Lipoid degeneration of bone marrow. Osteochondrosis is the result of fatty degeneration

Fatty degeneration bone marrow is a natural age-related process, which is characterized by the replacement of hematopoietic tissue with adipose tissue. Bone marrow degeneration can be caused by both pathological and physiological reasons. Treatment methods depend on the causative disease and the patient's health status. Symptoms are nonspecific, and sometimes the disorder is asymptomatic. The prognosis depends on the degree of fatty tissue degeneration, the patient’s age and concomitant diseases.

Age-related degeneration of yellow bone marrow increases the likelihood of developing spinal osteochondrosis

Bone marrow is a spongy red substance that is located in the inside of the bones. It plays an important role in the formation of bone tissue. It contains multipotent stem cells. They form white blood, red blood cells and platelets.

Yellow bone marrow is composed primarily of fat cells (hence the color), which increase in content as each person ages. Red bone marrow is the site of formation of cellular components of blood. In a child, bone marrow fills all the bones. Over time, red bone marrow turns yellow. In adults, red is found only in flat bones: sternum, vertebral bodies, ribs, cranial bones, pelvic bones. In case of anemia, yellow bone marrow can be replaced with red bone marrow.

The prevalence of early fatty degeneration caused by hypoplastic or aplastic anemia is low in the United States and Europe: 2–6 cases per million people. Much more often, fatty degeneration of the bone marrow occurs as a result of acute myelogenous leukemia and multiple myeloma: 27-35 cases per 1,000,000 people. The incidence of myelodysplasia has increased from 143 cases reported in 1973 to 15,000 cases annually in the United States.

In Japan and Far East the incidence of fatty bone marrow degeneration is at least 3 times higher than in the United States and Europe. Mexico and Latin America also have high performance morbidity, which are explained by the liberal use of chloramphenicol. Factors environment and widespread use of insecticides have been seen as causes of this disease. The incidence of myelodysplasia is estimated to be approximately 4-5 cases per 100,000 people per year in Germany and Sweden.

In the International Classification of Diseases, 10th revision (ICD-10), fatty degeneration in the bone marrow is designated by code M42.

Symptoms

Age-related degeneration of yellow bone marrow increases the likelihood of developing osteochondrosis (dystrophy) of the vertebral bodies (in the spinal region). In most cases, the pathological process is asymptomatic or manifests minor symptoms. Symptoms depend on the rate of lipoid bone marrow degeneration and the underlying disease.

Causes

Deficiency of folic acid in the body leads to fatty degeneration of the bone marrow

Degenerative bone marrow diseases can be inherited or acquired during life.

Main reasons:

• Decreased concentration or damage to hematopoietic stem cells, leading to hypoplastic or aplastic anemia.
• Deficiency of folic acid or vitamin B12.
• Myelodysplasia.

Damage to hematopoietic stem cells can be caused by congenital or acquired disorders. The main mechanisms of stem cell destruction:

• Acquired stem cell damage is caused by viruses, toxins, or chemicals(chloramphenicol, insecticides), which leads to a quantitative or qualitative change cellular composition.
• Abnormal humoral or cellular control of hematopoiesis.
• Antibody, T cell, or lymphokine-mediated suppression of hematopoiesis.
• Mutations in genes that accelerate fatty degeneration of the bone marrow. The identification of these mutations has led to progress in determining the precise functions of the corresponding proteins in normal cells
• Hereditary syndromes.

Hereditary syndromes that accelerate bone marrow degeneration:

• Fanconi anemia.
• Congenital dyskeratosis.
• Shwachman-Diamond syndrome.
• Diamond-Blackfan anemia.
• Amegakaryocytic thrombocytopenia.
• Congenital neutropenia.

Constitutional aplastic anemia is associated with chronic failure bone marrow, congenital anomalies, familial morbidity, or thrombocytopenia at birth.

Red bone marrow aplasia may be a consequence of thymoma. Sometimes it occurs as a result viral infection. Bone marrow aplasia can also be permanent, e.g. as a result of viral hepatitis. In rare cases, aplasia is caused malignant neoplasms lymphoid tissue or collagen vascular diseases(for example, systemic lupus erythematosus).

Decreased concentrations of all 3 types of blood cells are the most common manifestation of a bone marrow disorder. Aplastic or hypoplastic anemia can develop due to secondary causes. Myelodysplastic may also reduce all types of blood cells.

Dangerous complications

Severe bone marrow degeneration requires rapid initiation of therapy - early search for donors for bone marrow transplantation

The morbidity and mortality from fatty bone marrow degeneration is caused by low levels of mature blood cells. Severe anemia can cause heart failure and fatigue. Neutropenia can predispose people to bacterial and fungal infections. A decrease in platelet count can increase the risk of severe bleeding.

