radiology; in pre-radiological time, nothing was known about the existence of these diseases. Only the widespread use of X-rays showed that under the name "tuberculosis", "syphilis", "rickets", etc., a rather large number of lesions are hidden, which make up an independent nosological group.

Common to all osteochondropathy is the predominant lesion of childhood and adolescence; all of them are characterized by a chronic benign clinical course and a favorable outcome.

From a morphological and pathophysiological point of view, osteochondropathy is an aseptic bone necrosis that occurs with peculiar complications, such as pathological fractures. Spongy bone tissue undergoes necrosis, moreover, only certain certain epiphyses, short and small bones and apophyses, which, due to their anatomical location, are under conditions of increased mechanical stress.

The etiology of osteochondropathy is still not well understood. Osteo-necrosis develops as a result of a violation of local arterial nutrition of the bone substance and bone marrow. But what are the causes and what is the immediate mechanism of this pathological disruption of the local blood supply? Only one thing is firmly established - necrosis is not - the result of grossly mechanical blockage of blood vessels; The embolic theory of osteochondropathy is rightly regarded as speculative and untenable. At present, the leading and decisive role of neurovascular, ie, in the final analysis, precisely nervous factors, is increasingly being confirmed in the occurrence of these painful phenomena in the vital activity of the bones. Aseptic osteonecrosis is caused, obviously, by a violation of the innervation of blood vessels, which is under the control of higher regulatory systems in the entire human body.

The further presentation is based on a simple scheme for dividing all the various osteochondropathy into four groups.

A. Osteochondropathy of the epiphyseal ends of tubular bones 1. Osteochondropathy of the femoral head. 2. Osteochondropathy of the head of the II or III metatarsal bone. 3. Osteochondropathy of the sternal end of the clavicle. 4. Multiple Osteochondropathy of the phalanges of the fingers. 5. Osteochondropathy of the navicular bone of the foot. 6. Osteochondropathy of the lunate bone of the hand. 7. Osteochondropathy of the vertebral body. 8. Osteochondropathy of the sesamoid bone of the first metatarsophalangeal joint.

B. Osteochondropathy of the apophyses 9. Osteochondropathy of the tibial tuberosity. 10. Osteochondropathy of the calcaneal tuber. 11. Osteochondropathy of the apophyseal discs of the vertebrae or juvenile kyphosis. 12. Osteochondropathy of the pubic bone.

D. Partial (wedge-shaped) osteochondropathy of the articular surfaces (dissecting osteochondritis of the knee, elbow and other joints).

1. Osteochondropathy of the femoral head (Legg-Calve-Perthes disease)

This Osteochondropathy of the femoral head is one of the most frequent. The age most predisposed to this disease is from 5 to 12 years, but cases of the disease are not uncommon at an earlier and especially at a later age (up to 18-19 years). In adults, starting from the 3rd decade, only the results of osteochondropathy can be observed, but not a fresh disease. Boys and young men are affected 4-5 times more often than girls. In most cases, the process is unilateral, but there is also a bilateral lesion, the latter is more common in young men at the age limit for this disease. In this case, a bilateral lesion develops first on one side, then on the other.

Usually apparently healthy, normally developed children get sick with osteochondropathy of the femoral head. In most case histories, there are no indications of trauma in the anamnesis, sometimes the onset is associated with a certain traumatic moment, a fall or a bruise. Pains appear in the hip joint, usually slight and unstable, almost never reaching such a degree as in tuberculous coxitis. Sometimes these pains refer to the groin area and radiate to the knee joint, as with coxitis. Pain comes more often after walking, less often at night. The child begins to limp and slightly drag the injured leg. At times, all these phenomena disappear, then resume. General symptoms such as fever are absent. The blood is normal. The erythrocyte sedimentation reaction shows normal numbers. The disease has a relatively benign chronic slow course. On average, after 4-4/2 years, but often much earlier - after 2-2/2 years, as, however, sometimes and much later, 6-8 years after the onset of the disease, a cure invariably occurs. There is never the formation of fistulas or swell abscesses, and an outcome in ankylosis is also excluded.

Patients usually seek medical help after several months, and sometimes several years after the onset of the disease. Objectively, the absence of atrophy of the affected limb or a very slight degree of it is determined. A characteristic clinical symptom is a more or less significant limitation of abduction with normally preserved flexion and extension in the hip joint; rotation is somewhat difficult, especially inwards. In rare cases, it is necessary to observe such a clinical syndrome with osteochondropathy of the femoral head, which completely fits into the objective picture of early tuberculous coxitis. This is explained by the fact that even with osteochondropathy, the synovial membrane of the joint can be edematous, full-blooded and thickened at the height of the disease, and the soft tissues around the joint turn out to be swollen. Usually, the movements are slightly painful, the load does not cause pain, with pressure on the head or greater trochanter, there may be complaints. Trendelenburg's symptom in most cases is positive. The diseased limb is shortened within a few centimeters.

The pathological and histological changes occurring in the epiphyseal part of the femoral head are based on the so-called primary aseptic subchondral epiphyseonecrosis. The whole complex and variegated pathoanatomical and radiographic picture of osteochondropathy of the femoral head is explained by a number of secondary sequential changes that are partly the nature of complications following necrosis, but mainly the nature of regenerative processes that restore the dead head.

In the first stage of osteochondropathy of the femoral head, the stage of necrosis, a typical histological picture of complete necrosis of both the spongy bone substance of the epiphyseal head and its bone marrow is found. Only the cartilaginous cover of the head does not die, which is why the process is called subcartilaginous. Macroscopically, the femoral head in this initial stage of osteochondropathy does not present any deviations from the norm, and deep internal changes do not appear in any way when examining the preparation with the naked eye.

The presence of dead bone tissue causes a response from healthy, not subjected to necrosis, adjacent connective tissue elements. This is where regeneration comes from - the resorption of dead tissue and its replacement with living, newly formed bone tissue. The metaphyseal periosteum is introduced from the side of the femoral neck into the dead focus through the cartilage at the edge of its attachment to the bone; superficial - the marginal parts of the epiphysis, therefore, are undermined and loosened. In addition, the necrotic bone skeleton of the head naturally loses its normal mechanical properties.

The femoral head is no longer functionally sufficient, it loses its ability to withstand the usual load. A relatively small injury that a normal bone would withstand is enough for a complication to occur in the form of a so-called depressed subchondral fracture of the necrotic head. This fracture, or rather, an infinite number of microscopic fractures, is, therefore, not a primary one, but a pathological, secondary fracture occurring in an altered tissue. Bone beams are wedged into each other, compressed, closely adjacent to each other and form a single dense mass, the so-called bone meal. Macroscopically, in this second stage of osteochondropathy, stage and compression fracture, the head is flattened from top to bottom, the cartilaginous cap, otherwise unchanged, is depressed and thickened.

The third stage of osteochondropathy - the stage of resorption - is characterized by the elimination of pounded dense bone sand. The healing of a peculiar fracture of dead bone beams cannot proceed in the usual way, for example, with the help of a callus, as in a diaphya fracture. Bone fragments are slowly resorbed by surrounding healthy tissues. Connective tissue strands from the femoral neck penetrate deep into the dead field; from the articular cartilaginous shell and the epiphyseal cartilaginous disk, cartilaginous islands are laced off and introduced into the "fragment field", and the entire head is divided into separate sections. Separate areas of necrotic masses are surrounded on all sides by osteoclastic shafts. Histologically, various secondary changes appear at this stage, such as the formation of cysts with giant cells lining their walls, various processes of hemoglobin decomposition from hemorrhages, the so-called fatty cysts with remnants of fatty accumulations from bone marrow lipoids and other elements, etc.

Following resorption, or rather, almost simultaneously with it, the formation of new bone tissue is also introduced; this is the fourth stage - the stage of reparation. The reconstruction of the spongy bone substance of the head occurs due to the same connective tissue and cartilaginous elements that have grown into the epiphyseal head from neighboring tissues. These elements metaplastically transform into bone tissue. It is at this stage of recovery, and not at the beginning of the pathological process, that it is especially often necessary to observe racemose enlightenments of various p-sizes. Thus, instead of necrotic and crushed bone beams, a living dense spongy tissue of the head is recreated.

