The main differences between cartilage tissues from each other. Types of cartilage in the human body

Consisting of cartilage cells (chondrocytes) and a large amount of dense intercellular substance. Acts as a support. Chondrocytes have a variety of shapes and lie singly or in groups within cartilage cavities. The intercellular substance contains chondrin fibers, similar in composition to collagen fibers, and the main substance, rich in chondromucoid.

Depending on the structure of the fibrous component of the intercellular substance, three types of cartilage are distinguished: hyaline (vitreous), elastic (mesh) and fibrous (connective tissue).

Cartilaginous tissue (tela cartilaginea) is a type of connective tissue characterized by the presence of a dense intercellular substance. In the latter, the main amorphous substance is distinguished, which contains compounds of chondroitinsulfuric acid with proteins (chondromucoids) and chondrin fibers, similar in composition to collagen fibers. fibrils cartilage tissue belong to the type of primary fibers and have a thickness of 100-150 Å. Electron microscopy in the fibers of the cartilaginous tissue, in contrast to the actual collagen fibers, reveals only an indistinct alternation of light and dark areas without a clear periodicity. Cartilage cells (chondrocytes) are located in the cavities of the ground substance singly or in small groups (isogenic groups).

The free surface of the cartilage is covered with dense fibrous connective tissue - the perichondrium (perichondrium), in the inner layer of which there are poorly differentiated cells - chondroblasts. The cartilaginous tissue of the perichondrium that covers the articular surfaces of the bones does not have. The growth of cartilage tissue is carried out due to the reproduction of chondroblasts, which produce the ground substance and later turn into chondrocytes (appositional growth) and due to the development of a new ground substance around chondrocytes (interstitial, intussusceptive growth). During regeneration, the development of cartilage tissue can also occur by homogenizing the basic substance of the fibrous connective tissue and converting its fibroblasts into cartilage cells.

Cartilage nutrition goes the way diffusion of substances from the blood vessels of the perichondrium. In the tissue of the articular cartilage, nutrients penetrate from the synovial fluid or from the vessels of the adjacent bone. Nerve fibers are also localized in the perichondrium, from where individual branches of amyopiatic nerve fibers can penetrate into the cartilaginous tissue.

In embryogenesis, cartilaginous tissue develops from mesenchyme (see), between the approaching elements of which layers of the main substance appear (Fig. 1). In such a skeletal rudiment, hyaline cartilage is first formed, temporarily representing all the main parts of the human skeleton. In the future, this cartilage can be replaced by bone tissue or differentiate into other types of cartilage tissue.

The following types of cartilage tissue are known.

hyaline cartilage(Fig. 2), from which cartilage is formed in humans respiratory tract, thoracic ends of ribs and articular surfaces of bones. In a light microscope, its main substance appears to be homogeneous. Cartilage cells or their isogenic groups are surrounded by an oxyphilic capsule. In differentiated areas of cartilage, a basophilic zone adjacent to the capsule and an oxyphilic zone located outside of it are distinguished; Together, these zones form a cellular territory, or chondrin ball. A complex of chondrocytes with a chondrin ball is usually taken as a functional unit of cartilage tissue - a chondron. The ground substance between chondrons is called interterritorial spaces (Fig. 3).

Elastic cartilage(synonym: reticulate, elastic) differs from hyaline by the presence of branching networks of elastic fibers in the ground substance (Fig. 4). The cartilage of the auricle, epiglottis, vrisberg and santorin cartilages of the larynx are built from it.

fibrocartilage(a synonym for connective tissue) is located at the transition sites of dense fibrous connective tissue into hyaline cartilage and differs from the latter by the presence of real collagen fibers in the ground substance (Fig. 5).

Cartilage pathology - see Chondritis, Chondrodystrophy, Chondroma.

Rice. 1-5. The structure of cartilage.
Rice. 1. Cartilage histogenesis:
1 - mesenchymal syncytium;
2 - young cartilage cells;
3 - layers of the main substance.
Rice. 2. Hyaline cartilage (small magnification):
1 - perichondrium;
2 - cartilage cells;
3 - the main substance.
Rice. 3. Hyaline cartilage (large magnification):
1 - isogenic group of cells;
2 - cartilage capsule;
3 - basophilic zone of the chondrin ball;
4 - oxyphilic zone of the chondrin ball;
5 - interterritorial space.
Rice. 4. Elastic cartilage:
1 - elastic fibers.
Rice. 5. Fibrous cartilage.

cartilage tissue

General characteristics: relatively low level metabolism, lack of vessels, hydrophilicity, strength and elasticity.