The severity and extent of fatty degeneration determine the prognosis. Severe multiple bone marrow degeneration is an emergency medical situation, requiring a quick start of therapy - an early search for donors for bone marrow transplantation.

Long-term transfusion of donor red cells increases the overall burden on the patient. Increased levels iron are toxic to various organs, including for the heart. High dosages can cause arrhythmia, diabetes and cirrhosis of the liver. Iron may also produce a bronze coloration in people with soft skin. Therefore, it is necessary to measure the patient's reserves of the element (in the form of ferritin).

Administration of a chelating agent is an effective method for removing excess iron. Chelating agents are made up of molecules that bind tightly to free iron and remove it.

Monitoring serum ferritin levels and measuring total urinary excretion may determine the effectiveness of therapy. Most bone marrow tissue damage can be reversed with timely treatment.

Diagnostics

First, a physical examination is performed and a medical history is taken. Then the doctor prescribes blood tests that show the qualitative and quantitative composition of the blood. Red blood cells are morphologically normal in tests. The reticulocyte count is usually less than 1%, indicating a lack of red blood cell production. Sometimes the average cell volume increases.

The platelet count is lower than usual, and sometimes there is a severe decrease in platelet count. The platelet size is normal, but low level may lead to bleeding.

There is a decrease in all granular leukocytes, including neutrophils, eosinophils and basophils, as well as a decrease in monocytes. Sometimes relative lymphocytosis occurs. Folic acid, vitamin B12 and serum erythropoietin levels are usually elevated in fatty bone marrow degeneration.

Fanconi anemia should be considered in all young adults and children with hypoplastic or aplastic anemia, unexplained macrocytosis, myelodysplastic syndrome, acute myeloid leukemia, or cutaneous malignancies.

Bone marrow tests help confirm the diagnosis. Pure red cell aplasia characteristically affects red blood cell progenitor cells; amegakaryocytic thrombocytopenia is confirmed by the absence of megakaryocytes. Detection of bone marrow hypoplasia distinguishes aplastic anemia from aleukemic leukemia.

Classification

To assess changes in the bone marrow of the vertebral bodies using magnetic resonance imaging, the Modic classification is used:

• Type I: areas of low magnetic resonance signal intensity on T1-weighted images and high-intensity areas on T2-weighted images. Patients experience bone marrow changes due to inflammation and swelling.
• Type II: high signal intensity on T1- and T2-weighted images due to fatty degeneration of the bone marrow.
• Type III: low intensity signal on T1- and T2-weighted images. Sclerotic changes are visible in the spongy substance of the vertebral bodies.

Treatment

The choice of treatment method (conservative or surgical) depends on many factors - technical capabilities, age and health status of the patient, prognosis for the success of a particular method of therapy

Infections leading to neutropenia should be treated as an emergency medical conditions. After taking blood and other biological materials antibiotics are prescribed wide range actions. The choice of antibiotic may be changed later, depending on the results of the microbiological analysis.

Sepsis, pneumonia, infections urinary tract and cellulite are common complications of neutropenia.

Patients with severe aplastic anemia who receive antithymocyte or antilymphocyte globulin have a 1-year survival rate of 55%. Androgen supplementation increases treatment response rates to 70%, with a 1-year survival rate of 76%. Although their mechanism of action is unknown, antithymocyte or antilymphocyte globulin should be given with corticosteroids to prevent serum sickness.

Forecast

The prognosis of bone marrow degeneration depends on the underlying disease. Majority hereditary syndromes diseases, such as Fanconi anemia, can develop into leukemia after a few years. Acquired idiopathic aplastic anemia is usually a permanent and life-threatening blood disorder. Half of patients die within the first 6 months.

If fatty degeneration of the bone marrow is caused by harmless causes - aging - the prognosis is favorable and life expectancy does not decrease.

Bone marrow accounts for approximately 5% of the total body weight and plays an active role in hematopoiesis (blood formation). Bone marrow consists mainly of stem cells (all types of cellular elements of the blood), surrounding supporting cells - macrophages, adipocytes and large number others involved in nutrition, proliferation (growth) and differentiation of stem cells. Red bone marrow contains about 40% fat, yellow bone marrow contains up to 80%. This feature helps in identifying various pathologies associated with changes in this ratio using MRI of the spine.

T1-weighted MRI is most sensitive to adipose tissue. They are the basis of the MRI protocol. In addition, T2-weighted MRI with fat suppression is used. Below we will focus on the main pathologies that appear on MRI of the spine, such as bone marrow pathology in the first place.