The fifth stage of osteochondropathy of the femoral head is called the final stage and is characterized by a number of secondary changes in the hip joint such as disfiguring arthrosis. If the structure of the head is usually more or less completely restored, then its shape, of course, undergoes significant changes during the course of the disease. The depressed fracture and mainly the load on the head that has lost its normal strength, in which a long process of restructuring takes place, lead to the fact that the shape of the reconstructed head differs from the original. Along with this, the shape of the acetabulum changes again. Due to the rule that the shape of the articular cavity is always adapted to the shape of the head and changes in one of the articular surfaces are necessarily followed by changes in the other, the acetabulum also flattens a second time. The bag of the joint remains thickened and compacted. The anatomical outcome of osteochondropathy of the femoral head is a special kind of disfiguring osteoarthritis.

From an anatomical point of view, osteochondropathy can thus be characterized as a kind of regenerative-reparative process following primary aseptic bone necrosis. From beginning to end there are no purely inflammatory changes in the tissues. Therefore, names indicating inflammation, such as disfiguring juvenile osteochondritis of the hip, should not be used.

Such is the anatomical evolution of this disease, presented here in a somewhat schematic form. In fact, the individual stages do not follow one another with such regularity, but at the same moment there are signs of two, and sometimes three successive stages.

Anatomical and histological changes in osteochondropathy of the femoral head are very demonstratively depicted on the radiographs.

In the first stage (Fig. 428, A), when necrosis has already set in, but the macroscopic picture of the femoral head is still quite normal, the x-ray picture of osteochondropathy remains absolutely unchanged. This is of great practical importance; the radiologist is deprived of the right to exclude the possibility of osteochondropathy on the basis of negative radiographic data at the onset of the disease, if this disease is suspected from the clinical side. It is not known exactly how long this latent period lasts for X-ray diagnostics - in some cases, it takes several months to the second stage, in others - six months and rarely even more. The radiologist in such early doubtful cases should insist on repeated studies every 2-3 weeks, until the diagnostic problem is solved in one direction or another from the clinical or radiological side.

The second stage (Fig. 428, B, 429, 430) gives a characteristic x-ray picture. The femoral head is primarily uniformly darkened and devoid of a structural pattern; in the picture of the pelvis, the affected epiphyseal head is therefore sharply contrasted. The deep intense shadow of the epiphyseal head is explained by the fact that necrotic bone tissue itself is always marked by an increase in the density of its shadow compared to the norm. In addition, due to the compression of bone beams into bone meal, there are a significantly larger number of these beams per unit volume than under normal conditions. Osteosclerosis of the head, as previously assumed on the basis of x-rays, of course, no. Only in rare, very early cases of osteochondropathy, it is necessary to observe not a uniform darkening of the head, but a focal one - then separate darker structureless islands appear against a normal background, which very quickly merge with each other into one continuous dark hat. In isolated cases, it is possible to detect a sinuous serpentine line parallel to the epiphyseal strip, crossing the head at some distance from its surface, which can be used as a fracture line; usually, an impression fracture is not directly visible. The epiphyseal line in the second stage does not present any special changes, or it is "restless", more tortuous than under normal conditions, and sometimes bifurcates.

Of great diagnostic importance is the flattening or compression of the head from top to bottom; its height is reduced in comparison with the other normal side by one quarter or one third. The contours of the head are sharply limited, as in the norm, but lose their smoothness; flatter uneven places resembling facets appear on the surface of the head, or the whole head takes on a somewhat irregular multifaceted shape. Especially valuable in the diagnostic sense is the expansion of the joint space. This expansion is explained by the fact that there is already an early reactive process on the part of the articular cartilage, namely its proliferation, leading to a thickening of the transparent cartilage in the picture.

The second stage lasts, as shown by a series of photographs taken at regular short intervals, for a varying "long time - from several months to six months or more. It is impossible to determine its exact duration, because the appearance of initial symptoms has to be observed only in exceptional cases.

An extremely characteristic, almost pathognomonic picture is presented by radiographs in the third stage (Fig. 428, B, 431, 432). - The head no longer gives a homogeneous shadow - it is all broken into several dark structureless isolated fragments of a completely irregular shape, most often flat, flattened top down. The contours of these intense areas, corresponding to necrotic bone meal, are sharply limited and uneven, bay-like and tortuous. especially on the side of the neck. The light background on the roentgenogram corresponds to the growths of the connective tissue that are transparent to x-rays; tissue and cartilage. This is the so-called sequester-like picture, so typical of the third stage of osteochondropathy. In the early phases of the third stage, it is necessary to observe foci of resorption in the form of mainly marginal defects in the base of the epiphyseal head at the border with the femoral neck. The splitting of necrotic masses lying directly under the cartilaginous cap into larger lateral and smaller medial fragments also appears relatively early, which is due to the introduction of living and active connective tissue elements into the head through the round ligament.

The head of the femur, now consisting only of bone remnants, flattens even more. The joint space - the projection of the articular cartilage - is also wider than in the second stage. The epiphyseal line, initially sharply tortuous, loosens, breaks into several branches crossing each other, embracing the so-called bone islands, and then completely disappears, i.e., the initially flat cartilaginous epiphyseal disc turns into a very complex uneven relief due to the proliferation of its cells. bumpy elevations. In the stage of resorption, the light epiphyseal zone merges with enlightenments between individual sequester-like shadows. There is an introduction of cartilaginous growths and real islet formations into the spongy bone substance. In other words, gradually deepening, the cartilaginous sprouts lose their connection with the epiphyseal disc, are rejected, take on a rounded shape, and then gradually decrease, ossify, and are lost in the overall bone structure. These cartilage formations are thus temporary, in contrast to the more persistent fatty and bloody racemosus with their sclerotic rim. Osteoporosis at this stage, as well as throughout the disease, is absent or only barely noticeable.

The X-ray picture of the femoral neck also undergoes major changes. The neck first of all thickens and shortens; the first is due to a significant periosteal reaction and is best described in the upper-outer area between the greater trochanter and the head. Shortening is explained by a violation of the process of endochondral epiphyseal growth. In addition to this absolute shortening of the neck, on the radiograph, one can also note its relative shortening due to developing retroversion (Fig. 432).

In some severe cases of osteochondropathy, not only the epiphyseal head, but also a larger or smaller area of the femoral neck adjacent to it, undergoes necrosis. In these cervical foci of enlightenment, however, in no way should one see the primary localization of the osteochondropathic destructive process, which allegedly precedes changes in the epiphyseal head. The assumption that the main changes nest in the neck, under the head, and, adjacent to the epiphyseal cartilage, involve it in the process, contradicts all anatomical information; it is based on an erroneous interpretation of radiographs. Already in the second stage, when the shadow of the head is not yet completely homogeneous, the epiphyseal light line can bifurcate or break into several branches that intersect each other and form the so-called islands. These islets are often imaginary; they are the product of the projection on the radiograph of individual bone elevations corresponding to the bumpy relief of the growing epiphyseal cartilage. The islets sometimes appear very clearly on the pictures and in reality may resemble separate bone foci; they are certainly not located in the femoral neck itself. Even more can simulate subcapital foci and in the third stage of the disease, individual "sequester-like shadows", namely: if the radiograph was made in the position of turning the thigh outward or when the neck was turned back. Then the head "gets into the back of the head" and is projected on the radiograph not in profile, but more from front to back, sequester-like shadows are lying in the shadow of the femoral neck, and the head retains a more or less normal spherical shape and smooth outer contours (Fig. 433, 434).

Here also it is impossible to use only one typical direct projection, but it is obligatory to take additional pictures in other positions of the study. It is in the third stage that very valuable details are determined. The head in some cases is displaced posteriorly to such an extent that there is reason to talk about genuine pathological epiphyseolysis.

The third stage lasts the longest, namely about 1/2-2/2 or more years, and therefore the radiologist has to see the largest contingent of patients with osteochondropathy of the femoral head mainly at this stage. Diagnosis of this disease at this stage is the easiest.

