Human musculoskeletal system. Therapeutic massage against diseases of bones and muscles. Prevention of diseases of the musculoskeletal system

Bone muscular system.

A properly formed, well-functioning musculoskeletal system is one of the main conditions for the full development of a child. By the time of birth, its structural differentiation is far from complete. Very high rates of growth and restructuring, in particular, of bone tissue in early childhood, require constant supply:

2) vitamins

3) calcium, phosphorus and other trace elements, as well as

4) intensive blood supply

5) uninterrupted and error-free operation of the enzyme systems of the bone itself and other organs.

These processes are carried out under extremely difficult conditions:

1. age-restricted nutrition
2. functional imperfection of most organs
3. insufficient central and neuroendocrine regulation of metabolic processes.

The functioning of the musculoskeletal system largely depends on the state of the nervous system, which is functionally and morphologically undeveloped, often injured in utero or during childbirth.

All this creates a special vulnerability of the musculoskeletal system in early childhood, contributing to the emergence of pathological processes, the consequences of which are often difficult to correct. In addition, syndromes of damage to bones, muscles, and joints can also accompany various acute and chronic infections, kidney and liver pathologies, and endocrine disorders.

Anatomical and physiological features and semiotics of damage to the muscular system in children.

Muscle tissue (meaning skeletal muscle tissue) develops from the middle germ layer (mesoderm) to

3-4 weeks embryogenesis.

At birth, the muscles are relatively poorly developed. So in newborns the relative muscle mass is only

20 – 23%. During the period of teething - 16.6%; at 7 years 22%; in adults approximately 36%.

General mass increase muscle tissue in the process of postnatal development is 37-fold, while the mass of the skeleton increases only 27-fold. No other tissue produces such growth after birth.

There is also a peculiarity in the distribution of muscle tissue in newborns and older children. In newborns, most of its mass falls on the muscles of the trunk (40%), while in other periods it falls on the muscles of the limbs.

TO morphological features muscular system in children should include:

1) smaller thickness of muscle fibers (5 times)

2) a relatively larger amount of loose intertitial tissue and vessels

3) and a larger number of rounded nuclei both in the cells of the muscles themselves and in the interstitial connective tissue

Each muscle is characterized by a more or less stable number of muscle fibers, which is established in the first months after birth and remains until adulthood.

The muscle growth that accompanies the postembryonic development of the body is associated with the lengthening and thickening of existing muscle fibers; their growth is insignificant.

Muscles lengthen due to growth in the zones of transition of muscle fibers into the tendon, where greatest number cores. In parallel with the growth of myofibrils, the number of nuclei per unit area of ​​tissue decreases (from 45 in newborns, to 5 in

17-year-old teenager). In parallel, the formation of the connective tissue framework of the muscles occurs, which reaches the final degree of differentiation by 8-10 years.

As children age, the chemical composition muscles: the amount of dense substances increases, the amount of water decreases, the amount of globulins remains almost unchanged, myostromin progressively increases, the amount of glycogen, lactic acid, nucleic acids decreases, relative to the mass of muscle tissue. An important quantitative feature is the presence in the muscles of children of the fetal form of myosin - this is an enzyme that activates the conversion of ATP into ADP and the release of energy necessary for muscle contraction.

As the child grows, fetal myosin disappears.

The innervation apparatus of skeletal muscles is basically formed by the time of birth; in the first years of life, its differentiation continues, and myelination of nerve fibers occurs.

Functionally A child’s muscles are characterized by various features:

1) thus, the electrical excitability of the neuromuscular system in children during the newborn period is reduced compared to older children.

2) Mechanical muscle excitability in newborns is slightly increased. They are characterized by a proboscis reflex, the presence of carpopedal spasm, tonic convulsions in the hand, foot. At a later age, these symptoms indicate pathology, in particular tetany associated with hypocalcemia, alkolosis.

3) In children of the first months of life there is increased tone muscles that do not disappear even during sleep, the so-called physiological hypertension, it is associated with the characteristics of the central nervous system function. A feature of newborns is the predominance of flexor muscle tone, due to which a specific fetal position occurs in the prenatal period and after birth, children usually lie with bent arms and legs. Gradually, muscle hypertension disappears in 2-2.5 months. on the upper and at 3-4 months. on the lower extremities, which is important for the development of coordinated hand movements.

The motor ability of a child’s muscles first appears in the muscles of the neck and torso, and then in the muscles of the limbs. Muscle strength in children clearly increases with age; as a rule, the right hand is stronger than the left.

Boys have slightly more muscle strength than girls.

It is believed that rich blood supply and intense metabolism contribute to the rapid leaching of lactic acid from the muscles, therefore the functional activity of children’s muscles is high, children are very mobile and get tired less than adults.

For normal muscle development in children and adolescents, moderate physical activity is necessary.

Both hypokinesia and excessive loads unfavorable for physical development child.

The degree of muscle development depends on a number of exogenous and endogenous reasons.

In thin children, especially in children with a microsomatotype, the muscles are always much less developed than in children with a macrosomatotype.

In infants and very obese children, the muscles are also relatively poorly developed.

Some general underdevelopment muscles most often occurs in children who have been bedridden for many years due to some chronic disease, as well as in children who do not engage in sports, leading sedentary lifestyle life, etc.

In sharply expressed cases Poor muscle development can be referred to as muscle atrophy.

Atrophic conditions are most pronounced in various forms of progressive muscle atrophy, in which muscle atrophy and hypotonia develop in a certain sequence.

Severe muscle atrophy is observed in cerebral and spinal palsy. Typical for spinal paralysis is muscle atrophy during polio (this is a viral neuroinfection with damage to the motor neurons of the spinal cord), when there is pronounced atrophy of the muscles of any group or the muscles of the entire limb.

Peripheral paralysis is flaccid in nature, called. "flaccid paralysis" At central paralysis muscle atrophy is not so pronounced, and the paralysis itself is spastic in nature. This is cerebral palsy.

Reverse state– hypertrophy of certain muscle groups – most often it is working hypertrophy. It can be observed in children engaged in any physical work or, for example, as a result of prolonged stiffness of individual muscles. It is necessary to distinguish pseudohypertrophy from true muscle hypertrophy, when replacement fat deposition simulates the picture of well-developed muscles.

Muscle tone. Plays an important role in the life support of the body. Muscle tone is judged by the consistency of muscle tissue, determined by touch, and by the degree of resistance that occurs during passive movements.

General hypotension of the entire muscular system occurs with: rickets, chorea, congenital myopathy.

Limited hypotension usually depends on peripheral neuronal disease (poliomyelitis, neuritis).

General hypertension occurs as a result of damage to the central neuron (residual effects after encephalitis, birth trauma, underdevelopment of the cortex, hydrocephalus).

In early childhood, hypertension and hypotension are often observed in acute and chronic disorders nutrition and digestion, and for certain infections (tetanus, meningitis).

Cause limited hypertension may lie in the muscles themselves - with myositis. Increased tension in the muscles of the abdominal walls is typical for peritonitis.

Anatomical and physiological features and semiotics of damage to the skeletal system.

Bone also develops from mesenchyme - in 2 ways:

1) directly from the mesenchyme (dermal or connective tissue osteogenesis).

2) In place of previously laid cartilage (through the cartilage stage - chondral osteogenesis). The development of bone directly from mesenchyme without prior transformation into cartilage is characteristic of the formation of coarse-fiber bone tissue as a) the integumentary bones of the skull; b) facial bones; c) diaphysis of the clavicle.

The primary basis of the skeleton is cartilaginous tissue, which is gradually replaced by bone, and bone formation occurs both inside the cartilaginous tissue (endochondral ossification) and on its surface (perichondral ossification). Endochondral ossification is promoted by the pressure of the body's gravity on the skeleton, perichondral - by the action of traction of tendons and muscles. They go almost simultaneously.