• Hemangioma, single or multiple, accounts for 10-12% of changes in the vertebrae. It refers to vascular anomalies and has characteristic features on MRI of the spine - round or trabecular, light on T1-weighted and T2-weighted MRI, does not change MRI with signal suppression techniques from fat.
• Local fat deposits appear with age and are a variant of the norm. Fatty deposits are also observed in osteochondrosis along the endplates (fatty degeneration, or Modic type 2). They are bright on T1-weighted MRIs of the spine and become dark on fat-suppressed MRIs. Sometimes there are mixed variants of bone marrow changes in osteochondrosis, which are not completely suppressed when using the STIR MRI sequence.
• Paget's disease refers to metabolic disorders and is observed in 1-3% of people over 40 years of age. Damage to the vertebrae ranks second after the pelvic bones. In diagnosing Paget's disease, identifying lytic foci in the bones of the skull is very helpful. Paget's disease goes through 3 stages - lytic, mixed and blastic. In accordance with these stages, MRI of the spine shows a different picture. In the lytic stage, the lesion signal is bright on T2-weighted MRI and low on T1-weighted MRI, then becomes hypointense on both types of MRI as sclerosis and fibrosis increase. MRI of the spine also reveals other character traits Paget's disease - thickening of the cortical plates of the vertebral bodies, fatty degeneration at a late stage and during successful treatment.

MRI of the spine. T1-weighted sagittal MRI of the lumbosacral region. Replacement of sacral bone marrow with fat in Paget's disease.

• Lipoma refers to benign tumors from adipose tissue. They make up about 1% of all primary bone tumors and no more than 4% of them are localized in the vertebrae. On MRI of the spine, lipomas are difficult to distinguish from fat deposits, however, they are more clearly defined and may undergo internal necrosis and calcification
• hemorrhages in the vertebrae occur with injuries. MRI of the spine reveals characteristic blood dynamics depending on the duration of the hemorrhage.
• Consequence radiation therapy boil down to replacing red bone marrow with yellow. When the absorbed dose exceeds 36 Gy, this process becomes irreversible. MRI of the spine shows diffuse increase signal on T1-weighted MRI with a clear boundary corresponding to the irradiation field. After radiation therapy and chemotherapy, myelofibrosis - bone marrow replacement - can also develop fibrous tissue. In MRI of the spine, the signal is very low on both T1-weighted and T2-weighted MRIs.

MRI of the spine. T1-weighted sagittal MRI thoracic. Fatty bone marrow degeneration after radiation therapy.

• Osteoporosis leads to a decrease in the cellular composition of the bone marrow and an increase in fat. MRI of the spine often shows diffuse increased signal from the vertebral bodies on T1-weighted MRI. There are also focal changes that require MRI of the spine differential diagnosis with hemangiomas. MRI diagnostics for osteoporosis is also presented in a separate article.
• Spondyloarthropathy on MRI of the spine often manifests as “glowing” angles on T2-weighted MRI. This is especially true for acute stage ankylosing spondylitis. Change acute phase to chronic leads to transformation inflammatory reaction in a depot of adipose tissue, clear on T1-weighted MRI. MRI of the spine for various diseases belonging to the group of spondyloarthropathies is discussed in a special article on our other website.
• Anorexia is accompanied various changes in the body, including osteoporosis and decreased signal intensity on T1-weighted MRI, as well as bone marrow edema, which is referred to as “gelatinous transformation.” On T2-weighted MRI (especially fat-suppressed MRI), there is a slight diffuse increase in signal from the vertebrae. MRI of the spine with contrast shows amorphous signal enhancement.

MRI of the spine. T2-weighted sagittal MRI. Gelatinous transformation due to malnutrition.

• Hemosiderosis is a phenomenon observed in hemolytic anemia. MRI of the spine shows low signal in the bone marrow. In differential diagnosis, it is important that the liver and spleen acquire the same low signal.
• Gaucher disease is an autosomal recessive disorder hereditary disease classified as sphingolipidosis and manifested by the accumulation of glucocerebrosides in histiocytes. The diagnosis is made based on puncture of the spleen and detection of specific cells. On MRI of the spine, red bone marrow is replaced by Gaucher cells, which are hypointense on T1- and T2-weighted MRI. In addition, bone infarcts are often observed on MRI of the spine.

MRI of the spine. T1-weighted MRI of the thoracic spine. Gaucher's disease.

• Myeloproliferative and myelodysplastic syndromes, which include chronic myeloid leukemia and other chronic leukemias, polycythemia, mastocytosis, essential thrombocytopenia on MRI of the spine manifest as a uniformly reduced signal on T1-weighted MRI. T2-weighted MRIs of the spine often show “reverse” brightness intervertebral discs, they become lighter than the vertebral bodies. MRI of the brain for tumors of the hematopoietic system can also reveal its damage.