In the fourth stage (Fig. 428, D, 435), sequester-like areas are no longer visible on radiographs. Above the newly appeared epiphyseal line, the spongy bone shadow of the epiphyseal femoral head is again outlined. The head, however, still does not give a correct structural pattern, individual beams are usually thickened and partially merge with each other, forming areas of osteosclerosis. In some places, on the contrary, small light layers of not yet ossified strands of connective tissue or cartilage remain. Islets of live sclerosed bone may resemble necrotic dark areas; the difference between them lies only in the fact that the sclerosed areas lie among the spongy bone, while the necrosis is more sharply isolated against a light background of transparent soft tissues. In some cases, only a serial study can finally clarify the issue: on subsequent images, necrotic areas become smaller, while the size of dense living bone areas slowly increases until the entire head is completely rebuilt.

At this stage, the correct rounded racemose enlightenments, bordered by a thin sclerotic belt (Fig. 436), also stand out most clearly.

There are indications that cysts seem to develop especially often in cases of osteochondropathy in small children, when the disease begins at the age of 3-5 years. Our own observations, on the contrary, speak in favor of a greater frequency of racemose enlightenments in severe cases, especially bilateral ones, in adolescence. The duration of the recovery stage ranges from six months to one and a half years.

The recovery process, which has dragged on for years, is mainly due to repeated necrosis and pathological fractures, superimposed on previously existing ones.

No less characteristic are radiographic signs and the final stage of osteochondropathy of the femoral head (Fig. 428, D and D \\). The reconstructed head has a completely correct structural spongy pattern, but its shape has been drastically changed. The main thing is a noticeable flattening of the femoral head.

Recovery occurs in two ways. The first type (Fig. 428, E and 437) is characterized by the fact that the head again acquires a very regular spherical or slightly compressed from top to bottom, slightly ovoid shape, which differs from the original only by significantly increased sizes. Twice as often, however, the head is restored according to the roller-like type, that is, it is deformed in the form of a roller or mushroom (Fig. 428, D \, 438): the articular surface of the head takes on a shape resembling a truncated cone, the narrow part of which is directed to the medial side.

In both cases, the femoral neck is sharply thickened, shortened, somewhat arcuately curved, the cervical-diaphyseal angle decreases and true coxa vara develops; a frequent complication is the turning of the neck back combined with coxa vara. Sometimes the neck completely disappears, and the enlarged head almost comes close to the greater trochanter. The joint space is very different in the final stage of osteochondropathy, it most often expands, moreover, evenly in all parts of the joint or unevenly, rarely remains normal and even less often narrows to the same or unequal degree from the inside and outside. The acetabulum with its upper-outer quadrant is raised according to a greater or lesser flattening of the head, but at the same time it usually does not cover the entire head from above, and a significant part of the latter, sometimes its entire lateral half, remains outside the bony articular cavity, i.e., subluxation of the femoral head develops , functionally almost unaffected, Changes in the acetabulum with this osteochondropathy are secondary.

Sometimes the bone structure in the circumference of the cavity is quite significantly rebuilt, especially with bilateral lesions.

Lush bone growths as a result of osteochondropathy, in contrast to the primary cartilaginous disfiguring process, are usually not seen. The cartilaginous cover of the head remains intact all the time, and the bone head is not exposed in osteochondropathy. Therefore, the outcome in bone ankylosis never happens here.

These are the five stages in the evolution of osteochondropathy of the femoral head. Since one phase does not follow another through clear thresholds, attempts are being made by various authors to replace the breakdown into phases of the development of the disease with more advanced groupings at the stage. So, for example, D. G. Rokhlin distinguishes three successively developing phases of osteochondropathy - necrotic, degenerative-productive and the phase of outcome. The first and third phases are not objectionable. But the entire complex evolution of the disease, which usually lasts several years in the active stage and is of great practical and clinical importance, is reduced to only one second phase - the degenerative-productive one. V. P. Gratsiansky proposes to distinguish 8 periods during this disease. But it's too cumbersome. Therefore, being fully aware of certain conventions and shortcomings of the five-level breakdown, we continue to adhere to this grouping, most accurately and in the light of the latest data corresponding to the actual state of affairs.

Despite numerous theories based on a large collective experience and a significant amount of research, the cause of this disease remains unknown. The question of why head necrosis occurs is not resolved. The reasons given were: acute and chronic trauma, static moments, weakened infection, paratuberculous and parasyphilitic processes, late rickets, diseases of the endocrine system, constitutional congenital abnormalities of development, anomalies, pathological processes of ossification, beriberi. Osteochondropathy was considered as a special type of congenital dislocation of the hip, an irregularity. development of the acetabulum, fibrous osteitis, etc. Most of these assumptions lost their meaning when the formal genesis became clear.

One thing is certain - necrosis is caused by a violation of the arterial supply of the epiphyseal head of the femur. Burkhard's experimental studies show that bone tissue is very sensitive to interruption of blood supply. If with the help of an elastic tourniquet for a long time to squeeze the lumen of the arteries going to the periphery of the limb, then the bone tissue undergoes focal necrosis, which is only very slowly restored, as opposed to the reparative processes of "soft" connective tissue formations. Aseptic necrosis can be induced by blockage of arterial branches by injecting silver powder in liquid Arabica gum or by injecting carcass suspension into the artery. By cutting the corresponding arteries of the femoral head in a young dog, Nusbaum experimentally created a disease that is clinically, pathologically histologically and radiologically similar in all details with osteochondropathy of the femoral head in humans.

All these data on the role of the vascular factor were also confirmed by Tucker (Tucker) in 1950 using the most convincing method of labeled atoms. These studies showed that after the introduction of radioactive phosphorus, rushing into the bone, into the bloodstream, it is possible to show with accurate measurements a large difference of 1:16 and 1:20 in the content of isotopes in the femoral head and in the substance of the adjacent greater trochanter.

It is known from general pathology that aseptic bone necrosis in general can be caused by various causes: mechanical disruption of the integrity of the arteries, their twisting or compression, traumatic moments, embolism, possibly obliterating endarteritis, possibly also venous stasis, etc.

The most likely condition for the occurrence of necrosis is the constant traumatization of blood vessels in the form of their compression, tension or twisting at the sites of attachment of the articular bag, ligaments and muscles. From this point of view, numerous observations on the development of osteochondropathy after reduction of the hip due to its congenital dislocation are interesting, as well as a number of our observations when necrosis occurred with the so-called idiopathic coxa vara.

The most likely assumption seems to be that the violation of arterial nutrition occurs as a result of vasomotor innervation disorders, i.e. that osteochondropathy is aseptic osteonecrosis of neurovascular origin. Back in 1926, Bentzon experimentally obtained histologically proven changes in rabbits and goats, similar to osteochondropathy of the femoral head in humans, by injecting alcohol on the vasomotor nerves supplying the vessels of the upper epiphysis of the thigh. It can be assumed that a variety of general and local factors in the whole organism, as a result of violations of regulatory mechanisms, cause certain local circulatory disorders through the vascular nervous devices, which directly entail necrosis. This is not thought of as a mandatory vasospasm; theoretically, vascular paresis, i.e. active arterial hyperemia with blood stasis, should not be excluded. With this assumption, the occurrence of necrosis can be explained by only local functional disorders in the vessels, which are not detected by the usual rough histological methods of research. Thus, we can assume that osteochondropathy is caused in each individual case by the combined action of a number of causal factors, that its etiology is heterogeneous and cannot be reduced to just one factor. Osteochondropathy is a polyetiological concept.

As for the differential diagnosis of osteochondropathy of the femoral head, the X-ray examination, starting from the second stage, immediately brings complete clarity to the recognition of the disease. As a matter of fact, there is no differential X-ray diagnostics in typical cases of the disease, the X-ray picture in all stages, with the exception of the first, is almost pathognomonic. Typical cases of osteochondropathy can and should be recognized on the basis of clinical data alone, mainly symptoms of a favorable outpatient course, limited hip abduction with free flexion, a positive Trendelenburg phenomenon, etc. However, full confidence in the correctness of the clinical diagnosis without x-rays is never can't be.