Structure: chondrocyte cells and intercellular substance (fibers, amorphous substance, interstitial water).

Lecture: CARTILAGE TISSUE

Cells ( chondrocytes) make up no more than 10% of the cartilage mass. The bulk of the cartilage tissue is intercellular substance. The amorphous substance is quite hydrophilic, which allows nutrients to be delivered to the cells by diffusion from the capillaries of the perichondrium.

Differon chondrocytes: stem, semi-stem cells, chondroblasts, young chondrocytes, mature chondrocytes.

Chondrocytes are derivatives of chondroblasts and the only population of cells in cartilage, located in lacunae. Chondrocytes can be divided according to the degree of maturity into young and mature. Young retain the structural features of chondroblasts. They have an oblong shape, developed GREP, a large Golgi apparatus, are able to form proteins for collagen and elastic fibers and sulfated glycosaminoglycans, glycoproteins. Mature chondrocytes are oval or round in shape. The synthetic apparatus is less developed when compared with young chondrocytes. Glycogen and lipids accumulate in the cytoplasm.

Chondrocytes are capable of dividing and form isogenic groups of cells surrounded by a single capsule. In hyaline cartilage, isogenic groups can contain up to 12 cells, in elastic and fibrous cartilage - a smaller number of cells.

Functions cartilaginous tissues: supporting, formation and functioning of joints.

Classification of cartilage tissues

There are: 1) hyaline, 2) elastic and 3) fibrous cartilage tissue.

Histogenesis . In embryogenesis, cartilage is formed from mesenchyme.

1st stage. Formation of a chondrogenic island.

2nd stage. Differentiation of chondrroblasts and the beginning of the formation of fibers and cartilage matrix.

3rd stage. Cartilage growth in two ways:

1) Interstitial growth- due to an increase in tissue from the inside (formation of isogenic groups, accumulation of the extracellular matrix), occurs during regeneration and in the embryonic period.

2) Apposition growth- due to tissue layering due to the activity of chondroblasts in the perichondrium.

Cartilage regeneration . When cartilage is damaged, regeneration occurs from the cambial cells in the perichondrium, with the formation of new layers of cartilage. Full regeneration occurs only in childhood. Adults are characterized by incomplete regeneration: PVNST is formed in place of the cartilage.

Age changes . Elastic and fibrocartilage are resistant to damage and change little with age. Hyaline cartilage tissue can undergo calcification, sometimes transforming into bone tissue.

Cartilage as an organ consists of several tissues: 1) cartilaginous tissue, 2) perichondrium: 2a) outer layer - PVNST, 2b) inner layer - RVST, with blood vessels and nerves, and also contains stem, semi-stem cells and chondroblasts.

1. Hyaline cartilage

Localization: cartilages of the nose, larynx (thyroid cartilage, cricoid cartilage, arytenoid, except for the vocal processes), trachea and bronchi; articular and costal cartilages, cartilaginous growth plates in tubular bones.

Structure: cartilage cells, chondrocytes (described above) and an intercellular substance consisting of collagen fibers, proteoglycans and interstitial water. Collagen fibers(20-25%) consist of type II collagen, arranged randomly. proteoglycans, making up 5-10% of the mass of cartilage, are represented by sulfated glycosaminoglycans, glycoproteins that bind water and fibers. Hyaline cartilage proteoglycans prevent its mineralization. interstitial water(65-85%) provides incompressibility of the cartilage, is a shock absorber. Water promotes efficient metabolism in cartilage, carries salts, nutrients, metabolites.

articular cartilage is a type of hyaline cartilage, does not have a perichondrium, receives nutrition from the synovial fluid. In the articular cartilage, there are: 1) a superficial zone, which can be called acellular, 2) a middle (intermediate) zone containing columns of cartilage cells, and 3) a deep zone in which the cartilage interacts with the bone.