MRI of the spine. T2-weighted sagittal MRI cervical region spine. Chronic myeloid leukemia.

• Sarcoidosis affects the bone marrow in 1-3% of cases. Damage to the brain and spinal cord is much more common in sarcoidosis. MRI of the spine reveals sclerotic foci that closely resemble metastases, often multiple. The lesions can be mixed lytic with sclerotic rims. MRI of the spine with contrast may show increased signal from lesions.
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My son is 18 years old, he has had problems with his spine since he was 14, now in the lumbar region. 3 hernias and 2 in the thoracic, everything else is protrusion, recently an MRI showed that in the lumbar region. Fatty infiltration of the bone marrow, what is it and is it dangerous or not?

Tatyana, Moscow

ANSWERED: 03/19/2017

Hello, Tatyana. Fatty infiltration of the bone marrow is evidence of metabolic disorders and bone tissue formation. It is necessary to check the function of the liver, kidneys, and intestines. Make an appointment.

ANSWERED: 03/19/2017 Valeeva Elvira Raisovna Moscow 0.0 doctor oncologist gynecologist

Hello, Bone marrow is a collection of stem cells. These cells, transforming, become leukocytes - protecting the body from infections, platelets - ensuring blood clotting, and red blood cells - providing the body with oxygen. All three types of blood cells make up the bone marrow, which controls life processes living organism. In particular, he plays vital role, both in the formation and maintenance of the immune system. Due to some reasons, internal or external, the process of hematopoiesis, healthy functions bone marrow may be impaired. In particular, due to degenerative, dystrophic processes, its natural healthy tissue is gradually, little by little, replaced by connective or adipose tissue. Moreover, it is the latter, fat replacement that occurs most often. Fatty degeneration of the bone marrow occurs - a change, replacement of healthy tissue, deterioration of its condition caused by big amount fat in her cells. Why is fatty degeneration dangerous? Degenerative changes occurring in the bone marrow negatively affect the process of hematopoiesis, worsen the composition of the blood, negatively affect the blood circulation process, and affect the health of blood vessels. When the functions of this organ are impaired, the number of leukocytes, platelets, and red blood cells decreases. All these negative changes affect general health person. The nutrition of organs and tissues is disrupted, the composition of the blood changes, and it moves worse through the vessels. The functions of the entire body are impaired, its resistance to various diseases. Now, to confirm or exclude this diagnosis, a consultation with a hematologist is needed, taking into account the presence of hernias, protrusion, consultation with a neurologist and neurosurgeon to develop management and treatment tactics

Related questions:

Doctors say that the condition of the entire body largely depends on the health of the spine. But a person often does not take care of his musculoskeletal system, subjecting it to heavy loads, leading an inactive lifestyle, long time sitting at the computer. As a result of this, degenerative-dystrophic changes occur in the spine, subsequently causing osteochondrosis.

Fatty degeneration of the bone marrow of the vertebral bodies is a change in tissue, accompanied by the accumulation of a lot of fat in the cells. At the same time, the protoplasm of the cell can be converted into it due to the fact that fat grains get inside it. Such disturbances cause the death of the cell nucleus, and subsequently it dies.

In most cases, fatty degeneration occurs in the liver and blood vessels, but can also occur in other parts of the body. When fat replaces the cartilage of the intervertebral discs, they lose their ability to provide flexibility and springiness to the spine.

Even human bones can be replaced by fat. As a result, the vertebrae become less strong, which adversely affects the health of the spine as a whole. The vertebrae acquire excessive mobility, that is, they become unstable. These pathological abnormalities are clearly visible to doctors when performing magnetic resonance imaging.

Based on the nature of pathological changes, forms of degeneration can be different. If the spine is affected by this pathology, then there is a high probability of developing osteochondrosis.

Classification of degenerative-dystrophic changes in the spine

The course of pathology is divided by specialists into several stages, each of which is characterized in its own way. Thus, the following stages of dystrophy in the vertebrae are distinguished:

1. First stage. It shows no changes in the intervertebral disc yet, but upon examination one can already see that there are small tears inside the layers of the fibrous ring.
2. Second stage. At this stage, the outer layers of the annulus fibrosus are still preserved and can prevent the disc from bulging. But the patient already feels pain in the back area, which can radiate to the leg and knee.
3. Third stage. Extensive ruptures of the fibrous ring occur on it, resulting in protrusion intervertebral disc. Painful sensations V lumbar region become even stronger.