From a differential diagnostic point of view, it is possible to oppose the classical - true, so-called genuine osteochondropathy, a fairly large group of symptomatic osteochondropathy, etiologically very motley.

In a very sometimes complex differential X-ray diagnostics with tuberculous coxitis, it is necessary (p. 182) to keep in mind, together with P. G. Kornev, histologically proven combined, combined forms. The tuberculous process in the head of the femur can sometimes be complicated by necrosis, which develops evolutionarily as osteochondropathy. Then on a series of radiographs there are elements of both diseases - inflammatory and necrotic. These are undoubtedly compatible phenomena.

The same is true for purulent coxitis, especially septic, most often postocarlatinal. A complete and correct assessment of the combined lesion is based on important anamnestic data and on the presence of clinical and radiological symptoms, both of an inflammatory-destructive order from the side of the articular surfaces, and necrotic from the side of the structure of the epiphyseal head. In these cases, the picture of osteochondropathy is compatible with the formation of ankylosis of the joint. We have also repeatedly observed a picture of the gradual development of a false joint in the subcapital part of the femoral neck after the complete fusion of the first dead, and then restored, living femoral head with the acetabulum.

Aseptic necrosis of the femoral head after a gross trauma is not uncommon, mainly in adults and even old people. The picture of aseptic necrosis after a fracture of the femoral neck is now well known, especially after the hip is repositioned on the occasion of congenital and traumatic dislocation. The pathological process then plays out in the following sequence: trauma, reduction, a light period of several months, a recurrent period of pain, and then a typical clinical and radiological evolution of osteochondropathy. The prognosis in these cases is always worse than; with the so-called genuine osteochondropathy.

Particular attention deserves partial superficial intra-articular lesions of only narrow plates of bone substance under the cartilaginous cover. These fractures are defined radiologically as a serpentine strip crossing the epiphyseal head more or less parallel to the enchondral cartilage disc. Sometimes only the lateral half or some upper-outer part of the head segment is cut off. Then, in a shorter time than usual, a partial osteochondropathy process also develops with an outcome in a blurred disfiguring, osteoarthritis.

As for the differential diagnosis between osteochondropathy and partial dissecting osteochondropathy, it will be clear from what follows (p. 494) that we are talking essentially only about quantitatively different manifestations of the same pathological necrotic process.

The same can be said about epiphyseolysis and coxa vara. Osteochondropathy entails a kind of pathological epiphyseolysis. But epiphyseolysis, for its part, can cause osteochondropathy as a complication. As a result of osteochondropathy, a viral deformity of the upper end of the thigh necessarily develops. But we have repeatedly observed the reverse relationship, namely: typical coxa vara is secondarily complicated by osteochondropathy. It is clear that the clarification of such cases is possible only with the use of all anamnestic and clinical data, but it is unthinkable without the use of basic and decisive radiological data, especially in a dynamic section.

Especially important is the X-ray examination of the most indicative and decisive in the differential diagnosis of the skeleton in such congenital and systemic diseases as chondrodystrophy, multiple cartilaginous exostoses, Olier's disease, and primarily osteochondrodystrophy. Sometimes in cases of little known and poorly recognized, often congenital, osteochondrodystrophy (Fig. 237, 238), a diagnosis of some systemic osteochondropathic process is made, while in fact such a disease does not exist. So, in our practice, there were patients with osteochondropathy with very significant structural changes in the head and neck, which in oncological institutions were misunderstood for certain tumors, benign and malignant, primary and metastatic.

In the differential diagnosis of osteochondropathy, finally, disfiguring osteoarthritis also acquires important practical significance, for example, when, with an inferior history in a patient aged 25-30 years, a pattern of damage to the femoral head and the entire hip joint, to some extent characteristic of osteochondropathy, is radiologically detected for the first time. Differential diagnostic difficulties may arise especially when making a very late diagnosis, when it is no longer possible to restore the clinical and especially radiological dynamics of the disease transferred many years ago. Especially lush bone growths are observed with a bilateral process. It is clear that in some difficult cases in middle or old age, all retrospective X-ray diagnostics of osteochondropathy of the femoral head becomes very doubtful, since over many years, as a result of progressive deformity, the femoral head may completely lose its appearance characteristic of osteochondropathy. However, in the vast majority of cases, the features characteristic of osteochondropathy still remain: a typical correct flattened head shape and a wide joint space.

The prognosis of osteochondropathy of the femoral head in the sense of life, of course, is quite favorable, but functionally it can be different. In any case, this disease cannot be considered exclusively benign. Long-term observations of patients whose fresh disease ended several years ago show that approximately 10-15% after osteochondropathy experience pain of a rather constant nature, limited mobility, periodically occurring lameness and, consequently, a decrease in working capacity1!. In other more numerous cases, the result of osteochondropathy is only a limitation of mobility in the hip joint without subjective complaints, and, as in the height of the disease, hip abduction most often suffers. At the same time, in contrast to fresh cases, where the reason for the restriction of abduction is muscular phenomena and under anesthesia, abduction can be performed freely, in the final stage the obstruction is anatomical. These cases refer entirely to the roll-like type of deforming arthrosis. Complete clinical and anatomical cure, which usually corresponds to a spherical head, occurs in 20-25% of all cases. According to summary statistics, in 80-85% of all cases of Legg-Calve-Perthes disease, a clinical permanent cure occurs. Bilateral osteochondropathy, especially asymmetrical, always proceeds worse than unilateral; the onset of the disease at a later age also worsens the prognosis. In rare, exceptionally favorable cases, the radiologist has to detect an old cured oeteochondropathy of the femoral head unexpectedly for the clinician and even for the patient who is not very attentive to himself.

As for the treatment of osteochondropathy of the femoral head, all changes following the primary aseptic epiphyseonecrosis are restorative and lead to the reconstruction of the femoral head. Since the conditions for the onset of necrosis remain unknown, prevention and causal treatment are, of course, still unknown. Therefore, all therapeutic measures are reduced only to the usual symptomatic, for example, physiotherapy. With very severe pain, immobilization and temporary unloading with traction are indicated. However, the end results in terms of the formation of a spherical head and the restoration of the function of the hip joint are much better in cases where the patient was not immobilized. The opinion that it is possible to easily stop or even eliminate osteochondropathy of the femoral head at any stage of development should be considered erroneous, since a quick cure, at least from an anatomical and radiographic point of view, never occurs.

If the disease is prone to self-healing, surgical intervention is not only not indicated, but, according to the unanimous opinion of all authors, is contraindicated.

2. Osteochondropathy of the head of the II and III metatarsal bones - the so-called second disease of Alban Koehler

Since Koehler described two localizations of osteochondropathy of the foot and both are designated by his name, in order to avoid confusion, it is customary to call the osteochondropathy of the scaphoid bone of the foot "the first Koehler's disease", and the osteochondropathy of the head of the metatarsal bone - the "second". Mnemonically, this is easy to remember, as Kohler's second disease affects the second metatarsal. It is best to leave your own names in general and define the disease with the word "osteochondropathy" indicating its localization.

Osteochondropathy of the II metatarsal bone is, together with osteochondropathy of the femoral head, one of the most common localizations of osteochondropathy. L. L. Golst and G. V. Khandrikov in 1926 published 29 cases of Koehler's second disease; we investigated over 180 cases of this disease during the 8 years up to 1934.

Unlike osteochondropathy of the femoral head, this disease affects the female sex four times more often, and mainly during puberty, i.e., at the age of 13 to 18 years. There are patients at an earlier and especially at a later age, and the development of the disease is often affected by everyday and especially professional moments; for example, the metatarsal bones are often affected by osteochondropathy in young textile workers and weavers who work standing with the torso tilted forward and resting on the area of the heads of the protruding metatarsal bones. Often, the disease was observed earlier in young workers in clothing factories, often resorting to flexion movements of the feet with pressure on the heads of the metatarsal bones from the sole.