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2. ELASTIC CARTILAGE

Localization: auricle, cartilages of the larynx (epiglottic, corniculate, sphenoid, as well as the vocal process at each arytenoid cartilage), Eustachian tube. This type of tissue is necessary for those parts of organs that are able to change their volume, shape and have reversible deformation.

Structure: chondrocytes cartilage cells (described above) and intercellular substance consisting of elastic fibers (up to 95%) fibers and amorphous substance. For visualization, dyes are used that reveal elastic fibers, such as orcein.

3. FIBROUS CARTILAGE

Localization: fibrous rings of intervertebral discs, articular discs and menisci, in the symphysis (pubic articulation), articular surfaces in the temporomandibular and sternoclavicular joints, at the sites of attachment of tendons to bones or hyaline cartilage.

Structure: chondrocytes (often singly) of an elongated shape and an intercellular substance consisting of a small amount of amorphous substance and a large amount of collagen fibers. The fibers are arranged in orderly parallel bundles.

All our bones in the process of embryonic (embryonic) development are formed from cartilage. In an adult, they make up no more than 2% of body weight. Bones grow thanks to the diaphyseal cartilage, they lengthen until the so-called growth zones are closed1. However, some of them increase throughout a person's life. It has been established that constantly growing, albeit at a slow pace, lower jaw, nose, auricles, feet and hands.

Most often, athletes leave the sport due to injuries of the articular-ligamentous apparatus. His weakness- cartilage. Problems with the spine are also mainly due to the pathology of the intervertebral cartilage.
It can be said that cartilage treatment is the No. 1 concern in sports traumatology. At the same time, some authors believe that cartilage is restored by no more than 50%, thus casting doubt on the possibility of a complete restoration of sports performance. Let's try to consider in more detail what cartilage is and determine the limits and methods of its regeneration.

Cartilage is a type of connective tissue that performs supporting functions in the body. An indispensable attribute of cartilage, with the exception of articular cartilage, is the perichondrium, which provides its nutrition and growth. In the joints, the cartilage is exposed and is in direct contact with the internal environment of the joint - the synovial fluid. It acts as a kind of lubricant between the rubbing surfaces of the joints, covered with smooth gliai cartilage. The cartilage of the bones and spine is constantly experiencing both static and dynamic loads. The cartilages of the nose, larynx, bronchi, fibrous triangles in the heart also perform a supporting function.

The structure of the cartilage allows it to experience reversible deformation and at the same time retain the ability to metabolize and reproduce. Its main components are cartilage cells (hendrocytes) and an extracellular matrix consisting of fibers and ground substance. Moreover, most of the mass of cartilage is precisely the intercellular substance.
Depending on the predominance of collagen, elastic fibers or the ground substance, hyaline, elastic and fibrous cartilage are distinguished.

A feature of cartilage, in comparison with other types of tissues in the body, is that there are few cells in it and they are surrounded by a large amount of intercellular space - the matrix. Cartilage recovers so poorly after damage precisely because there are very few cells in it that can multiply and the main part of the repair (recovery) comes from the extracellular matrix. The elastic cartilage (larynx, nose, auricle) contains a lot of elastin (for example, 30% of the human ear consists of it).

There is a lot of water in the articular cartilage (in the cartilage of the head of the femur young man- 75 g per 100 g of tissue). Glauronic acid helps the matrix bind water, which ensures the elastic and elastic properties of the tissue.
In hyaline cartilage, which most often represents the intraarticular surface, half of the entire matrix is ​​collagen, the main protein of connective tissue. Only the tendons and dermis (deep layer of the skin) surpass the matrix in terms of collagen saturation. Its highest concentration in articular cartilage is concentrated in the superficial zone.
Collagen is a collective concept, there are several types of it. Different in chemical composition, all of them, nevertheless, consist of very large molecules, folded into triple helixes. This structure of the fibers makes them very resistant to twisting, stretching and tearing. Each of the three chains has a polypeptide structure.
If we analyze the composition of the polypeptide chains of any of the three types of collagen (in humans, there are exactly three of them), we will see that the specific gravity of the amino acid glycine is the largest. It is followed in terms of specific gravity by the amino acids promen (proline -?) and alanine. Sometimes alanine "outweighs" proline, and sometimes vice versa, proline surpasses alanine in its specific gravity.