Reasons for the development of the disease

The main cause of fatty degeneration is poor nutrition of the vertebral cells. They are the ones who are most sensitive to the fact that a small amount of oxygen and glucose is supplied and changes occur acid-base balance in blood. All this provokes the development of disc disorders.

Deterioration in performance circulatory system may occur due to various reasons, for example, due to anemia, spinal overload and poor nutrition. Deviations can also develop due to age.

Changes can even occur as a result of poisoning with a substance, such as alcohol. Certain infectious pathologies can also cause fatty degeneration.

Treatment methods for fatty degeneration of the bone marrow of the vertebral bodies

Fatty degeneration of the vertebrae is treated with both conservative and surgical method. If the pathology appears due to the aging of the body, then the process cannot be cured, since it is irreversible.

Whenever unpleasant symptoms, processes of inflammation and compression of nerves, experts prescribe the following medications:

• non-steroidal anti-inflammatory drugs aimed at relieving inflammation and relieving pain;
• muscle relaxants to eliminate spasms of muscle tissue;
• blockades with novocaine in the form of injections;
• chondroprotectors that help restore damaged cartilage.

Except medicines patients are prescribed physiotherapeutic procedures, for example, magnetic therapy and electrophoresis. Also great help physiotherapy, but it can only be used during remission. Good methods of treatment are massage and acupuncture.

Surgery is performed only if there is a narrowing of the spinal canal. In this case, without the help of a doctor, the patient risks losing sensitivity and acquiring paralysis.

In this case, it is possible to restore bone tissue only in the first stages of the disease, but basically therapy can only stop the development of the pathological process.

Arachnodactyly or Marfan syndrome is genetic disease autosomal dominant type, affecting connective tissue. Characterized by long arms and legs, very thin and skinny fingers, as well as a thin physique.

Such people have cardiovascular defects, often manifesting themselves in the form of pathologies of the heart valves and aorta. The disease got its name from the name of the French pediatrician Marfan, who was the first to describe a 5-year-old patient with long thin legs and fingers.

This genetic disease occurs as a result of dysfunction of connective tissue and is associated with significant polymorphism of symptoms. This may be an aortic aneurysm, myopia, gigantism, chest deformation, ectopia of the lens, kyphoscoliosis, ectasia of the solid meninges and other deviations.

Arachnodactyly does not depend on the gender of the patient. Among children, the percentage is 6.8%, with the majority of them being boys. The prevalence of the disease is 1:10,000 people.

Causes of mutation

Marfan syndrome is an anomaly from birth that is inherited in an autosomal dominant manner. The reason for this is a mutation in the FBN1 gene, which is responsible for the synthesis of the structural protein of the intercellular matrix - fibrillin. It is this that affects the elasticity and contractile properties of connective tissue. Lack of fibrillin and its pathology contribute to disruption of the formation of the fibrous structure, loss of connective tissue strength and the inability to tolerate physical activity.

In 3/4 of all cases, the cause of Marfan syndrome is hereditary, and in the rest it is a primary mutation. If a father over 35 years of age has a history of cases of this anomaly, the likelihood that the child will also suffer from the disease is very high.

The main symptoms that accompany Marfan syndrome

There are two forms of manifestation of arachnodactyly syndrome, which depend on the degree and number of affected systems and organs:

1. erased, weakly expressed in 1-2 systems;
2. expressed with weakly expressed changes in 3 systems, in one system or in 2-3 systems or more.

The severity is divided into mild, moderate and severe. According to the characteristic features of the course of the disease, stable and progressive Marfan syndrome are distinguished.

Signs of the disease are divided depending on the location of the manifestation of connective tissue dysplasia. The main symptoms of the disease include:

Changes in the musculoskeletal system

Most of the symptoms of the disease are associated with disorders of the skeletal system. The patient's height is usually above average. Characterized by an asthenic body type, a narrow skull with bird-like facial features, a too narrow and deformed chest, flat feet, bone arachnodactyly, spinal deformity, hypermobility of tendons and joints.

In addition to limb disproportions and high growth, other malfunctions in the functioning of the skeletal system occur. Most often this is scoliosis, a deformed funnel chest, very flexible joints, malocclusion And high sky, deformation of the toes. Muscle, joint and bone pain may be present. Speech disturbances may also sometimes occur, and osteoarthritis at an early age is possible.

Visual impairment

The disease can also affect vision. Very often, patients are diagnosed with myopia and astigmatism, less often - farsightedness. The following disorders are also possible: myopia, blue sclera, aniridia, ectopia and subluxation of the lens, hypermetropia high degree, coloboma, aphakia.

In 80% of cases, there is a violation of the position of the lens, in one or both eyes. Vision problems can occur after weakening of the connective tissue caused by a retinal detachment. Another ophthalmological problem associated with arachnodactyly is glaucoma, which occurs at a fairly early age.