A radiologist relatively often has to deal with patients and in adulthood up to 40-50 years old, in whom the disease has allegedly just appeared. Collecting an anamnesis in such cases with special care, one can always be convinced that this is not a fresh case, but the result of a process forgotten, transferred in adolescence, complicated at the present time by trauma.

The right foot is somewhat more frequently affected than the left. In 10% of all cases, the disease nests in the head not II, but III, and very rarely - in the head of the IV metatarsal bone. Also, in 10% of all cases, there is a bilateral disease of both second metatarsal bones, less often II and III on both sides, and very rarely two adjacent heads on one foot.

Everything that has been said about the evolution of osteochondropathy of the femoral head, with minor changes, can be repeated about osteochondropathy of the metatarsal head. From a clinical point of view, osteochondropathy of the metatarsal head proceeds extremely typically, so that all case histories are very uniform. In the anamnesis most often there is no acute traumatic moment. The process usually begins gradually, sometimes - immediately. Pain appears in the front end of the foot, periodically causing a slight lameness. The pains become very sharp when the patient accidentally steps on some object, the pain is especially significant when the patients walk without shoes.

In an objective clinical study, metatarsal heads suffering from osteochondropathy appear to be otherwise perfectly healthy young people. Often there is a flat or splayed foot. On the back of the foot, in the region of the metatarsophalangeal joints, swelling is found, so that the longitudinal depressions between the extensor tendons disappear. In some cases, there is also a slight reddening of the skin. When palpating, slight, and sometimes quite large, bone growths are determined on the head of the affected metatarsal bone. The affected finger II is somewhat shortened. Movement in the metatarsophalangeal joint is limited. Pressing on the head and pushing along the axis of the affected bone cause sharp pain. The general course is quite favorable; after 2-2/2 years, all phenomena disappear or only pains recur from time to time, especially during work or after an injury. There is never decay or suppuration, fistulas, ankylosis. The pathoanatomical and histological picture of osteochondropathy of the metatarsal head corresponds to the smallest detail to the already known picture of formal evolution in osteochondropathy of the femoral head. The X-ray picture is exactly the same.

The latent period of x-ray diagnostics - the time from the onset of clinical phenomena to the appearance of the first x-ray symptoms - lasts no more than 10-12 weeks.

In the second stage on the radiograph (Fig. 439, B), in full accordance with the anatomical data, the epiphyseal head loses its regular spherical or ovoid shape and flattens, its height decreases two to three times against the norm - one of the main radiological symptoms of osteochondropathy of the head metatarsal bone. Thus, due to the shortening of the head, the entire II metatarsal bone is shortened, and behind it the II toe; radiographically, this immediately catches the eye, since the light joint space of the second metatarsophalangeal joint becomes on the same level with the spaces of the joints of the I and III fingers (Fig. 440).

In addition to flattening, in the second stage there are still profound structural changes: the spongy pattern of the epiphysis disappears, and the entire head gives an intense, uniform, structureless shadow, which stands out very contrastingly in the picture in the form of a dark strip. The epiphyseal line is loosened. The joint space expands due to thickening of the cartilage of the articular head (Fig. 441).

In the third stage (Fig. 439, B), the solid shadow of the head is broken into "sequester-like shadows." At the edges of the head, necrotic bone masses disappear most quickly; therefore, sequester-like shadows have the form of flattened islands with uneven, sharply limited contours, and in some cases appear as transverse stripes with a smoother distal edge. The epiphyseal line merges with a light moat that delimits sequester-like shadows (Fig. 442).

The response activity of the periosteum affects the significant periosteal layers, typical for the third stage, evenly enveloping the distal end of the metatarsal bone in the form of a cone and leading to a typical thickening of the bone metadiaphysis. Due to the fact that ossification occurs relatively early along the edges of the metaepiphyseal growths, the affected metatarsal resembles an overturned bottle with a depressed bottom, and the head resembles a saucer in which dark sequester-like shadows lie. The metatarsal head becomes much wider than the opposite base of the phalanx. The joint space is even more expanded than in the second stage (Fig. 443).

In the fourth stage (Fig. 439, D), there are no sequester-like shadows. Periosteal bone layers are in the stage of reverse development, the meta-diaphysis of the metatarsal bone becomes thinner. The head is saucer-shaped with a central recess and raised pointed edges. Its structural pattern is rough and disordered (Fig. 444).

Finally, in the fifth stage of osteochondropathy of the head of the metatarsal bone, radiographs show a picture of disfiguring osteoarthritis (Fig. 439, D and 445, 446). The head is persistently deformed, its articular surface is tuberous, typical bony growths in the form of lips and ridges are outlined at the edges, the entire head is significantly flattened and enlarged in diameter. The final stage differs from the previous ones in secondary successive changes on the part of the main phalanx - its base, as well as the head of the metatarsal bone, is expanded, flattened, unevenly tuberous. The articular fissure of the second phalangeal joint gives a complex tortuous, sometimes expanded, sometimes narrowed projection. In the obligatory lateral photograph of the foot, lush bone ridges are also found on the dorsum of the head of the metatarsal bone.

This disease does not always lead to significant joint deformity; in some cases it is necessary to observe a more perfect restoration of not only the structure, but also the shape of the head. Apparently, not every primary necrosis is necessarily complicated by a fracture. In these cases, the restoration of the head will be more complete and the entire process, which is probably hidden, will end with a complete restoration.

In most cases, except for the initial and persistent end-stage metatarsal head osteochondropathy, radiographs at the onset of the disease show signs of not one stage, but transitional changes from one stage to another. Anatomically, this is quite understandable.

Recognition of osteochondropathy of the metatarsal bone currently does not present any difficulties already on the basis of clinical signs alone. A typical lesion in a typical place at a certain age, a benign general course, isolated pain on pressure on the head of the second metatarsal bone, the absence of decay and fistulas - all these signs are completely sufficient to justify a clinical diagnosis.

In all cases, X-ray examination makes it possible to discard any diagnostic doubts. In the second, third and fourth stages, the x-ray picture is pathognomonic; in the fifth, it is extremely characteristic, almost pathognomonic, or rather, it is not the picture of changes that is pathognomonic, but their localization in the head of the II or III metatarsal bone; only in the first stage is recognition entirely based on the clinical picture. Repeated x-ray examinations at the beginning of the disease, at the latest after 2-3 months, decide the issue definitively. However, most patients go to the doctor already with the third stage or even later, and the first stages are rarely observed in practice. A fairly common radiological error is the diagnosis of completed osteochondropathy of the head of the first metatarsal bone; here deforming osteoarthrosis in the first metatarsophalangeal joint is not primary bone, as in osteochondropathy, but primary cartilaginous (p. 589).

Treatment for osteochondropathy of the head of the II metatarsal bone should be conservative. Symptomatic treatment, as a rule, quite achieves the goal; of particular benefit is the partial unloading of the affected head with a special insole and appropriate shoes. Surgical removal of the head in fresh cases is contraindicated.

Only patients with an old and persistent fifth stage of the disease can be referred for surgery, when there is severe pain and large bone growths that make it difficult to wear comfortable shoes.

When assessing the condition of the foot, we are guided by the following criteria

Criteria for the normal position of the foot

1. The center of the hip, knee and ankle joints lie on one straight line drawn from the center of the hip joint to the ankle joint.

As mentioned above, pathological pronation of the foot, as well as the anterior tilt of the pelvis, can lead to an inward deflection of the knee joint.

There are also varus and valgus deformities of the lower extremities of a different nature, and these will also affect the position of the foot.

2. The lateral malleolus is below and posterior to the medial

A change in the normal ratio of the heads of the fibula and tibia indicates dysfunction of the tibial ligaments and the interosseous membrane. It is necessary to correct these structures.

3. In the standing position and lying on the stomach with the feet hanging down, the central axis of the ankle coincides with the axis of the calcaneus
Those. the heel is neither in supination nor in pronation.

The causes of the pathology are described in sufficient detail earlier, here I would like to draw attention to the difference in these provisions.

In the prone position, there is no static load and heel deviation, if any, occurs due to muscle imbalance (hypertonicity of the long peroneal muscle, for example).