Elastic cartilage (for example, nose and ears) contains in its matrix mainly elastin, which, like collagen, forms strong fibers. They are thinner than collagen, but they are very durable. Fabrics containing a large amount of elastin are capable of very large reversible deformations. The main amino acid of elastin (as well as collagen) is glycine. It is followed in percentage by alanine, proline and valine.
Elastin, like collagen, has several types. Elastin fibers also have a peptide character and a spiral shape. This explains their great extensibility. The helix, however, is not triple, but single, so elastin fibers are thinner than collagen ones. In different cartilages, either collagen or elastin fibers predominate in the matrix. All of them are intertwined in a strong three-dimensional network. The collagen (elastin) network “holds” other molecules inside the cartilage, both mechanically and with the help of electrostatic bonds.

The biomechanical properties of cartilage make them highly specific and essentially unique components of the musculoskeletal system.
They:
a) take on the action of external mechanical forces of compression and tension; distribute these forces evenly, absorb and dissipate them, converting axially directed forces into tangential ones (in the joints of the limbs, spine, etc.);
b) form wear-resistant surfaces of the joints of the skeleton, participate in the formation of a lubricating apparatus in synovial joints;
c) are the place of attachment and support for soft tissues and muscles; form cavities at the points of contact with the external environment (cartilage of the nose, ears, respiratory organs).

It is believed that the cartilage matrix consists of 3 main components:
1) a fibrous collagen scaffold that forms a three-dimensional network of weaves;
2) proteoglycan molecules that fill the loops of the fibrous framework;
3) water moving freely between the tangles of the scaffold and proteoglycan molecules.

Articular cartilage has no blood vessels. It feeds diffusely, absorbing nutrients from the synovial fluid.

The collagen framework is, as it were, the "skeleton" of cartilage. It has a high elasticity in relation to tensile forces and at the same time has a relatively weak resistance to compressive loads. Therefore, intra-articular cartilage (for example: menisci and articular surfaces of the femur and tibia) are easily damaged under compressive (compressive) loads and almost never under tensile loads ("break").
The proteoglycan component of the matrix is ​​responsible for the ability of cartilage to bind water. It can be removed outside the cartilage into the synovial fluid and return to it back. It is water as an incompressible substance that provides sufficient rigidity to the cartilage. Its movement evenly distributes the external load throughout the cartilage, resulting in the weakening of external loads and the reversibility of deformations arising under loads.

The elastic cartilages of the larynx and trachea contain a very small number of vessels. The collagen cartilage of the joints does not contain vessels at all. A large mechanical load on the cartilage is incompatible with vascularization (vascular supply). The exchange in such cartilage is carried out due to the movement of water between the components of the matrix. It contains all the metabolites necessary for cartilage. Therefore, both anabolic and catabolic processes are sharply slowed down in them. Hence their poor post-traumatic recovery, in contrast to cartilage with vascularization.
In addition to gliain and elastic cartilage, another group is distinguished - fibrous, or fibrous cartilage. Fibrosis means "fiber". The matrix of fibrous cartilage is formed by collagen fibers, however, compared to, say, gliai cartilage, the bundles of collagen fibers are thicker and do not have a three-dimensional weave structure. They are oriented, basically, parallel to each other. Their direction corresponds to the vectors of tension and pressure forces. Intervertebral discs are composed of fibrous cartilage and are highly durable. Large collagen fibers and their bundles are located in the intervertebral discs circularly. In addition to the intervertebral discs, fibrocartilage is found at the points of attachment of tendons to bones or cartilage, as well as at the articulation of the pubic bones.
The maintenance of the entire structural integrity of the cartilage matrix depends entirely on chondrocytes. And although their mass is small, they nevertheless synthesize all the biopolymers that make up the matrix - collagen, elastin, proteoglycones, glycoproteins, etc. With a specific gravity of 1 to 10% of the total volume of cartilage tissue, chondrocytes provide the formation of large masses of matrix. They also control all catabolic reactions in the cartilage.

What is the reason for the low metabolic activity of cartilage? Only in one - in a small number of cells (1-10%) per unit volume of tissue. In terms of pure cell mass, the metabolic rate of chondrocytes is no less than that of other body cells. Articular cartilages and pulpal nuclei of intervertebral discs are especially characterized by low metabolism. It is these structures that are distinguished by the smallest number of chondrocytes (1% of the total mass of cartilage) and it is they that are the worst to recover from damage.