In young children, the tubular bones are filled with actively functioning red bone marrow and consist of several parts - the diaphysis and epiphyses, connected to each other by a layer of non-calcified cartilage. By the time a child is born, the diaphyses of the tubular bones are already represented by bone tissue, while the vast majority of the epiphyses, all the spongy bones of the hand and part of the spongy bones of the foot still consist only of cartilaginous tissue. By birth, only points of ossification are visible in the central parts of the epiphyses of the femur and tibia, in the talus, calcaneus and cuboid bones, in the bodies of all vertebrae and their arches, other ossification points appear after birth. Their sequence of appearance is quite specific.

The totality of ossification points present in a child is an important characteristic of the level of his biological development and is called bone age.

The growth of tubular bones in length until the appearance of ossification points in the epiphyses is carried out due to the development of germinal cartilaginous tissue, which forms the end sections of the bones.

After the appearance of ossification points in the epiphyses, growth occurs due to the development of germinal cartilaginous tissue in the metaphyseal zone, and the epiphyses increase as a result of the development of germinal cartilaginous tissue surrounding the corresponding ossification points.

In the metaphyseal zones of bone growth there is a very rich blood supply and slow blood flow, which ensure active bone formation, so microorganisms easily settle in these places, as a result of which metaphyseal osteomyelitis often occurs in children 1 year of age. At the age of 2-3 years, when ossification nuclei are formed in the epiphyses, osteomyelitis is often epiphyseal; in adults, it is diaphyseal.

At the same time, the diaphyses of long tubular bones increase in diameter due to the bone formation process from the periosteum, while from the bone marrow space the cortical layer undergoes constant resorption. The consequence of these processes is an increase in the diameter of the bone and an increase in the volume of the bone marrow space, which is very small at birth.

The bone tissue of newborns has a coarse fibrous mesh structure. A few bone plates are located incorrectly; the Haversian canals are represented by randomly scattered cavities. The periosteum is thick, its intrauterine layer is especially well defined due to which the processes of bone growth in diameter occur, which explains the high frequency of subperiosteal fractures in 1-year-old children - of the “green twig” type. The bones of children are poor in mineral salts, rich in water and blood vessels. Therefore, the child’s bones are soft, flexible, do not have sufficient strength, are easily bent and become irregular shape with compression and bending, with systematic incorrect position: in arms, bed.

It is unacceptable to sit a child up early and put him on his feet. At the same time, the child’s bone is more resistant to injury due to its elasticity.

The energy of bone growth and regeneration in childhood is much greater than in adults, so healing of fractures in children requires a shorter period of time. As the child grows, bone restructuring occurs, replacing the fibrous, mesh structure with a lamellar one. The amount of water decreases, the ash residue increases. Cartilage tissue is gradually replaced by bone tissue. In the process of bone formation and remodeling of bone tissue, there are 3 stages:

Stage 1 of osteogenesis - the formation of the protein basis of bone tissue - the bone matrix. For this process it is necessary to provide the child with protein, colloid, vitamins A, C, etc. B. Hormones take part in this process: thyroxine, somatomidins, activated somatotropic hormone of the pituitary gland, insulin, parathyroid hormone.

Stage 2 – mineralization of the bone matrix, i.e. deposition of mineral salts. For this stage, the body’s supply of calcium, phosphorus, microelements (manganese, magnesium, zinc, copper), and vitamin D is crucial.

The course of this stage is disrupted when acidosis develops in the child’s body. Both of these stages are regulated by muscle tone, as well as movements, so massage, gymnastics, and physical activity are very important during this period.

Stage 3 of osteogenesis is a process of remodeling and constant self-renewal of bone, which is regulated by the parathyroid glands and depends on the availability of vit. "D".

By the age of 3-4 years, the child’s bones acquire a lamellar structure, and by the age of 12 they no longer differ from the bones of an adult.

Skull bones . Skull box In contrast to an adult, a child's facial skeleton is much more developed. It depends on the lack of small child teeth and from poor development of the nose and its accessory cavities.

The skull of a small child is distinguished by the following features: it consists of bones separated from each other by sutures; at the junction of several bones there are gaps completely devoid of bone - fontanelles.

Lateral fontanelles (2 of them): between the occipital, temporal and parietal bones. These fontanelles are normally closed at the time of birth; if they are open, this indicates either the baby’s prematurity or cephalic dropsy.

Small, or posterior, fontanel, lying between the occipital and parietal bones, also closes in most full-term children by birth. However, in approximately 20-25% of newborns it is open and closes at 3-4 weeks.

The anterior, or large, fontanel (between the frontal and parietal bones) remains after birth and in a full-term healthy child; its normal size is 2-2.5x3 cm. The dimensions of the fontanel are determined by measuring the distance between the opposite sides of the fontanel. You cannot measure it diagonally, because... in this case, it is difficult to decide where the suture ends and the fontanel begins. Later, the fontanel gradually decreases and closes normally by 1 or 1.5 years.

Later closure of the large fontanel may be due to: rickets, hydrocephalus, myxedema. Premature closure can occur: with microcephaly (due to underdevelopment of the brain) or due to premature fusion of cranial sutures - craneostenosis.

It is necessary to pay attention to other properties of the fontanel: normally, the fontanel “breathes” - fluctuations in its surface are clearly visible simultaneously with the child’s breathing and pulse. In this case, the fontanel remains at the same level with the bones of the skull.

During feverish conditions, the fontanel usually protrudes somewhat and pulsates more strongly. And with a significant increase in intracranial pressure (hydrocephalus, meningitis), the fontanel protrudes above the level of the bones and becomes very tense. It should be remembered that the fontanel can be tense even in a healthy child during a cry.

When intracranial pressure decreases (decline in cardiac activity or dehydration of the entire body due to fluid loss due to vomiting or diarrhea), the fontanel sinks and appears below the level of the bones.

The sutures between the bones of the skull in a healthy child are clearly palpable only in the newborn period. When you feel the bones of the skull of a healthy child, you feel hardness above the middle. The pliability of bones that sag like parchment is called craniotabes, what is observed in rickets. This is especially common on the occipital and parietal bones. The normal shape of the skull is round. Some newborns experience a so-called birth tumor in the form of a soft, harsh swelling of the skin, which depends on the serous permeation of the soft tissues and spontaneously resolves within a few days. Another type of tumor can form outside the skull as a result of a more severe birth injury: this is hemorrhage under the periosteum - cephalohematoma. It differs from a birth tumor in that it does not go beyond the sutures, whereas a birth tumor also goes through the sutures.

With rickets it may also be change in the shape of the head - quadrangular shape (enlargement of the frontal and parietal tubercles), buttock-shaped head, tower skull.

Spine . The spine of a newborn child is devoid of physiological curvatures; it is almost straight, or rather, has a general convexity posteriorly.

When a child begins to hold his head up, he appears cervical lordosis; later (at the 6th month), when he begins to sit, thoracic kyphosis forms; When learning and walking, lumbar lordosis is formed.

At first, these bends are unstable and smooth out when the child lies down. Lateral curvature of the spine is called scoliosis. Severe degrees of scoliosis, as well as kyphosis, in young children usually occur with rickets.

In school children and preschool age Curvature of the spine of another etiology is often noticed - the so-called “habitual” or “school” kyphoscoliosis.

The formation of such habitual or “school” kypho-scoliosis depends on insufficient tone and partly on insufficient development of muscles in general and back muscles in particular. This is observed both due to late rickets and in the wrong way life. For these pathologies, it is recommended to use a bed with an orthopedic mattress, which slows down the process of spinal deformation and also reduces the load on it.

The chest of a child has a number of features. In a newborn and up to 1.5-2 years of age, it appears barrel-shaped - the transverse size is almost equal to the anteroposterior. Later it takes on the shape of a cylinder and at school age the shape of a truncated cone.

In the first year of life, a child’s ribs extend from the spine almost at a right angle and have a horizontal direction. This structure of the chest leads to difficulty in inhaling in young children - it is only possible due to the lowering of the diaphragm, while the ribs are always in the position of maximum inhalation. With rickets, the following deformations of the ore cell are possible:

“chicken breast”, when the chest is as if compressed from the sides with the sternum protruding forward. Other deformation -

"shoemaker's chest". In such cases, the sternum, especially the xiphoid process, seems to be depressed or sunk.

When the heart enlarges due to congenital or early acquired heart defects, a cardiac hump develops - a bulging of those parts of the chest that cover the outside of the heart.