In the standing position, a number of other forces arise (pressure of body weight, support reaction, etc.), ligamentous-articular mechanisms come into play, so static dysfunction will be a total phenomenon from many factors.

4. With a vertical heel, the forefoot must be horizontal

This statement repeats the previous one, i.e. we are talking about the absence of pronation and supination of the foot, but in this case, the examination is performed in a sitting position with the heel hanging vertically, and the anterior section is evaluated, i.e. a line drawn along the tops of the fingers. It should be parallel to the floor.

5. Each finger is on the same axis with the metatarsal bone of the same name

An example of a deviation from this rule is transverse flat feet and the subsequent changes in the toes.

6. In the standing position and at the moment of support when walking, the foot is in a neutral position.

The meaning of this position is as follows: the subtalar and talo-navicular joints must be congruent and held without resorting to ligaments. The axis of the subtalar joint should be located in such a way that its vertical component coincides with the axis of the lower leg, and the horizontal component coincides with the axis of the foot.

Neutral position means equal opportunities for pronation and supination.

All this is necessary in order for the talus to successfully perform its main function - to distribute force in three directions.

- back through the posterior articular joint with the calcaneus,
- anteriorly and medially through the talo-navicular joint,
- anteriorly and outward through the anterior articular surface of the talocalcaneal joint

7. A plumb line, lowered from the center of the lateral ankle, cuts off at least a third of the distance from the heel to the end of the little finger.

This criterion makes it possible to evaluate the ratio of the force vectors of the Achilles tendon and gastrocnemius muscle, directed upwards, and the plantar aponeurosis and short flexor of the fingers, the vector of which is directed along the foot towards the toes. If there is no balance and there is hypertonicity of the Achilles tendon, this distance will be less

Vectors of muscle traction in the foot, transverse and longitudinal stretching

From the point of view of mechanics (or, in this case, biomechanics), the system is in equilibrium if the resultant of the forces that make up its composition is equal to zero. If it is not equal to zero, it will move in the direction of the greater force until a new equilibrium is reached. Our body and any part of it, considered from this point of view, is a combination of multidirectional forces that are in balance.

True balance implies the absence of additional tension to compensate for the difference in forces. That is, with true equilibrium, there is simply no such difference. In this case, the bony landmarks correspond to a neutral, or zero, or simply normal position.

The criteria for this position for the foot and lower leg were listed above. Let us consider in more detail some pairs of force vectors with the foot.

It is easy to see that two independent force directions work in the area of the foot. For convenience, we will call them longitudinal and transverse power struts.

The longitudinal strut consists of two differently directed force vectors applied to the calcaneus. The first one is directed up and back. This is a powerful Achilles tendon with a calf muscle. In the opposite direction, along the foot towards the fingers, another force is applied, the material carrier of which is the plantar aponeurosis together with the short flexor of the fingers and partially the long plantar ligament.

If these forces are in balance, the calcaneus is positioned in relation to the ankles so that a plumb line dropped from the center of the lateral malleolus will cut off at least one third of the length of the foot from the heel to the end of the little toe. A decrease in this distance will indicate hypertonicity of the gastrocnemius muscle and shortening of the Achilles tendon. This is just that new balance, the mechanism of which can be briefly described as follows: an increase in the posterior-vertical force vector leads to a compensatory increase in the tone of the foot flexors and plantar aponeurosis, and the heel, as it were, is squeezed out by the resultant of these forces. It is clear that the correction in this case should begin with the Achilles tendon and calf muscle

Another power strut, let's call it transverse, comes from the bone center, grouped around the navicular bone: the sphenoid bones, the proximal head of the first metacarpal bone.

As you can easily see, two muscle groups are attached to this zone.

The first includes both tibial muscles, the second long peroneal. The power levers create a balance between pronation-abduction and supination-adduction. When we consider a freely hanging foot with a vertically located heel, then with the balance of these forces, we will observe the horizontal position of the forefoot. Hypertonicity and relative shortening of the long peroneal muscle will lead to the lowering of the inside of the foot, changes in the tibial muscles will lead to supination of the forefoot. When correcting, it should be noted that pain on palpation, sometimes quite significant, will be manifested by a muscle that is spasmodic in a stretched position, but correction must begin with its antagonist, because. that is the cause of the dysfunction.

Algorithm for correcting the musculoskeletal structures of the foot

General correction plan

1. Correction is always better to start with soft tissue techniques or foot and lower leg massage.

A. Correction of muscular-fascial structures of vertical stretching
to. gastrocnemius muscle
k. plantar aponeurosis and flexor digitorum brevis

IN. Correction of transverse stretch muscles
to. anterior tibial muscle
to. posterior tibial muscle
to. long peroneal muscle

WITH.Foot muscle correction
Correction of the flexor muscles of the fingers

3. Correction of the bone structures of the foot

A. Subtalar Joint Correction

IN.Correction of the talocalcaneonavicular and calcaneocuboid joints separately and the Chopard joint as a whole

WITH.Wedge-navicular-cube joint correction

D.Lisfranc Joint Correction:
correction of the articulation of the medial sphenoid bone and 1 metatarsal bone
k.s. intermediate cuneiform and 2 metatarsal bones
k.s. lateral cuneiform and 3rd metatarsal
k.s. cuboid and 4th metatarsal
k.s. cuboid and 5th metatarsal

E.Metatarsophalangeal Joint Correction
k. metatarsophalangeal joints
k. intermetatarsal joints
F.Correction of interphalangeal joints

Description of algorithm techniques

(for convenience, the description is given for the left foot, the technique for the right foot is the same, but the right hand changes from the left).

Correction of the interosseous membrane and tibial ligaments.

The position of the patient. Lying on your back. The feet are on the couch.
The position of the osteopath. Standing on the correction side.
Left hand. The thumb is on the head of the fibula, the remaining fingers cover the upper part of the lower leg.
Right hand. Thumb on the lateral malleolus, middle or index finger on the medial malleolus.
From. Fascial indirect technique. Initiation - bringing the bones together and moving the arms towards each other.

Ankle correction.

P.p.
By. Standing on the correction side.
L.r. Grabs both ankles.
Etc. Covers the foot. Thumb and index (middle) finger on the talus.
From.

Subtalar joint correction.

P.p. Lying on the stomach, the leg is bent at an angle of 90 degrees.
By. Standing on the correction side.
Etc. Covers the rear of the foot, fingers on the talus.
L.r. Covers the sole of the foot. Thumb and forefinger on the calcaneus.
From. Fascial indirect technique. The initiating movement is the convergence of the bones.

Correction of the talocalcaneal-navicular joint.

P.p.
By.
L.r. The thumb lies on the plantar side of the foot on the talocalcaneal joint near the joint space, the remaining fingers cover the talus and calcaneus from the back.
Etc. The thumb is fixed on the navicular bone from the plantar side, the index (middle) covers the foot from the medial side and is also fixed on the navicular bone but from the back side.
From. Fascial indirect technique. The main movement is between the thumbs.

Correction of the calcaneocuboid joint.

P.p. Lying on the stomach, the foot hangs freely.
By.
Etc. The thumb is on the heel bone from the plantar side, the remaining fingers cover the heel bone.
L.r. The thumb is on the cuboid bone from the plantar side, the index or middle finger covers the foot and is located on the cuboid bone from the back side.
From. The technique is the same. The main movement is carried out between the thumbs. Initiation - movement to bring articular surfaces closer together.

Chopard joint correction in general.

P.p. Lying on the stomach, the foot hangs freely.
By. Standing (sitting) facing the foot side of the couch.
L.r. Captures the calcaneus and talus.
Etc. Covers the scaphoid and cuboid bones.
From.

Correction of the sphenoid-navicular-cuboid joint.

P.p. Lying on the stomach, the foot hangs freely.
By. Standing (sitting) facing the foot side of the couch.
L.r. The thumb fixes the cuboid and navicular bones from the plantar side, the index (middle) from the back.
Etc. The thumb firmly fixes the three cuneiform bones from the plantar side, the index finger from the back.
From. Fascial indirect technique. The initiating movement is the convergence of the articular surfaces.