Oxidative processes in cartilage proceed mainly in an anaerobic (oxygen-free) way. So, for example, chondrocytes of the pulpous nuclei of intervertebral discs are 99% anaerobic and only 1% aerobic. On average, oxygen oxidation in cartilage tissue is at least 50 times less intense than in normal body tissues. The anaerobic nature of oxidation in chondrocytes is a protective and adaptive reaction that has developed in the course of evolution. And this is not surprising, given that the cartilage has no (glainous, fibrous) or almost no (elastic) blood supply. If you start introducing oxygen into the space bordering the cartilage, then O2 diffusion into the cartilage not only does not improve its trophism, but, on the contrary, sharply worsens it.

How low the metabolic activity of cartilage is can be understood from the following comparison. The protein composition of the liver is completely renewed in 4 (!) days. Cartilage collagen is renewed by only 50% in 10 (!) years. Therefore, it becomes clear that any injury to the cartilage tissue is practically incurable, unless special measures are taken to increase the number of chondrocytes that will form a new matrix.

Cartilage tissue regeneration, both physiological and reparative (restorative), directly depends on hormonal background and modulating action of certain hormones. For example, glucocorticoid hormones inhibit anabolic reactions in chondrocytes, inhibit the synthesis of collagen and proteoglycans, and cause a deficiency of glauronic acid in the synovial fluid and matrix. And this inhibitory effect of glucocorticoids is more pronounced if it is combined with compression (compression) of the cartilage. In principle, this is not surprising, given that glucocorticoids inhibit glycolysis - anaerobic oxidation of glucose in cartilage. Regeneration without energy supply becomes simply impossible. Insulin stimulates collagen synthesis in the cartilage matrix, but this stimulation is small and indirect.

The strongest factor stimulating both physiological and reparative synthesis in cartilage tissue is somatotropic hormone. There is no affinity of cartilage for somatotropic hormone as such. However, under the action of somatotropic hormone, an insulin-like growth factor (IGF-1) is formed in the liver, which has its own anabolic effect on all tissues, including cartilage. By itself, growth hormone is able to have an anabolic effect on cells only if its concentration is 2000 times higher than physiological. This is possible only in a test tube and is completely excluded in real life. When using somatotropin for reparative purposes, it must be remembered that its effect on the synthesis of IGF-1 is possible only under conditions of normal liver function, in the absence of serious diseases, otherwise IGF-1 simply will not be synthesized and the introduction of somatotropin will not give any result. The ability of somatomedin to enhance the regeneration of cartilage tissue is 100 times greater than the effect of the introduction of insulin and testosterone into the body. IGF-1 is the only factor that causes division (multiplication) of chondrocytes. Other anabolic factors of the body (and there are quite a lot of them) do not have this ability.

Thyroid hormones can enhance the repair and physiological growth of cartilage when used in small amounts close to physiological. Then they have an anabolic effect on all tissues of the body. In the middle and large quantities thyroid hormones have an even greater anabolic effect, however, they also cause an energy deficit (thermogenic effect) and increased catabolism.
At the same time, catabolism is enhanced to a greater extent than anabolism, and the activity of destructive processes exceeds the synthetic activity. No matter how much anabolism increases with increasing doses of thyroid hormones, catabolism increases even more and this must be remembered.
Thyrocalcitonin is the only thyroid hormone that enhances the restoration and growth of cartilage tissue in any amount, but for this it must be used in isolation, separately from thyroxine and triyedironin, the “main” thyroid hormones.
The parathyroid hormone (parathyroid hormone) has a moderately stimulating effect on cartilage regeneration.

Testosterone, the main androgen of the body, moderately stimulates biosynthetic processes in cartilage, and estrogens, female sex hormones, on the contrary, inhibit it.
Anabolic steroids have the ability to induce cartilage regeneration to a much greater extent than pure testosterone, and this is not surprising, given that they have an anabolic effect several times greater than the anabolic effect of testosterone.