Rib beads, as a manifestation of rickets, are formed at the site of the transition of the bone tissue of the rib into cartilage. Palpated approximately along the parasternal line.

The pelvic bones are relatively small in young children. The shape of the pelvis resembles a funnel. The growth of the pelvic bones occurs relatively rapidly until the age of 6 years. From 6 to 12 years of age, there is a relative stabilization of the size of the pelvis, and subsequently its development is most intensive in girls, and moderate growth in boys.

In children in the first months of life, apparent curvature of the legs is often observed. This has no pathological significance and is not associated with true curvature of the limbs, which can occur with rickets (X-, O-shaped legs) or with syphilis, but depends on the peculiar development of soft tissues.

Teeth . Newborns have no teeth. They occur as an exception and usually fall out quickly. Teething begins at healthy children at the age of 6-7 months. Teeth of the same name on each half of the jaw erupt simultaneously. The lower teeth tend to erupt earlier. Than the top ones. The only exceptions are the lateral incisors - here upper teeth appear before the lower ones. U one year old child d.b. 8 teeth. In the primary occlusion there are 2 periods: 1 to 3-3.5 years, orthognathic bite, 2 - from 3.5 to 6 years, straight bite.

The period of preservation of milk teeth and the appearance of permanent teeth is called the period mixed bite. All milk teeth erupt at about 2 years of age and there are 20 in total.

Formula for calculating baby teeth n – 4, where n is the number of months of a child’s life.

First permanent teeth erupt at approximately 5-5.5 years. These are the first molars. Then the sequence of appearance permanent teeth, approximately the same as when dairy products appeared. After the primary teeth are replaced by permanent teeth at approximately 11 years of age, the second molars appear. Third molars (wisdom teeth) erupt between the ages of 17 and 25, and sometimes later.

For an approximate assessment of permanent teeth, regardless of gender, you can use the formula:

X (number of permanent teeth) = 4n – 20.

The formation of both primary and permanent dentition in children is an important indicator of the level of biological maturation of the child. Therefore, in assessing the biological maturity of children, the concept of “dental age” is used. There is a table for assessing the level of age development by “dental age”.

Of particular importance is the determination of dental age in assessing the degree of maturity of children of preschool and primary school age, where other criteria are more difficult to use.

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In the musculoskeletal system, the soft tissue component is the muscles. In the clinic they matter various injuries muscles, their inflammation is myositis, they can undergo various dystrophic and necrotic changes in various diseases. However, tumors of muscle tissue are of independent and very important importance. They can develop from smooth muscle, and their benign forms are called leiomyomas, and their malignant forms are called leiomyosarcoma. If the tumor grows from the striated muscle, it is called rhabdomyoma, and its malignant counterpart is rhabdomyosarcoma. Tumors from muscle tissue belong to a large group of soft tissue tumors, including various neoplasms from mesenchymal derivatives. Each of these tumors, including neoplasms from muscle tissue, have many forms and variants; their detailed study is the task of oncology. Here it makes sense to show only the fundamental features of the morphology and clinical picture of muscle tumors.

Smooth muscle tumors. Leiomyoma is a mature benign tumor of smooth muscle that occurs at any age in people of both sexes, most often at 30-50 years of age. The tumor is a dense elastic node, covered with a connective tissue capsule, clearly demarcated from the surrounding tissue. The sizes of the tumor vary widely - from 0.5 cm in the wall of the stomach or intestine to 20-30 cm in the retroperitoneum or mediastinum. Leiomyomas are often multiple (that is, they grow in multicentric growth), and in such cases they speak of leiomyomatosis. Leiomyoma develops especially often in the myometrium; it often grows from the smooth muscles of various parts gastrointestinal tract, but, in principle, this tumor occurs wherever there is smooth muscle tissue.

Microscopically, the tumor consists of slightly enlarged muscle cells with a denser nucleus, forming swirls and tufts running in different directions. The stroma consists of argyrophilic and collagen fibers, also arranged randomly. As the duration of its existence increases, neoplasms may develop in its stroma dystrophic changes ending in hyalinosis. All this serves as a manifestation of tissue atypia of the tumor. Leiomyoma grows expansively and at the same time puts pressure on the surrounding tissue. As a result, atrophy occurs from the pressure of both the muscle cells of the periphery of the tumor and the surrounding tissue and their replacement with connective tissue, forming the leiomyoma capsule. If a leiomyoma contains a lot of stroma, consisting of randomly arranged collagen fibers, the tumor acquires a dense consistency and is called fibroleiomyoma. Sometimes in a smooth muscle tumor there are many vessels, which are usually polymorphic and around them muscle cells are located in a very peculiar way, somewhat reminiscent of epithelial ones. This type of leiomyoma is called “bizarre” or epithelioid. The prognosis for leiomyoma is favorable; malignancy is rare.

Leiomyosarcoma is very malignant tumor from smooth muscles, metastasizes early by hematogenous route, and gives abundant distant metastases; relapses may occur after tumor removal. The tumor most often arises from the smooth muscle elements of the skin, retroperitoneal space and omentum, grows by infiltrating growth, but more often has the shape of a node. Microscopically, sharply atypical polymorphic cells with high mitotic activity, atypical mitoses, giant multinucleated cells and muscle symplasts are revealed. Sometimes, to diagnose the muscle origin of leiomyosarcoma cells, electron microscopy is necessary, which makes it possible to detect myofilaments in their cytoplasm. Muscle tumor cells form bundles of unequal size, arranged randomly. The stroma is represented by a loose network of argyrophilic fibers. The prognosis of the tumor after removal is difficult.

Tumors of striated muscles. Rhabdomyoma is a mature benign tumor that has all the signs of striated muscle tissue. This is an uncommon tumor, mainly in children, that occurs deep in the muscles of the limbs, in the myocardium, and in the area of ​​the root of the tongue. It consists of nodules from 1 cm to 10-15 cm in diameter, grayish-white when cut. The tumor consists of large spindle-shaped and round cells containing a light nucleus. The cytoplasm usually has transverse, sometimes longitudinal, striations and contains a lot of glycogen. The stroma is composed of a delicate argyrophilic network. After tumor removal, the prognosis is favorable.

Rhabdomyosarcoma is a relatively rare, very malignant tumor that occurs in people of both sexes at any age, but more often in children under 5 years of age, growing from the muscles of the limbs, torso, sometimes arising out of connection with muscle tissue - in the retroperitoneal tissue, mediastinum, face and neck , in the nasopharynx, genitourinary tract, and in the female genital organs. Tumor growth accelerates after biopsy. Metastasis is extensive, sometimes after removal of the sarcoma. Relapses are frequent.

The tumor is a node in the thickness of the muscles with a diameter of up to 20 cm or more. Microscopically, cellular polymorphism is characteristic, reminiscent of embryonic muscle cells at different phases of embryogenesis, sharp nuclear atypia, irregular, sometimes “monstrous” mitoses in large tumor cells.

Depending on the degree of anaplasia of rhabdomyosarcoma cells, there are 4 variants of its structure: 1) embryonic type: found mainly in children, perhaps this variant is associated with dysembryoplasia; characterized by cells resembling embryonic myoblasts, myosymplasts, sometimes with striations of the cytoplasm, arranged randomly, sometimes forming something like muscle bundles; 2) alveolar type: This rhabdomyosarcoma most often occurs in the limbs of people aged 10-25 years. It forms pseudoglandular and pseudoalveolar structures, formed due to the presence of connective tissue layers, bordered by tumor cells with pronounced polymorphism, but generally also having an embryonic structure - oval or round in shape with a large light core; 3) the pleomorphic type is relatively rare, the tumor has the most variegated structure and can consist of small round, oval or spindle-shaped cells, as well as a variety of giant multinucleated cells, sometimes resembling a tennis racket. There are no rhabdomyoblasts. In the cytoplasm, myofibrils with transverse striations can be seen. The cells lie in the form of fields or form various bundles, surrounded by argyrophilic fibers. Ingrowth of tumor cells into the vessels of rhabdomyosarcoma is often visible; 4) mixed type, usually having the structure of both embryonal and alveolar rhabdomyosarcoma. The prognosis of rhabdomyosarcoma, even after removal and appropriate treatment of the tumor, is questionable, and more often than not, poor.