Correction of the articulation of the medial sphenoid bone and 1 metatarsal bone.

P.p. Lying on the stomach, the foot hangs freely.
By. Standing (sitting) facing the foot side of the couch.
l.r. The thumb and forefinger encircle the medial cuneiform bone.
etc. The thumb and forefinger cover the head of the 1st metacarpal bone.
From. Fascial indirect technique. The initiating movement is the convergence of the articular surfaces.

Correction of the articulation of the intermediate sphenoid and 2 metatarsal bones.

P.p. Lying on the stomach, the foot hangs freely.
By. Standing (sitting) facing the foot side of the couch.
l.r. The thumb and index finger encircle the median sphenoid bone.
etc. The thumb and index finger cover the head of the 2nd metatarsal bone.
From. Fascial indirect technique. The initiating movement is the convergence of the articular surfaces.

Correction of the articulation of the lateral sphenoid and 3 metatarsal bones.

P.p. Lying on the stomach, the foot hangs freely.
l.r. The thumb and index finger cover the lateral sphenoid bone.
etc. The thumb and index finger cover the head of the 3rd metatarsal bone.
By. Standing (sitting) facing the patient's feet.
From. Fascial indirect technique. The initiating movement is the convergence of the articular surfaces.

Correction of the articulation of the cuboid and 4 metatarsal bones.

P.p. Lying on the stomach, the foot hangs freely.
By. Standing (sitting) facing the patient's feet.
L.r. The thumb is on the cuboid bone from the plantar side, the index (middle) from the back.
Etc. Fingers cover the head of the 4th metatarsal bone.
From. Fascial indirect technique. The initiating movement is the convergence of the articular surfaces.

Correction of the articulation of the cuboid and 5 metatarsal.

P.p. Lying on the stomach, the foot hangs freely.
By. Standing (sitting) facing the corrected foot.
L.r. The thumb and forefinger encircle the cuboid bone.
Etc. The thumb and index (middle) fingers cover the head of the 5th metatarsal bone.
From. Fascial indirect technique. The initiating movement is the convergence of the articular surfaces.

Correction of the metatarsophalangeal joints.

P.p. Lying on the stomach, the foot hangs freely.
By. Standing (sitting) facing the patient's feet.
L.r. The fingers wrap around the metatarsal.
Etc. Thumb and index finger on the proximal phalanx of the corresponding finger.
From. Fascial indirect technique. The initiating movement is the convergence of the articular surfaces.

Intermetatarsal joints correction.

P.p. Lying on the stomach, the foot hangs freely.
By. Standing (sitting) facing the patient's feet. Thumbs and forefingers encircle the heads of adjacent metatarsal bones
From. Fascial indirect technique. The initiating movement is the convergence of the articular surfaces.

Correction of interphalangeal joints.

P.p. Lying on the stomach, the foot hangs freely.
By. Standing (sitting) facing the patient's feet.
L.r. The thumb and forefinger cover the proximal bone.
Etc. The thumb and index finger cover the distal bone.
From. Fascial indirect technique. The initiating movement is the convergence of the articular surfaces.

Correction of the calf muscle and Achilles tendon.

P.p.
By. Standing (sitting) facing the patient's feet.
L.r. Supports the back of the leg.
Etc. Presses on the plantar side of the foot, producing dorsiflexion of the foot.
From. PIR technique is used. On inspiration, the patient tries to bend the foot, the osteopath resists. The position is fixed for 4-7 seconds. On exhalation, the doctor increases the extension of the foot, stretching the muscle. The procedure is repeated 3 times.

Correction of the plantar aponeurosis and flexor digitorum brevis.

P.p. Lying on the stomach, the leg is bent at a right angle.
By. Facing the couch.
L.r. Fixes the ankle joint and heel.
Etc. Presses on the foot in the area of the distal heads of the metatarsal bones, bringing the fingers into dorsiflexion.
From. PIR technique. On inspiration, the patient tries to bend his fingers, the position is fixed for 4-7 seconds, on exhalation, the doctor increases the extension of the fingers, stretching the aponeurosis.

Tibialis posterior correction.

P.p. Lying on the stomach, the foot hangs freely from the couch.
By. Standing on the side of the opposite correction. In this case, on the right.
Etc. Fixes the back of the leg.
L.r. The thumb is tightly fixed on the navicular and medial sphenoid bones, the finger is directed towards the navicular bone. The remaining fingers cover the foot.
From. Combined technique. At the first stage, we bring the ends of the muscle together: the foot goes into flexion-adduction-supination. Further indirect technique 20-30 seconds until the state of release. Against the background of the release - pronation-abduction-extension. The right hand at the same time moves to the foot, helping the left. On inspiration, we fix the position for 4-7 seconds, on exhalation we increase pronation-abduction-extension.

Correction of the long peroneal muscle.

P.p. Lying on your back, feet hang freely.
By. Standing on the correction side.
Etc. The thumb fixes the medial sphenoid and 1 metacarpal bone from the plantar side. The remaining fingers cover the foot.
L.r. The thumb is fixed on the lateral ankle, the palm covers the upper part of the lower leg.
From. First stage. The foot is brought into flexion-pronation-abduction until movement is initiated. Indirect technique before release. Next, against the background of the release, we introduce the foot into a state of supination-adduction-extension and hold this state against the background of holding the breath on a deep breath for 4-7 seconds. On exhalation, we strengthen supination-adduction-extension. We repeat 3 times.

Correction of the flexor muscles of the fingers.

P.p. Lying on your stomach, leg bent at a 90 degree angle
By. Standing on the side of the couch
L.r. Lies on the heel, gently fixing it and the ankle joint
etc. Grabs the fingers, bringing them into a state of extension to the barrier
From. The patient tries to bend his fingers, the osteopath prevents this. The position is fixed for 4-7 seconds. During the relaxation period, we increase the extension to the next barrier. We repeat 3 times.

Correction of the extensor muscles of the fingers

P.p.
By.
L.r.
Etc. Grabs the fingers, bringing them into a state of flexion to the barrier.
From. The patient tries to straighten his fingers, the osteopath prevents this. The position is fixed for 4-7 seconds. During the relaxation period, we increase the flexion to the next barrier. We repeat 3 times.

Thumb flexor correction

P.p. Lying on the stomach, the leg is bent at the knee joint at 90 degrees.
By. Standing on the side of the couch on the correction side.
L.r. Supports the heel and ankle.
Etc. Grabs the thumb, bringing it into a state of extension to the barrier
From. The patient tries to bend the finger, the osteopath prevents this. The position is fixed for 4-7 seconds. During the relaxation period, we increase the extension to the next barrier. We repeat 3 times.

Thumb extensor correction

P.p. Lying on the stomach, the leg is bent at the knee joint at 90 degrees.
By. Standing on the side of the couch on the correction side.
L.r. Supports the heel and ankle.
Etc. Grabs the thumb, bringing it into a state of flexion to the barrier.
From. The patient tries to straighten the finger, the osteopath prevents this. The position is fixed for 4-7 seconds. During the relaxation period, we increase the flexion to the next barrier. We repeat 3 times.

Foot and leg massage

Foot and lower leg massage can be considered both as a preparatory procedure before a specific correction, and as an independent procedure with a pronounced effect. Massage allows you to restore muscle tone and elasticity of the ligaments, normal pressure in the sheaths of the neurovascular bundles. Before the correction, massage helps to relax the muscle structures. In addition, it should be remembered that the foot is a reflexogenic zone, and foot massage has a fairly powerful general health effect.

It is quite difficult to work out the feet with your fingers, so it is more convenient to use special wooden sticks.

Before the procedure, the patient should wash their feet, massage oil and cream are not necessary, but after the procedure, the feet and lower legs should be treated with cream.

When massaging the feet, the initial position of the patient is lying on his stomach with his feet hanging freely. The masseur sits at the foot end of the couch. The working finger or stick is located at right angles to the surface, pressing and pulling along the course of the ligaments and fascia is carried out. Ligaments seem to be stretched. The procedure is carried out quite slowly - 10-12 movements per minute and deep enough, but without pain.