It is interesting that the matrix - the product of chondrocytes - lives its own independent life. It is able to modulate the action of various hormones on chondrocytes, weakening or enhancing their action. By acting on the matrix, it is possible to change the state of chondrocytes, both for the better and for the worse. Removal of a part of the matrix causes an immediate intensification of the biosynthesis of macromolecules missing in it. Moreover, at the same time, proliferation (growth) of chondrocytes is enhanced. Quantitative changes in the matrix can cause their qualitative changes.
Prolonged restriction of movement in the joint (gypsum immobilization, etc.) leads to a decrease in the mass of cartilage. The reason is surprisingly simple: there is no mixing of synovial fluid in an immobile joint. At the same time, the diffusion of molecules into the cartilage tissue slows down and the nutrition of chondrocytes worsens. The lack of a direct compressive load (on compression) also leads to a deterioration in the nutrition of chondrocytes. Cartilage needs at least a minimal compression load to maintain normal trophism. Excessive tensile load in the experiment causes cartilage degeneration with the development of coarse fibrous fibers.

The synovial membrane has a very complex effect on the state of intraarticular cartilage. It can both enhance the anabolism of cartilage tissue and enhance its catabolism. Removal of the synovial membrane sharply worsens the trophism of cartilage, which is restored only after its growth.
Chondrocytes are also capable of autoregulation. They synthesize special growth factors that stimulate the growth of neighboring chondrocytes. Until their structure is fully deciphered. It is only known that they have a polypeptide nature.

All cartilages, but especially the cartilages of the musculoskeletal system, are constantly exposed to microtrauma. First of all, this applies to the intervertebral discs, the most vulnerable part of which is the nucleus pulposus. Already in adolescence (starting from the age of 16), dystrophic changes begin in the intervertebral discs of the cervical spine. In terms of a unit of cross section, it bears a load much greater than any other part of the spine, including the lumbar. First of all, dystrophic changes concern the nucleus pulposus. Some of its cells die and are replaced by coarse connective tissue. Similar, but less pronounced changes occur in the intervertebral disc itself. In places, focal proliferation of chondrocytes occurs. The body seeks to restore damaged cartilage and starts reparative processes. However, in the places of death of chondrocytes there is a coarse fibrous connective tissue - a kind of scar. And just in it, where they are needed, chondrocytes cannot recover. Their growth occurs along the periphery of the scar tissue, where they are, in fact, not needed. This leads to unnecessary deformation of the cartilage, which further impairs its function. The main function of cartilage is supporting and stabilizing. With the development of degenerative and dystrophic processes in the intervertebral discs, the vertebrae lose their stability and gradually become hypermobile, easily displaced. Their hypermobility can cause compression of the surrounding soft tissues. Edema of soft tissues, in turn, causes compression of the vessels and nerves passing through them with the development of corresponding symptoms. The body seeks to restore the stability of the articular-ligamentous apparatus. There is an overgrowth of individual sections of the vertebrae in the form of a kind of bone outgrowths - "whiskers". These "whiskers" squeeze nearby soft tissues, causing their swelling and secondary compression of nearby vessels and nerves. The whole complex of changes in the osteochondral apparatus in this case is called osteochondrosis, although this term is very vague, non-specific, and, in fact, unscientific.

If in cervical region spine negative phenomena develop with adolescence, then in lumbar, where the load per unit of cross section is much lower - starting from 25-30 years. In general, they have the same morphological character as in the cervical region, but differ in clinical (medical) signs. In the cervical spine, large arteries pass through the transverse processes of the cervical vertebrae, feeding the entire base of the brain and its stem part, where the vital centers (respiration, blood circulation, etc.) are located. With development cervical osteochondrosis there is a gradual imperceptible squeezing of these arteries with the development of cerebrovascular insufficiency. At the same time, there are practically no (or they are very rare) any pain signs of the process. In the lumbar spine, the picture is somewhat different. Nerve roots come out of this department, carrying sensory fibers from lower extremities and motor fibers to the leg muscles. Lumbar osteochondrosis is primarily manifested by various pain symptoms, impaired sensitivity and motor sphere. At the same time, no vital important functions it does not harm the body. Cervical osteochondrosis does not reveal itself with any pain signs and does not cause any particular inconvenience, however, it can lead to serious disorders of cerebral circulation, up to strokes with the development of paralysis.