Granular cell myoblastoma or myoblast myoma (Abrikosov tumor) is a benign tumor unknown origin. A.I. Abrikosov, who described this tumor in 1925, believed that the source of its growth were myoblasts that arise during the regeneration of damaged muscle tissue, but did not exclude that outside the muscles these cells are of dysontogenetic origin. The tumor is observed at any age in people of both sexes, is localized in the muscles, especially in the muscles of the tongue, shoulder, thigh, calf muscles, but can also occur outside of connection with the muscles - in the skin, larynx, gums, pituitary gland. Abrikosov's tumor has the shape of a node, sometimes reaching 20 cm, but can grow in the form of multiple nodes, not always clearly demarcated from the surrounding tissues. It grows relatively slowly, with expansive growth, but a connective tissue capsule does not form around the tumor. Microscopically, large cells of various shapes with centrally located round, often pyknotic nuclei with a mesh chromatin structure are characteristic. Mitoses are not typical. The cytoplasm is granular and rich in glycogen. Sometimes myofibrils with transverse striations can be seen in the cytoplasm. The stroma is tender, fibrous, and forms cells surrounding complexes of tumor cells. There are few vessels in the tumor. After its removal the prognosis is good.

Of course, the information presented in the lecture does not exhaust the entire variety of pathologies of the musculoskeletal system. At the same time, this information allows us to understand the patterns of development and features of the patho- and morphogenesis of the main, most common and most important diseases of bones and joints.

Lecture equipment

Macroscopic specimens: chondrosarcoma, osteosarcoma, cancer metastases in the lumbar vertebra, osteomyelitis of the leg.

Microspecimens: giant cell tumor of bone, Ewing's sarcoma, adenocarcinoma metastasis to bone, osteopetrosis, chronic osteomyelitis.

On-line consultations with doctors

Muscles

Human movements are provided by the musculoskeletal system, which consists of a passive part - bones, ligaments, joints and fascia, and an active part - muscles.

There are three main types of muscles. The first is the striated muscles, which are controlled by the brain. Contractions of these muscles are called voluntary, because they are subject to the will. Together with bones and tendons, they are responsible for all our movements.

The second is smooth muscle, which gets its name because this is what it looks like under a microscope. They are responsible for involuntary movements internal organs, for example, Bladder or intestines.

And the third is the cardiac muscle, of which the heart almost entirely consists. The heart muscle does not stop its rhythmic work throughout life. The nervous system regulates the frequency, strength, and rhythm of heart contractions.

Striated muscles are widely distributed throughout our body, even in a newborn baby making up a significant part of the weight - up to 25%. They control the movements of a wide variety of parts of the skeleton - from the tiny stapedius muscle, which moves the stapes in the ear, to the gluteus maximus, which forms the buttock and commands hip joint. Striated muscles are divided into muscles of the trunk, head and neck, upper and lower limbs.

Muscles are attached to the skeleton by tendons. The end of the tendon closest to the center of the body is called the muscle insertion, and is shorter than the tendon at the other end. Typically, one tendon attaches the muscle to the near end of the joint, and the other to the far end, due to which, by contracting, it sets it in motion.

Striated muscle can be thought of as a series of bundles of muscle fibers assembled together. The smallest of them, and the main working element of the muscle, are actin and myosin filaments. They are very thin and can only be seen under an electron microscope. They consist of a protein, which is sometimes called contractile protein. When all the myosin filaments slide along the actin filaments, the length of the muscle shortens.

All these threads are collected in bundles, or myofibrils. Between them, reserves of muscle fuel are stored in the form of glycogen and cellular energy generators, or mitochondria, are located, in which oxygen and fuel supplied with food are burned, producing energy. Myofibrils are collected in larger bundles or muscle fibers. These are already real muscle cells with a nucleus located on the outer edge.

The muscle fibers are also bundled together in a sheath of connective tissue, similar to the insulation of copper wires in a thick cable. A small muscle may consist of only a few bundles, while a large one may consist of many hundreds.

The entire muscle is enclosed in the same fibrous sheath, akin to the insulating coating of a multi-core cable. In smooth muscles we will not see such a geometrically ordered structure of threads and fibers, but they also contract due to the sliding of the threads. At the same time, the cardiac muscle looks under a microscope the same as striated muscle, with the difference that the individual bundles of fibers are connected by jumpers.

From the motor (movement-controlling) areas of the cerebral cortex, nerves travel along the spinal cord and branch into many muscle-controlling endings. Without nerve signals, the muscle loses its ability to contract and gradually atrophies.

Nerves are “connected” to muscle fibers in certain areas of the surface. Electric power entering the muscle nerve impulse is insignificant compared to the electrical changes occurring in it, so an amplifier is needed. The contractile impulse is supplied at the motor ending, where the motor nerve joins the muscle fiber. An electrical impulse passing along the nerve releases the substance acetylcholine, which causes the muscle to contract.

The sliding of myosin filaments along actin filaments is a complex process during which a number of chemical compounds are continuously formed and broken down between them. This requires energy, which is produced by the combustion of oxygen and fuel supplied with food in the mitochondria. Energy is stored in reserve and transferred in the form of a substance called ATP (adenosine triphosphate), rich in phosphates. Muscle contraction begins with the influx of calcium into muscle cells through many microtubules flowing between myofibrils.

In addition, there are two more groups of fibers in the muscle. One registers the force of contraction, and the other, located inside the tendons, controls its stretching. This key information for controlling muscle activity is transmitted back to the brain.

Muscles have different shapes. They are: biceps, triceps, quadriceps, quadrate, triangular, pyramidal, teres, serratus, soleus muscles. Based on the direction of the fibers, the muscles are divided into rectus, oblique and orbicularis muscles. Depending on their functions, muscles are divided into flexors, extensors, adductors, abductors, rotators, tension muscles, facial muscles, masticatory muscles, respiratory muscles, etc.

Striated muscles have auxiliary apparatus: fascia, fibro-osseous canals, synovial sheaths and bags. The muscles are abundantly supplied with blood thanks to a large number of blood vessels and have developed lymphatic vessels.

Muscles performing the same movement are called synergists, and opposite movements are called antagonists. The action of each muscle can only occur with the simultaneous relaxation of the antagonist muscle; such coordination is called muscle coordination.

Muscle strength depends on the number of myofibrils in muscle fibers: in well-developed muscles there are more of them, in poorly developed muscles there are fewer. Systematic training and physical work, which increase myofibrils in muscle fibers, lead to an increase in muscle strength.

Diseases of the muscular system.

Tumors in the muscles are relatively rare.

Among the malformations of muscle development, there are disturbances in the development of the diaphragm with the subsequent formation of diaphragmatic hernias. Muscle necrosis can occur as a result of metabolic disorders, inflammatory processes, trauma, exposure to a nearby tumor, as well as blockage of large arteries.

Dystrophic processes of various origins can develop in muscle tissue, including lipomatosis (excessive fat deposition), observed, in particular, with general obesity.

The deposition of calcium salts in the muscles is observed as a manifestation of a general or local disturbance of mineral metabolism.

Muscle atrophy is expressed in the fact that their fibers gradually become thinner. The causes of atrophy are varied. As a physiological phenomenon, muscle atrophy can occur in older people due to their low physical activity. Sometimes atrophy develops due to impaired muscle function due to diseases of the nervous system. Muscle atrophy can also develop when the patient is immobilized due to severe trauma or joint diseases, in severe debilitating diseases, etc.

Hypertrophy (increase muscle mass) muscles are mainly of a physiological, working nature. It can be observed during severe physical exertion, as well as with some hereditary diseases.

Common diseases of the muscular system include the so-called. aseptic muscle inflammation - myositis. Muscle damage associated with inflammatory process, occur in a number of systemic (Collagen diseases, Rheumatism) and infectious (Myocarditis) diseases.

The development of purulent inflammation - an abscess - refers to severe forms lesions of the muscular system requiring surgical treatment.