Disturbance of the central nervous system

One of the serious consequences of Marfan syndrome is dural ectasia, which is characterized by stretching and weakening of the dura mater (membrane). Pain in the back, lower back, legs, pelvis and abdomen, headache may not appear or immediately disappear as soon as the person lies down on a flat and level surface on his back. In this regard, X-rays of the lower back and magnetic resonance imaging are prescribed.

Neurological problems with arachnodactyly include degenerative disease intervertebral bones and discs of the back and the development of pathology of the autonomic nervous system.

Disorders in the cardiovascular system

The following systems and organs malfunction:

• heart and great vessels;
• violation of intraventricular conduction;
• moderate hypertrophy of the left ventricular myocardium;
• aortic aneurysm;
• aortic insufficiency;
• prolapse mitral valve;
• hypoplastic expansion pulmonary artery and the root of the aorta, the “hanging” heart;
• bicuspid or dilated aortic root;
• failure of intracardiac dynamics;
• mitral insufficiency (myxomatous degeneration of the leaflets, an increase in their area and expansion of the fibrous ring, increased prolapse and looseness of the leaflets).

General clinical picture

IN general outline signs of the disease look like this: patients have muscle weakness, decreased activity during physical activity. The patient has low body weight, muscle hypotonia, hypoplasia of muscles and adipose tissue, small lung size, long intestines, and aneurysms of the sinuses of Valsalva.

The patient may also have a pituitary disorder: high growth, diabetes insipidus, acromegaloid disorders, long limbs and feet, disorder autonomic system, acromegaloid disorders.

Methods for diagnosing the disease used by modern medicine

Diagnosis of Marfan syndrome is made on the basis of hereditary factors, severe symptoms, examination of the patient, X-ray results, ophthalmological and genetic examinations, as well as echocardiography, electrocardiogram and laboratory tests.

During diagnosis, phenotypic tests are performed to determine the ratio of the hand and height, the length of the middle finger, the Varga index, test thumb for arachnodactyly and wrist coverage.

Using ECG and ECHO, cardiac arrhythmias, myocardial hypertrophy, mitral valve prolapse, chord rupture and left ventricular enlargement are determined.

Using radiography, you can see the expanded arches of the root and aorta, and the large size of the heart. X-ray hip joints will show protrusion of the acetabulum.

MRI of the spine allows you to determine ectasia of the dura mater, dilatation and aortic aneurysms will show CT and MRI of the heart and blood vessels.

Using biomicroscopy and ophthalmoscopy, ectopia of the lens can be detected. Gene identification will indicate mutations in the FBN1 gene.

Treatment of arachnodactyly in all its manifestations

To date, there is no cure for Marfan syndrome as such. But for recent years The life expectancy of patients with Marfan syndrome has become significantly longer. Treatment methods are determined as the disease progresses, and ways to prevent its occurrence are especially important. Therefore, the main course of treatment is aimed at preventive measures on the development of the disease and subsequent complications of the heart and blood vessels. This also applies to young children - all actions should be aimed at slowing down the development of aortic aneurysm.

The course of treatment of the disease includes conservative and surgical techniques corrections cardiovascular disorders, damage to the organs of vision and skeleton. If the aorta is no more than 4 cm in diameter, the patient is prescribed calcium antagonists, ACE inhibitors or β-blockers.

Surgical intervention must be performed if the aorta diameter is is more than 5 cm, there is mitral valve prolapse, heart valve insufficiency and aortic dissection. In some cases, mitral valve replacement is performed.

In case of vision problems, patients are prescribed its correction by selecting glasses and contact lenses. In especially severe cases, vision correction is performed by laser or surgical intervention.

IN childhood in case of skeletal disorders, surgical stabilization of the spine, hip replacement and thoracoplasty are performed.

The course of treatment also includes taking vitamins, metabolic and pathogenetic therapy with normalization of collagen. An important component is the work of a physiotherapist, who in the treatment of Marfan syndrome includes electric shock (TENS therapy), as well as ultrasound and other methods to improve the functioning of the skeleton, affecting the height and length of the arms, and life expectancy.

Video: The dangers of excessive joint flexibility

Damage to the meniscus of the knee joint: symptoms (signs and photos), treatment, causes

To learn more…

Damage to the meniscus in the knee joint is a very common disease. Athletes and people doing physical work are susceptible to this disease.

A meniscal injury is a tear cartilage tissue. Knee injuries are divided into several types. One of the groups is degenerative changes. The likelihood of a lateral meniscus injury increases if there is an old injury to the meniscus, for example, senile arthrosis or hereditary diseases were not cured.