The study is carried out in the following sequence: the calcaneal tuber and tissues around it (1), we descend along the plantar aponeurosis, the navicular bone (3), the sphenoid bones (4,5,6), the proximal (7) and distal (8) heads of the metatarsal bones , fingertips. Each point is processed 10-15 times.

Thus, the zone of the lateral and medial ankles is processed along the tendons of the muscles of the lower leg and the muscles of the lower leg themselves.

The peroneal muscles (1), as well as the anterior group of muscles of the lower leg (2), including the extensors and the anterior tibial muscle, are easily accessible for exposure. In order to work out the calf flexor group, it is necessary to move the fibers of the gastrocnemius muscle (3) and go deeper.

Massage movements are made with the pad of the thumb, directed vertically. Pressing and dragging is performed. Painful points are pressed through within 90 seconds.

Keller's diseases 1 and 2 refer to osteochondropathy - pathologies of bone and cartilage tissue that develop on the basis of local circulatory failure.

Causes

Pathological changes that are observed in the bones and articular cartilage in this disease are called aseptic necrosis. What can cause problems with microcirculation:

Frequent trauma.
Wearing uncomfortable and tight shoes.
Excessive load on the musculoskeletal system.
Endocrine disorders (diabetes mellitus, disorders of the thyroid gland, adrenal glands, etc.).
and other deformities of the foot.
genetic predisposition.

Regardless of the localization of the pathological process, this group of diseases is characterized by a chronic course and a fairly favorable prognosis with timely and proper treatment. Also quite typical is a slow onset and a long course without pronounced exacerbations.

Thanks to modern diagnostic methods, in most cases it is possible to detect disorders in bone and cartilage tissue at an early stage of their development.

Osteochondropathy of the scaphoid

Keller's disease 1 is called osteochondropathy of the navicular bone. The vast majority of patients are young children (3 to 12 years of age). Pathological changes can be observed immediately on both feet. According to clinical statistics, boys are much more likely to get sick than girls. The disease usually lasts for 8-15 months. Then the symptoms begin to slowly pass.

Clinical picture

Keller's disease 1 develops gradually. Usually, the first manifestations of osteochondropathy of the navicular bone is the appearance of pain on the dorsum of the foot. Features of the clinical picture:

Basically, increased pain is noted with walking and physical activity.
Complaints of increased leg fatigue.
Sometimes the pain occurs at night.
Probing the back of the foot can cause some pain.
Because of the expressed painful sensations, a characteristic lameness appears. The child tries to walk, leaning on the outer edge of the foot.
In the region of the back surface, some swelling may be determined, but without clinical symptoms of the inflammatory process.

Despite the duration of the course, cases of self-healing are quite often recorded.

Diagnostics

The main method for diagnosing Keller's disease 1 is a survey radiography of the feet, which allows you to identify the initial signs, a violation of the processes of ossification of the navicular bone and its deformation. In addition, adjacent joint spaces may be slightly dilated. But what to do when there is no bone pathology yet (pre-radiological stage)? In the early stages of the development of the disease, diagnostic methods with high resolution will help to identify the pathological process:

CT scan.
Densitometry (determination of bone density).

The arsenal of diagnostic methods makes it possible to detect even the most insignificant changes in the structure of the bones and joints of the foot. With osteochondropathy of the navicular bone of the foot, it is also necessary to do clinical blood tests to exclude the presence of inflammation.

In adults, Keller's disease 1 does not occur.

Treatment

The main goal of the treatment of all forms of osteochondropathy, including Keller's disease 1, is to ensure the restoration of the normal development of bone that has undergone pathological disorders. It is necessary to ensure that at the end of the formation of the skeleton, the bone has the optimal size and shape. If you completely go through the entire therapeutic course prescribed by the attending physician, then getting a complete cure is quite realistic.

As soon as a child is diagnosed with Keller's disease 1, physical activity on the affected limb is immediately completely excluded. The foot should be immobilized (immobilized) by applying a plaster boot or splint for a period of 30–45 days. After the termination of immobilization, it is recommended to limit the physical load on the foot and wear. In addition, various types of physiotherapy are actively used, including:

Electrophoresis with vasodilator drugs.
ultrasound therapy.
Electrotreatment.
Balneotherapy.
Mud applications.

The course of treatment and recovery is prescribed by a specialist doctor (usually an orthopedist), taking into account the stage of the disease and the condition of the child.

Osteochondropathy of the metatarsal head

Keller's disease 2 is an osteochondropathy of the heads of the metatarsal bones. The main category of patients are children, adolescents and young men aged 10 to 21 years. As statistics show, boys are more often affected than their peers. The duration of the disease is 1-3 years and depends on the timeliness and effectiveness of therapy.

Metatarsals II and III are most commonly affected.

Clinical picture

The main complaints of patients are intense. There is a significant increase in pain during exercise, walking barefoot or in shoes with soft soles. What other clinical symptoms will be characteristic:

The pain syndrome is chronic with a tendency to decrease in intensity.
Night pain is not uncommon.
Sometimes there is some swelling of the rear of the foot, without signs of an inflammatory process.
It is impossible not to notice that the heads of the metatarsal bones are clearly enlarged and deformed.
Children try to walk on their heels. This helps them take the load off the forefoot.
The fingers are shortened.
Injury or injury to the foot can exacerbate the disease.
Development at a late stage of the disease leads to the resumption of pain.

Diagnostics

Pathological changes in the head of the metatarsal bone can be detected using the X-ray method of examination. What structural disorders will be characteristic for Keller's disease 2:

1 stage. Only a slight compaction of the head of the metatarsal bone is determined.
2 stage. There are changes in its articular surfaces. Increases bone density. The joint space will gradually expand.
3 stage. Metatarsal head shattered into small fragments. Resorption of necrotic (dead) areas of bone tissue is observed. The joint space is expanded.
4 stage. There is a restoration of the structure of the affected bone. However, the head still remains deformed. In shape, it may resemble a saucer. The bone itself is somewhat shortened. In addition, narrowing of the joint space is revealed.
5 stage. At this stage, the metatarsal head cannot fully recover. Characteristic symptoms appear.

Nevertheless, in the early stages of the disease, X-ray diagnostics is ineffective and one has to resort to additional research methods. What types of diagnostics can be prescribed to clarify the nature of the lesion in the small bones and joints of the foot:

CT scan.
Magnetic resonance imaging.
Scintigraphy.

Treatment

In most cases, conservative treatment methods are used. At the stage of exacerbation, when the pain syndrome is expressed and there is swelling of the foot, a plaster splint is used. Foot immobilization (immobilization) continues for 3-4 weeks. At the same time, various physiotherapeutic procedures are actively involved:

Electrophoresis.
Ultrasound.
Diathermy.
Mud compresses.
Laser therapy.
Warm compresses.
Radon and hydrogen sulfide baths.

After the elimination of swelling and pain, they switch to the use of special orthopedic shoes, the wearing of which allows you to unload the forefoot. In parallel, physiotherapy exercises and massage sessions are prescribed.

If severe deformities and pronounced signs of osteoarthritis are observed in Keller's disease 2, then the issue of surgical treatment is considered. For children and adolescents, they try to carry out conservative therapy as long as possible. Radical resections in childhood are contraindicated. Surgical intervention is tried to be used only in extreme cases, when all other methods of treatment have been ineffective.

Prevention of osteochondropathy

Prevention plays an important role in preventing the development of osteochondropathy. First of all, it is necessary to exclude possible causes and risk factors. Of decisive importance is weight control, avoidance of injuries and injuries, treatment of secondary osteoarticular pathology, correction of endocrine disorders. What other recommendations for the prevention of Keller's diseases 1 and 2 can doctors give:

Adhere to the optimal motor mode.
Regular exercise, especially in childhood, contributes to the proper formation of the musculoskeletal system.
Balanced diet.
Identification of risk groups (for example,).

Do not ignore preventive medical examinations that will help determine the pathology at an early stage of its development. In addition, it is necessary to contact a specialist doctor immediately after the first clinical symptoms of the disease appear.