Muscle damage occurs in the form of bruises or tears; both manifest as painful swelling and hardening as a result of hemorrhage.

Open muscle injuries (wounds) are usually accompanied by significant external bleeding, which requires urgent hospitalization of the victim.

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Diseases of the musculoskeletal system are extremely diverse. They can be roughly divided into diseases of the skeletal system, joints and skeletal muscles.

Diseases of the skeletal system

Diseases of this group can be dystrophic, inflammatory, dysplastic and tumoral in nature. Dystrophic bone diseases (osteodystrophy) are divided into toxic (for example, Urovsky disease), nutritional (for example, rickets - see. Vitamin deficiencies), endocrine, nephrogenic (see. Kidney diseases). Among dystrophic bone diseases, the most important is parathyroid osteodystrophy. Inflammatory bone diseases are most often characterized by the development of purulent inflammation of the bone marrow (osteomyelitis), often bone tissue is affected by tuberculosis and syphilis (see. Infectious diseases). Dysplastic bone diseases are most common in children, but can also develop in adults. Among them, the most common fibrous bone dysplasia, osteopetrosis, Paget's disease. Against the background of dysplastic bone diseases, bone tumors(cm. Tumors).

Parathyroid osteodystrophy(Recklinghausen's disease, generalized osteodystrophy) is a disease caused by hyperfunction of the parathyroid glands and accompanied by generalized skeletal damage. The disease occurs mainly in women 40-50 years old, rarely in childhood.

Etiology. Parathyroid osteodystrophy is associated with primary hyperparathyroidism, which is caused by adenoma of the parathyroid glands or hyperplasia of their cells (cancer is very rare). Primary hyperparathyroidism should be distinguished from secondary hyperparathyroidism, which develops with chronic renal failure, multiple cancer metastases to the bones, etc. The importance of hyperfunction of the parathyroid glands in the development of bone pathology was first substantiated by A.V. Rusa-

kov (1924), who proposed for treatment bone pathology surgical removal of tumors of the parathyroid glands.

Pathogenesis. Increased synthesis of parathyroid hormone causes increased mobilization of phosphorus and calcium from the bones, which leads to hypercalcemia and progressive demineralization of the entire skeleton. Osteoclasts are activated in bone tissue, and foci of lacunar bone resorption appear. Along with this, diffuse fibroosteoclasia increases - bone tissue is replaced by fibrous connective tissue. These processes are most intensely expressed in the endosteal parts of the bones. In areas of intense restructuring, bone structures do not have time to mature and calcify; osteoid tissue, cysts, cavities filled with blood and hemosiderin are formed. Bone deformation and osteoporosis progress, and pathological fractures often occur. Formations appear in the bones that are indistinguishable from giant cell tumors (osteoblastoclastoma, according to A.V. Rusakov). In contrast to true tumors, these are reactive structures, which are giant cell granulomas in foci of organization of blood accumulations; they usually disappear after removal of the parathyroid tumor.

Hypercalcemia, which develops with parathyroid osteodystrophy, leads to the development of calcareous metastases, see. Disorders of mineral metabolism (mineral dystrophies). Nephrocalcinosis often develops, combined with nephrolithiasis and complicated by chronic pyelonephritis.

Pathological anatomy. In the parathyroid glands, adenoma is most often found, cell hyperplasia is less common, and cancer is even less common. The tumor may have an atypical localization - in the thickness thyroid gland, mediastinum, behind the trachea and esophagus.

Skeletal changes in parathyroid osteodystrophy depend on the stage and duration of the disease. IN initial stage illness and low parathyroid hormone activity external changes bones may be missing. In an advanced stage, deformation of bones is detected, especially those that are subject to physical stress - limbs, spine, ribs. They become soft, porous, and can be easily cut with a knife. Bone deformation can be caused by multiple tumor-like formations, which have a variegated appearance when cut: yellowish areas of tissue alternate with dark red and brown ones, as well as cysts.

At in the bone tissue, foci of lacunar resorption are identified (Fig. 243), neoplasms of fibrous tissue, and sometimes osteoid beams. In the foci of tumor-like formations, giant cell granulomas, accumulations of erythrocytes and hemosiderin, and cysts are found.

Death In patients, it often occurs from cachexia or uremia due to shrinkage of the kidneys.

Rice. 243. Parathyroid osteodystrophy. Lacunar bone resorption (shown by arrows) and new formation of fibrous tissue (according to M. Eder and P. Gedik)

Osteomyelitis

Under osteomyelitis(from Greek osteon- bone, myelos- brain) understand inflammation of the bone marrow, spreading to the compact and spongy bone and periosteum. Osteomyelitis is divided into the nature of the current - on spicy And chronic, according to the mechanism of bone marrow infection - on primary hematogenous And secondary (a complication of injury, including a gunshot wound, during the transition of the inflammatory process from surrounding tissues). Primary hematogenous osteomyelitis is of greatest importance.

Primary hematogenous osteomyelitis can be acute and chronic. Acute hematogenous osteomyelitis, usually develops in at a young age, 2-3 times more often in men. usually the outcome of an acute

Etiology. In the occurrence of osteomyelitis, the main role is played by pyogenic microorganisms: hemolytic staphylococcus (60-70%), streptococci (15-20%), coliform bacilli (10-15%), pneumococci, gonococci. Less commonly, fungi can be causative agents of osteomyelitis. The source of hematogenous spread of infection can be an inflammatory focus in any organ, but often the primary focus cannot be detected. It is believed that such patients have transient bacteremia due to minor intestinal trauma, dental diseases, and upper respiratory tract infections.

Pathogenesis. Features of the blood supply to bone tissue contribute to the localization of infection in long tubular bones. Usually the purulent process begins from the bone marrow spaces of the metaphyses, where blood

the flow is slow. Subsequently, it tends to spread, causing extensive necrosis and spreading to the cortical bone, periosteum and surrounding tissues. Purulent inflammation spreads along the bone marrow canal, affecting more and more areas of the bone marrow. In children, especially newborns, due to the weak attachment of the periosteum and the peculiarities of the blood supply to the cartilage of the epiphyses, the purulent process often spreads to the joints, causing purulent arthritis.

Pathological anatomy. At acute hematogenous osteomyelitis the inflammation is phlegmonous (sometimes serous) in nature and involves the bone marrow, Haversian canals and periosteum; Foci of necrosis appear in the bone marrow and lamina compacta. Severe bone resorption near the epiphyseal cartilage can cause separation of the metaphysis from the epiphysis (epiphysiolysis), mobility and deformation of the periarticular zone appear. Around the foci of necrosis, tissue infiltration with neutrophils is determined, and blood clots are found in the vessels of the lamina compacta. Abscesses are often found under the periosteum, and phlegmonous inflammation is found in the adjacent soft tissues.

Chronic hematogenous osteomyelitis associated with chronic suppurative process, formation bone sequesters. Granulation tissue and a capsule are formed around the sequesters. Sometimes the sequestrum floats in a cavity filled with pus, from which fistulous tracts extend to the surface or cavities of the body, to the cavity of the joints. Along with this, bone formation is observed in the periosteum and medullary canal. Bones become thick and deformed. Endosteal bone growths (osteophytes) can lead to obliteration of the medullary canal, and the compact lamina thickens. At the same time, focal or diffuse irritation of the bone occurs due to its resorption. Foci of suppuration in soft tissues during chronic course hematogenous osteomyelitis usually scars.

Special shape chronic osteomyelitis is Brody's abscess. It is represented by a cavity filled with pus, with smooth walls, which are lined from the inside with granulations and surrounded by a fibrous capsule. In granulation tissue, many plasma cells and eosinophils are detected. No fistulas are formed, bone deformation is insignificant.

Complications. Bleeding from fistulas, spontaneous bone fractures, formation of false joints, pathological dislocations, development of sepsis; in chronic osteomyelitis, secondary amyloidosis is possible.

Fibrous dysplasia

Fibrous dysplasia(fibrous osteodysplasia, fibrous bone dysplasia, Lichtenstein-Braitsev disease) is a disease characterized by the replacement of bone tissue with fibrous tissue, which leads to bone deformation.