Arthrosis can last for more than one year. Sometimes the pathology enters a chronic phase, so its symptoms appear in old age.

Unfortunately, even a careless step can cause injury to the anterior meniscus. Treatment for such damage takes quite a long time. For these reasons, senile arthrosis is very dangerous for healthy joints and ligaments of the knee.

Therefore, you need to be regularly examined by a doctor and, if necessary, do everything necessary procedures. After all, arthrosis destroys the joint, causing the knee function to be impaired and the leg to become less mobile.

In cases where treatment of arthrosis was untimely or incorrect, people become disabled. The knee joint is a complex structure, so treat the damage medial meniscus quite difficult.

The knee is the largest joint that, despite being susceptible to numerous injuries, can recover.

As a rule, treatment of knee injuries is conservative and comprehensive. Surgical intervention is necessary if traditional medicine, physiotherapy and other methods of therapy are ineffective.

Structure, functioning of the knee joint and location of the anterior meniscus

The knee joint is located between the tibia and femur. There is a cup located in the front of the knee. This joint is made up of menisci, cartilage and cruciate ligaments.

The knee contains anterior and posterior ligaments that perform the following functions:

• resistance to movement of the ankle forward or backward beyond the established limits;
• stabilization of the entire joint;
• holding the bony protrusion.

The surface of the knee is covered with cartilage tissue, and between the bones there are menisci, which are also called crescent cartilages.

There are two types of menisci: external (lateral) and internal (medial). Menisci are layers of cartilage located in the middle of the knee. Their main tasks are shock absorption and stabilization of the joint.

Damage to the internal meniscus of the knee significantly complicates motor function. Until recently, it was believed that the lateral, as well as the medial, meniscus had no specific purpose. It was believed that the meniscus was just a remnant of muscle.

But the results of various studies have shown that these processes have more than one function. It turned out that the menisci are involved in the correct distribution of the load on the joint, which protect it from the development of arthritis and arthrosis. Also, the crescent cartilages reduce the force of the push on the knee joint, stabilizing it.

Moreover, the presence of a right and left knee meniscus reduces contact stress. They limit the range of motion, which helps prevent the occurrence of dislocation.

In addition, the purpose of the meniscus is to send a signal to the brain indicating the condition of the joint.

How often does a meniscus injury occur?

A torn meniscus usually occurs in professional athletes. But everyday physical exercise may also cause damage.

Men are at risk. After all, they are the ones who perform all the physical work, so their body undergoes changes this kind. Also, the likelihood of pathologies occurring in knee joint increases in older people and men aged 18 to 30 years.

In people who have crossed the forty-year mark, damage to the internal meniscus occurs due to factors such as developing pathology joint, which has become chronic. Thus, every degenerative change that occurs in the knee joint is accompanied by consequences.

After all, even flick or a push can provoke a tear of the lateral meniscus.

So which falciform cartilages are damaged more often: external or internal? Statistics say that most of patients are diagnosed with damage to the lateral meniscus.

This is explained by the fact that internal meniscus anatomically, it is more susceptible to injury. But there are cases when degenerative changes spread throughout the entire joint, in which, in addition to the diseased meniscus, the ligamentous apparatus is damaged.

Symptoms of ruptured falciform cartilages are severe. As a rule, they are manifested by frequent pain, the frequency and severity of which is related to the severity of the damage.

Symptoms of anterior and posterior meniscus damage

Injuries to cartilage tissue often occur if a person twists on his leg. Often the rupture occurs while running when the limb hits a protruding surface. In this case, a fall occurs, as a result of which the knee is injured, and pain occurs in the area of ​​\u200b\u200bthe bruise.

Signs of meniscal damage depend on where the tear occurs. Thus, in the case of more extensive damage to the meniscus, a hematoma occurs. If the injury to the lateral meniscus is minor, then movement becomes difficult, and a characteristic crunching sound is heard while walking.

The symptoms of a lateral meniscus tear in the knee are different from the obvious features of a medial meniscus injury. If the gap is external, then the person experiences severe pain, due to tension in the collateral ligament. Moreover, she gives to anterior section joints and has a shooting character.

When turning the shin, sharp pain occurs. And in the outer part of the thigh there is a feeling of weakness. It is these symptoms that worry a person if there is a tear of the external meniscus.

Note! Symptoms of the disease appear as early as initial stage its development, so that timely treatment can begin.

Internal meniscus injuries have the following symptoms:

1. feeling of discomfort inside the joint;
2. lumbago that occurs when the joint is tense;
3. increased sensitivity of the affected area (the area where cartilage tissue and ligaments join);
4. pain when bending the knee;
5. swelling (shown in the photo);
6. weakness appearing in the front of the thigh.