Etiology and pathogenesis. Reasons for development fibrous dysplasia are not clear enough, the role of heredity cannot be ruled out. Think that

The disease is based on a tumor-like process associated with improper development of osteogenic mesenchyme. The disease often begins in childhood, but can develop in young adulthood and old age. The disease predominates in females.

Classification. Depending on the distribution of the process, two forms of fibrous dysplasia are distinguished: monoosseous, in which only one bone is affected, and polyostotic, in which several bones are affected, mainly on one side of the body. The polyostotic form of fibrous dysplasia can be combined with melanosis of the skin and various endocrinopathies (Albright's syndrome). The monostotic form of fibrous dysplasia can develop at any age, the polyostotic form - in childhood, therefore, patients with this form of fibrous dysplasia have diffuse skeletal deformation and a predisposition to multiple fractures.

Pathological anatomy. In the monoosseous form of fibrous dysplasia, the ribs, long tubular bones, scapulae, and skull bones are most often affected (Fig. 244); with the polyostotic form - over 50% of the bones of the skeleton, usually on one side. The lesion may involve small area or a significant part of the bone. In tubular bones it is localized mainly in the diaphysis, including the metaphysis. The affected bone at the beginning of the disease retains its shape and size. Subsequently, areas of “bloating”, bone deformation, elongation or

shortening. Under the influence of static load, the femurs sometimes take on the shape of a shepherd's crook. When the bone is cut, clearly defined foci of a whitish color with reddish inclusions are identified. They are usually round or elongated, sometimes merging with each other; in places of “swelling” the cortical layer becomes thinner. The medullary canal is expanded or filled with newly formed tissue, in which lesions are identified bone density, cysts.

At microscopic examination foci of fibrous dysplasia are represented by fibrous fibrous tissue, among which poorly calcified bone beams of a primitive structure and osteoid beams are identified (see Fig. 244). Fibrous tissue in some areas consists of chaotically located bundles of mature collagen fibers and spindle cells, in other areas - from developing (thin) collagen fibers and stellate cells. Sometimes myxomatous foci, cysts, accumulations of osteoclasts or xanthoma cells, and islands of cartilaginous tissue are found. Some features of the histological picture of fibrous dysplasia of the facial bones are noted: the dense component in the foci of dysplasia can be represented by cement-type tissue (cementicle-like formations).

Complications. Pathological bone fractures are the most common. In young children, often during their first attempts to walk, the femur is especially likely to break. Fractures upper limbs rare. Typically, fractures heal well, but bone deformation increases. In a number of observations, sarcoma develops against the background of fibrous dysplasia, often osteogenic.

Osteopetrosis

Osteopetrosis(marble disease, congenital osteosclerosis, Albers-Schönberg disease) is a rare hereditary disease in which there is generalized excessive bone formation, leading to thickening of the bones, narrowing and even complete disappearance of the medullary spaces. Therefore, osteopetrosis is characterized by a triad: increased density bones, their fragility and anemia.

Etiology and pathogenesis. The etiology and pathogenesis of osteopetrosis have not been sufficiently studied. Undoubtedly, the participation of hereditary factors is associated with impaired development of bone and hematopoietic tissue. In this case, excessive formation of functionally inferior bone tissue occurs. It is believed that the processes of bone production prevail over its resorption, which is associated with the functional failure of osteoclasts. Increasing displacement of bone marrow by bone is associated with the development of anemia, thrombocytopenia, and the appearance of foci of extramarrow hematopoiesis in the liver, spleen, and lymph nodes, which leads to their enlargement.

Classification. There are two forms of osteopetrosis: early (autosomal recessive) and late (autosomal dominant). Early

form osteopetrosis manifests itself at an early age, has a malignant course, and often ends in death; late form proceeds more benignly.

Pathological anatomy. With osteopetrosis, the entire skeleton can be affected, but especially the tubular bones, bones of the base of the skull, pelvis, spine, and ribs. In the early form of osteopetrosis, the face has a characteristic appearance: it is wide, with widely spaced eyes, the root of the nose is depressed, the nostrils are deployed, and the lips are thick. With this form, hydrocephalus, increased hair growth, hemorrhagic diathesis, multiple lesions bones, whereas in the late form of osteopetrosis, bone damage is usually limited.

The outlines of the bones may remain normal; only a flask-shaped expansion of the lower parts of the femur is characteristic. Bones become heavy and difficult to saw. On cuts in long bones the medullary canal is filled with bone tissue and is often not detected. In flat bones, the medullary spaces are also barely visible. In place of the spongy substance, dense, homogeneous bone tissue is found, reminiscent of polished marble (marble disease). Bone growth in the area of ​​the holes and canals can lead to compression and atrophy of the nerves. This is what is associated with the most common optic nerve atrophy and blindness in osteopetrosis.

Microscopic picture extremely unique: pathological bone formation occurs throughout the entire bone, the mass of bone substance is sharply increased, the bone substance itself is randomly piled up in the internal parts of the bones (Fig. 245). Bone marrow

Rice. 245. Osteopetrosis. Disorderly pile bone structures(according to A.V. Rusakov)

the spaces are filled with randomly arranged layered bone conglomerates or lamellar bone with arcuate lines of adhesion; Along with this, beams of embryonic coarse fibrous bone are found. Single areas of ongoing bone formation are visible in the form of clusters of osteoblasts. Osteoclasts are rare, signs of bone resorption are insignificant. The architecture of the bone, due to the disordered formation of bone structures, loses its functional characteristics, which is obviously associated with bone fragility in osteopetrosis. In zones of enchondral ossification, cartilage resorption is practically absent. On the basis of the cartilage, peculiar rounded islands of bone beams are formed, which gradually turn into wide beams.

Complications. Bone fractures often occur, especially the femur. In places of fractures, purulent osteomyelitis often develops, which is sometimes a source of sepsis.

Causes of death. Patients with osteopetrosis often die in early childhood from anemia, pneumonia, and sepsis.

Paget's disease

Paget's disease(deforming ostosis, deforming osteodystrophy) - a disease characterized by increased pathological restructuring of bone tissue, a continuous change in the processes of resorption and new formation of bone substance; in this case, the bone tissue acquires a peculiar mosaic structure. The disease was described in 1877 by the English physician Paget, who considered it inflammatory and called it deforming osteitis.

Later, the inflammatory nature of the disease was rejected, and the disease was classified as a dystrophic disease. A.V. Rusakov (1959) was the first to prove the dysplastic nature of Paget's disease.

The disease is observed more often in men over 40 years of age, progresses slowly, and usually becomes noticeable only in old age. It is believed that asymptomatic forms of the disease occur with a frequency of 0.1-3% in different populations. The process is localized in long tubular bones, skull bones (especially facial), pelvic bones, vertebrae. The lesion may involve only one bone (monostotic form) or several often paired or regional bones (polyostotic form), but it is never generalized, which distinguishes Paget's disease from parathyroid osteodystrophy.

Etiology. The reasons for the development of the disease are not known. Disorders of phosphorus-calcium metabolism and viral infection as a possible cause of Paget's disease are excluded, but the familial nature of the disease is noted. The dysplastic nature of bone lesions in Paget's disease is evidenced by the non-functional nature of bone restructuring and the frequent development of sarcoma against this background.

Patho- and morphogenesis. The processes of bone tissue restructuring in Paget's disease occur continuously, and there is no connection with the functional load. Depending on the relationship between the process of osteolysis and osteogenesis, 3 phases of the disease are distinguished: initial (osteolytic), active (a combination of osteolysis and osteogenesis) and inactive (osteosclerotic). IN initial phase Bone resorption processes predominate with the participation of osteoclasts, and therefore deep lacunae are formed in the bone tissue. IN active phase deforming ostosis, along with osteolysis, new bone formation is also expressed; osteoblasts appear, lacunae are filled with newly formed bone substance. Wide, clear bonding lines appear where the old and new bone meet. Due to the constant repetition and change of the processes of osteolysis and osteogenesis, bone beams are built from small fragments that form a characteristic mosaic. For inactive phase characterized by the predominance of the process of osteosclerosis.

Pathological anatomy. Bone changes in Paget's disease are quite characteristic. Long tubular bones especially the femur and tibia, are curved, sometimes spiral-shaped, which is explained by the growth (elongation) of the bone during its restructuring. At the same time, the length of a healthy paired bone does not change. The surface of the affected bone is rough, cuts reveal a narrow medullary canal, sometimes it is completely obliterated and filled with randomly alternating beams. When the periosteum is removed, small numerous openings of the vascular canals are usually visible on the surface of the cortical layer (normally they are almost invisible). This is due to the fact that bone restructuring is accompanied by intense resorption of the bone walls of the vascular canals and a sharp dilation of blood vessels. When cut, the cortical layer of the bone loses its compact structure and becomes spongy. However, this is only an external resemblance to spongy tissue, since the restructuring in Paget's disease is afunctional in nature.

In case of defeat skull bones the process usually involves only the bones of the skull. In the bones of the roof of the skull there is no division into the inner, outer plate and middle spongy layer; the entire bone mass has an unevenly spongy structure with areas of rarefaction and compaction. If the bones of the facial skull are also changed, then the face becomes sharply disfigured. The thickness of the bones when cut can reach 5 cm, and the thickening of the bone can be either uniform or uneven. Despite the increased volume, the bones are very light, which is due to the decrease in lime in them and the presence of a large number of pores.

IN spine the process involves one or more vertebrae in any of its parts, but the whole thing is never affected spinal column. The vertebrae increase in volume or, on the contrary, flatten, which depends on the stage of the disease. Foci of osteoporosis are found on the cuts and

osteosclerosis. Pelvic bones may also be involved in pathological process, which captures one or all bones.

Microscopic examination convinces us that the structural features of bone tissue in Paget's disease reflect its pathological restructuring. The mosaic structure of bone structures characteristic of Paget's disease is associated with the continuous change in the processes of resorption and construction of bone substance (Fig. 246). Small fragments of bone structures with uneven contours and wide, clearly defined basophilic adhesion lines are identified. The areas of bone fragments of the mosaic are usually well calcified, their structure is disordered, fine-fibrous or lamellar. Sometimes osteoid structures are found. In the deep lacunae of bone structures, a large number of osteoclasts and axillary resorption cavities are found. Along with this, signs of new bone formation are noted: expanded bone spaces are filled with soft fibrous tissue. Bone remodeling processes also involve vascular bed, usually the caliber of the feeding arteries is sharply increased, they acquire a sharp tortuosity.

Complications. Hemodynamic disorders, pathological fractures, development osteosarcoma. Hemodynamic disorders, associated with vasodilation in the affected bone tissue, in the skin over the lesions, can cause heart failure in patients with bone lesions of more than a third of the skeleton. Pathological fractures usually develop during the active phase of the disease. Osteogenic sarcoma develops in 1-10% of patients with deforming ostosis. Sarcoma is most often localized in the femur, tibia, pelvic bones, zygomatic bone, and scapula; primary multiple sarcomas have been described.

Rice. 246. Paget's disease. Mosaic bone structure (according to T.P. Vinogradova)

Joint diseases

Joint diseases may be associated with dystrophic (“degenerative”) processes structural elements joints (arthrosis) or their inflammation (arthritis). The synovium of the joint and cartilage can be a source of tumor (see. Tumors). Arthritis may be associated with infections(infectious arthritis), be a manifestation rheumatic diseases(cm. Systemic connective tissue diseases), metabolic disorders(For example, gouty arthritis, cm. Disorders of nucleoprotein metabolism) or other diseases (for example, psoriatic arthritis).

The most important among arthrosis is osteoarthritis, among arthritis - rheumatoid arthritis.

Osteoarthritis

Osteoarthritis- one of the most frequent illnesses joints of dystrophic (“degenerative”) nature. Elderly women are more often affected. Osteoarthritis is divided into primary (idiopathic) and secondary (for others, such as endocrine diseases). As you can see, osteoarthritis is a collective concept that unites a large number of diseases. However, there are no significant differences between primary and secondary osteoarthritis. The joints of the lower extremities are most often affected - the hip, knee, ankle, and somewhat less frequently - the large joints of the upper extremities. Usually the process simultaneously or sequentially involves several joints.

Etiology and pathogenesis. For the development of osteoarthritis, predisposing factors are important - hereditary and acquired. Among hereditary Factors of particular importance are attached to genetically determined metabolic disorders in articular cartilage, especially the disruption of the catabolism of its matrix. From acquired Mechanical injury plays a leading role.

Classification. Based on clinical and morphological manifestations, 3 stages of osteoarthritis are distinguished. In stage I, pain in the joints is noted during exercise, and x-rays reveal a narrowing of the joint space and osteophytes. In stage II, pain in the joints becomes constant, narrowing of the joint space and the development of osteophytes with x-ray examination more pronounced. In stage III, along with constant joint pain functional joint insufficiency is noted due to the development of subchondral sclerosis.

Pathological anatomy. Macroscopic changes in osteoarthritis depend on the stage of its development. In the early (I) stage, roughness and tissue disintegration appear along the edges of the articular cartilage. Later (stage II) on the articular surface of the cartilage they find patterns And lumps, bone growths are formed - osteophytes. In advanced (III) stage of the disease articular cartilage disappears on the bones of the joints

Dents form and the joints themselves become deformed. The intra-articular ligaments are thickened and loosened; the folds of the articular capsule are thickened, with elongated papillae. The amount of synovial fluid is sharply reduced.

Microscopic characteristics stages of osteoarthritis have been well studied (Kopyeva T.N., 1988). In stage I, articular cartilage retains its structure; in its superficial and intermediate zones, the content of glycosaminoglycans decreases. In stage II, shallow lesions appear in the superficial zone of the cartilage, along the edge of which chondrocytes accumulate, and the content of glycosaminoglycans in all zones of the cartilage decreases. If there are no abnormalities in the superficial zone of cartilage, then in the superficial and intermediate zones the number of “empty lacunae”, chondrocytes with pyknotic nuclei, increases. The subchondral part of the bone is also involved in the process. In stage III of osteoarthritis, the superficial zone and part of the intermediate zone of the cartilage die, deep lesions are found, reaching the middle of the intermediate zone; in the deep zone, the content of glycosaminoglycans is sharply reduced, the number of chondrocytes with pyknotic nuclei is increased. The damage to the subchondral part of the bone intensifies. In all stages of osteoarthritis, in the synovial membrane of the joints they find synovitis varying degrees of severity, lymphomacrophage infiltrate and moderate proliferation of fibroblasts are found in the synovium; as a result of synovitis, sclerosis of the stroma and vascular walls develops.

Rheumatoid arthritis

Rheumatoid arthritis- one of the most bright manifestations rheumatic diseases (see Systemic connective tissue diseases).

Skeletal muscle diseases

Among skeletal muscle diseases, the most common are diseases of striated muscle dystrophic (myopathies) and inflammatory (myositis) character. Muscles can be the source of a number of tumors (see. Tumors). Of particular interest among myopathy are progressive muscular dystrophy (progressive myopathy) and myopathy in myasthenia gravis.

Progressive muscular dystrophy(progressive myopathy) includes various primary hereditary chronic diseases of the striated muscles (they are called primary because there is no damage to the spinal cord and peripheral nerves). The diseases are characterized by increasing, usually symmetrical, muscle atrophy, accompanied by progressive muscle weakness, up to complete immobility.

Etiology and pathogenesis little studied. The significance of anomalies in structural proteins, sarcoplasmic reticulum, innervation, and enzymatic activity of muscle cells is discussed. Characterized by an increase in the activity of muscle enzymes in the blood serum, corresponding electrophysiological disorders in damaged muscles, and creatinuria.

Classification. Depending on the type of inheritance, age, gender of patients, localization of the process and course of the disease, there are 3 main forms of progressive muscular dystrophy: Duchenne, Erb and Leiden. The morphological characteristics of these forms of muscular dystrophy are similar.