Factors of appearance are also of no small importance. Therefore, treatment is prescribed after identifying the causes.

If a person is elderly and has all of the above symptoms, then most likely this indicates the presence of a chronic degenerative rupture. As a rule, people young do not suffer from such pathologies.

Diagnosis and treatment

To get a diagnosis, a person complaining of knee pain should see a doctor. First, he will find out what is bothering the patient, and then he will examine the sore leg. The doctor will then check to see if there is any fluid accumulation in the kneecap or muscle atrophy. If these pathologies are detected, then the patient will be referred for examination to a traumatologist.

After an oral interview and examination of the limb, an experienced doctor will immediately establish the correct diagnosis. But to make sure it is correct, the doctor may prescribe additional examinations.

The patient will undergo magnetic resonance imaging, X-ray examination And ultrasound examination. By the way, an X-ray of the knee must be done, since it is the main way in which even damage can be detected posterior horn medial meniscus.

Today, treatment of anterior and posterior meniscus injuries is carried out various methods. A common method is surgery. The surgical method is used when it is difficult for the patient to flex and straighten the joint, and most importantly, it is relevant if conservative treatment turned out to be ineffective.

The surgical procedure performed to remove a lateral meniscus that has been damaged is called arthroscopy. Basically, such an operation is considered uncomplicated, and the rehabilitation process lasts about 14 days.

Traditional medicine can also eliminate painful symptoms meniscal injuries. But doctors say that such treatment can only eliminate the symptoms, but it is impossible to completely get rid of the pathology using home therapy methods.

Therefore, treatment with traditional medicine recommended as additional activities. Often this therapy is used during the recovery period.

During rehabilitation, you can make compresses with honey. In addition, lotions based on onions and burdock leaves are no less effective. But before making such compresses, you should definitely consult with a doctor who will approve or disprove these methods of treatment.

• Relieves pain and swelling in joints due to arthritis and arthrosis
• Restores joints and tissues, effective for osteochondrosis

To learn more…

Osteoporosis is a severe metabolic disease of the human musculoskeletal system. In many countries, this disease is detected on initial stages thanks to early diagnosis. But, unfortunately, this is not always the case, and osteoporosis can progress slowly and unnoticed, causing irreparable damage to the body.

Description of the disease

To begin with, it is worth considering the topographic classification of the disease. There are two main forms of osteoporosis: local (local) and general (generalized). The local form is divided into two more subgroups - spotted and uniform osteoporosis.

The main difference between these subgroups is the distribution of the pathological process zone on a specific bone. If the zone of bone depletion has a focal, chaotically located character and on the radiograph it looks like circles and ovals of different sizes, then this is a focal subgroup.

If the pathological process is evenly distributed over the bone area and looks on the radiograph as a general clearing of the bone compared to the other, this is a uniform option.

So, focal osteoporosis can be diagnosed only by visual inspection of the radiograph. Another name for this disease is found in the literature – spotted osteoporosis.

For a more accurate assessment of the radiograph, the focus of the image is made not on one limb, but on two at once. This allows you to clearly differentiate the pathological area and healthy bone tissue.

Causes

The local form of osteoporosis most often occurs against the background of local tissue damage. These include fractures, displacements, cuts, bruises, inflammatory processes, hypothermia, burns, intoxication, radiation, toxins. Drug use and alcoholism can also lead to pathology.

Iatrogenic etiology of osteoporosis occurs when injection techniques, manipulations and surgical interventions. Also, the causes of occurrence may be generalized processes - diabetic neuropathy and angiopathy, autoimmune diseases (red systemic lupus or systemic scleroderma).

This disease is characterized by periods of exacerbation and remission. During periods of exacerbation, pain in bones and joints increases, and the patient needs non-narcotic painkillers. Pathological processes during an exacerbation, they “plow” to the maximum, all the time reducing the percentage of working bone matter.

During remission, the process stops, the pain subsides, as a result of which the patient begins to feel much better.

Severe complications

Patchy osteoporosis of the femur can lead to very dangerous fracture neck of the femur. In this case, the patient will not be able to walk for a long time, and bed rest may well lead to congestive pneumonia.

Embolism is also a serious consequence of osteoporosis. Indeed, during minor fractures and cracks, yellow bone marrow from the bone enters the bloodstream. Through the vessels, these fat emboli enter the pulmonary arteries, clogging them. This process called pulmonary embolism (PE). This leads to pneumonia, pulmonary edema, ischemia and pulmonary infarction.

Displacement of the ridge can lead not only to changes in posture, but also to pinching of the spinal roots. This variant of pathogenesis is characterized by pain along the innervation of the nerve and impaired sensitivity in its zone.