Duchenne muscular dystrophy(early form) with a recessive type of inheritance associated with the X chromosome, usually appears at the age of 3-5 years, more often in boys. First, the muscles of the pelvic girdle, thighs and legs are affected, then the shoulder girdle and torso. Erb's muscular dystrophy(adolescent form) has an autosomal dominant type of inheritance and develops from puberty. The muscles of the chest and shoulder girdle, sometimes the face, are mainly affected (myopathic face - smooth forehead, insufficient eye closure, thick lips). Possible atrophy of the muscles of the back, pelvic girdle, proximal sections limbs. Muscular dystrophy Leiden with an autosomal recessive type of inheritance begins in childhood or during puberty and proceeds more quickly compared to the juvenile form (Erba), but more favorably than the early form (Duchenne). The process, starting with the muscles of the pelvic girdle and hips, gradually involves the muscles of the torso and limbs.

Pathological anatomy. Usually the muscles are atrophic, thinned, and depleted of myoglobin, so when cut they resemble fish meat. However, muscle volume can be increased due to the vacant growth of fatty tissue and connective tissue, which is especially typical for Duchenne muscular dystrophy (pseudohypertrophic muscular dystrophy).

At microscopic examination muscle fibers have different sizes: along with atrophic ones, there are sharply enlarged ones; the nuclei are usually located in the center of the fibers. Dystrophic changes in muscle fibers (accumulation of lipids, decrease in glycogen content, disappearance of cross-striations), their necrosis and phagocytosis are pronounced. Signs of regeneration are determined in individual muscle fibers. Accumulate between damaged muscle fibers fat cells. At severe course The disease reveals only single atrophic muscle fibers among extensive growths of adipose and connective tissue.

Ultrastructural changes in muscle fibers have been studied in more detail in Duchenne muscular dystrophy (Fig. 247). At the onset of the disease, expansion of the sarcoplasmic reticulum, foci

Rice. 247. Duchenne muscular dystrophy. Necrosis of muscle fiber with destruction of myofibrils. x 12,000

destruction of myofibrils, expansion of interfibrillar spaces in which the amount of glycogen increases, movement of nuclei to the center of the fiber. In the late stage of the disease, myofibrils undergo fragmentation and disorganization, mitochondria are swollen, the T-system is expanded; in muscle fibers the number of lipid inclusions and glycogen increases, and autophagolysosomes appear. At the end of the disease, the muscle fibers become denser, surrounded by a hyaline-like substance, and macrophages and fat cells appear around the necrotic muscle fibers.

Death In patients with severe progressive muscular dystrophy, it usually occurs from pulmonary infections.

Myasthenia gravis

Myasthenia gravis(from Greek myos- muscle, asthenia- weakness) is a chronic disease, the main symptom of which is weakness and pathological fatigue of the striated muscles. Normal muscle contraction after vigorous activity decreases in strength and volume and may stop completely. After rest, muscle function is restored. In an advanced stage of the disease, the rest time increases, creating the impression of muscle paralysis. With myasthenia gravis, any muscles of the body can suffer, but more often the muscles of the eyes (ptosis develops in 80% of cases), chewing, speech, and swallowing. In the extremities, the proximal muscles of the shoulder and thigh are most often affected. The respiratory muscles may also be affected.

The disease occurs at any age (peak incidence is 20 years), 3 times more often in women compared to men.

Etiology and pathogenesis. Etiology unknown. There is a correlation between anomalies thymus gland and myasthenia. Thymectomy often gives positive effect. The development of the disease is associated with a decrease of up to 90% in the number of acetylcholine receptors per unit of muscle plate, which is caused by autoimmune reactions. Antibodies to acetylcholine receptors were extracted from the thymus gland, they were found in the blood serum (in 85-90% of patients), using the immunoperoxidase method, IgG and C 3 were constantly detected in postsynaptic membranes. It is possible that not only antibodies, but also effector immune cells are involved in the blockade of acetylcholine receptors.

Pathological anatomy. In the thymus gland of patients with myasthenia gravis, follicular hyperplasia or thymoma is often found. Skeletal muscles are usually slightly changed or are in a state of dystrophy, sometimes their atrophy and necrosis, focal accumulations of lymphocytes among muscle cells are noted. Using immune electron microscopy, it is possible to detect IgG and C 3 in postsynaptic membranes. In the liver thyroid gland, adrenal glands and other organs find lymphoid infiltrates.

The skeleton and muscles are the supporting structures and organs of human movement. They perform a protective function by limiting the cavities in which they are located. internal organs. So, the heart and lungs are protected chest and muscles of the chest and back; abdominal organs (stomach, intestines, kidneys) - lower spine, pelvic bones, back and abdominal muscles; the brain is located in the cranial cavity, and spinal cord- in the spinal canal.

Bone

The bones of the human skeleton are formed by bone tissue, a type of connective tissue. Bone tissue is supplied with nerves and blood vessels. Its cells have processes. Bone cells and their processes are surrounded by tiny “tubules” filled with intercellular fluid, through which bone cells feed and respire.

General information about muscles

Muscles are made up of many elongated cells called muscle fibers that can contract and relax. A relaxed muscle can be stretched, but due to its elasticity, it can return to its original size and shape after stretching. The muscles are well supplied with blood, which supplies them with nutrients and oxygen and removes metabolic waste. Blood flow to the muscles is regulated in such a way that every this moment the muscle receives it in the required quantity.

There are three histological types of muscles:

• 1. Smooth muscles are located in the walls of the tubular organs of the body and ensure the movement of the contents of these organs; they slowly contract spontaneously. Smooth muscles are innervated by the autonomic nervous system.
• 2. Cardiac muscle, found only in the heart, contracts spontaneously and is not subject to fatigue. The cardiac muscle is innervated by the autonomic nervous system.
• 3. Skeletal muscles (striated muscles or voluntary muscles), attached to bones, they contract quickly and tire quite quickly. Skeletal muscles are innervated by the somatic nervous system.

The striated muscles are the most specialized apparatus for performing rapid contractions. There are two types of striated muscles - skeletal and cardiac.

Skeletal muscles are made up of long, thin muscle fibers. Skeletal muscles attach to bone in at least two places, one fixed and one movable part of the skeleton, the first of which is called the "origin" of the muscle, and the second the "insertion". The muscle is attached with the help of dense, low-extensibility tendons - connective tissue formations consisting almost exclusively of collagen fibers. One end of the tendon passes into outer shell muscles, and the other is very firmly attached to the periosteum.

Muscles are able to develop force only when shortened, so in order to displace a bone and then return it to its original position, it is necessary to at least, two muscles or two muscle groups. Pairs of muscles that act in this way are called antagonists.

Skeletal muscles are composed of muscle fibers, each of which is a multinucleated cell resulting from the fusion of a large number of cells. The functional unit of muscle fiber is the myofibril. Myofibrils occupy almost the entire cytoplasm of the muscle fiber, pushing the nuclei to the periphery

There are two types of skeletal muscle fibers.

red muscle fibers (type 1 fibers - tonic), which contain a large number of mitochondria with high activity of oxidative enzymes. The strength of their contractions is relatively small, and the rate of energy consumption is such that aerobic metabolism is sufficient for them. They are involved in movements that do not require significant effort, such as maintaining a pose. Smooth voluntary movements begin with the activation of red fibers. Slow (tonic) muscle fibers are located in the deep layers of the muscles of the limbs.

white muscle fibers (type 2 fibers - physical), which are characterized by high activity of glycolytic enzymes, significant contractile force and such a high rate of energy consumption for which aerobic metabolism is no longer sufficient. Therefore, motor units consisting of white fibers provide fast but short-term movements that require jerking efforts. Fast muscle fibers are located in the superficial layers of the muscles of the limbs.

Smooth muscles, unlike skeletal muscles, lack transverse stripes. They consist of long, pointed-ended cells that have only one nucleus and contain both thick and thin filaments oriented along the long axis of the cell. However, these filaments are not as ordered as in skeletal muscle cells and cardiac muscle cells, and apparently do not form myofibrils. Smooth muscles are specially adapted to maintain long-term tension, spending 5 to 10 times less ATP than would be needed to perform the same task. skeletal muscle. The slow formation and destruction of actin-myosin cross-links does not allow smooth muscle to contract quickly, but it gives it the opportunity to maintain constant muscle tone.