Cervical osteochondrosis is manifested by a variety of symptoms that can simulate other diseases. The deterioration of cerebral circulation is manifested by a decrease in efficiency, fatigue, headache. Tired eyes, flies before the eyes, a feeling of "sand in the eyes" are characteristic features cervical osteochondrosis. Ringing in the ears and hearing impairment are more likely to indicate cerebrovascular accident due to osteochondrosis than about diseases of the hearing aid. According to the latest data, 85% of all cerebral hemorrhages at a later age are not caused by age-related arterial pathology as such, but by compression of the cervical arteries as a result of widespread cervical osteochondrosis.

Age-related changes in elastic cartilage are not fatal. They are expressed mainly in ossification - the accumulation of calcium and do not lead to any noticeable dysfunction.
In the gliamine cartilage of the joints, already starting from the age of 30, fibrillation is detected - defibration of the cartilaginous surface. Microscopic examination reveals fractures and splits on the surface of the cartilage. Cartilage splitting occurs both vertically and horizontally. At the same time, in places there are accumulations of cartilage tissue cells as a response of the body to the destruction of cartilage. Sometimes there is an age-related increase (!) in the thickness of the articular cartilage as a response to the actions of mechanical (training) factors. Many researchers note the age evolution of the cartilage of the knee joint starting from the age of 40. The most significant change seen with cartilage aging is a decrease in water content, which automatically leads to a decrease in its strength.

Hence the extreme complexity of his post-traumatic treatment. Moreover, sometimes it is not easy even to maintain the normal state of the cartilage during the normal training process. Height muscle tissue ahead of the strengthening of the articular-ligamentous apparatus and especially its cartilaginous part. Therefore, sooner or later, the loads reach such a value that the cartilaginous part of the musculoskeletal system can no longer withstand. As a result, there are "inevitable" hard-to-heal injuries, due to which the athlete sometimes leaves the sport. Self-healing cartilage is never complete. In the best case, the cartilage is restored by 50% of its original value. However, this does not mean that its further restoration is impossible. It is possible with a competent pharmacological effect, designed to cause, on the one hand, the reproduction of chondrocytes, and on the other hand, a change in the state of the cartilage matrix. The problem of cartilage restoration is greatly complicated by the fact that scar tissue develops in place of the dead cartilage tissue. It does not allow cartilage to regenerate in the right place. Compensatory growth of cartilage areas in the vicinity of the injury site leads to its deformation, making it difficult to stimulate growth pharmacologically. However, all these difficulties can be overcome if the deformed cartilage is first subjected to surgical correction.

The potential for cartilage regeneration is quite large. It can regenerate at the expense of its own potential (proliferation of chondrocytes and growth of the matrix) and, no less important, at the expense of other types of connective tissue that have a common origin with it. The tissues adjacent to the cartilage have the ability to reorient their cells and turn them into cartilage-like tissue, which copes well with its functions. Take for example the most common type of damage - damage to intra-articular cartilage.

The source of regeneration are:
1) the cartilage itself;
2) the synovial membrane of the joint, growing from the edges of the defect and turning into a cartilage-like tissue;
3) bone cells, which, let's not forget, are of cartilage origin and, if necessary, can be transformed "back" into a tissue resembling cartilage in its structure;
4) bone marrow cells, which can serve as a source of regeneration in case of deep cartilage damage in combination with bone damage.

Immediately after injury, there is an "explosion" of mitotic activity of chondrocytes, which multiply and form a new matrix. This process is observed within 2 weeks after the injury, however, remodulation of the cartilage surface lasts at least 6 months, and completely stops only after a year. The quality of the "new" cartilage, of course, is inferior to the quality of the "old". If, for example, the hyaline intra-articular cartilage is damaged, then after 3-6 months a regenerate grows, which has the character of a hyaline-fibrous young cartilage, and after 8-12 months, it already turns into a typical fibrous cartilage with a matrix consisting of tightly adjacent to each other collagen fibers.
All researchers of cartilage tissue are unanimous in one thing: cartilage is not able to restore what has been lost only at the expense of its own internal resources and mechanisms. They are enough for a maximum of 50% regenerate. Some more growth of the regenerate is carried out at the expense of other types of connective tissue, which we have already talked about, but it is still not necessary to speak of a complete 100% restoration of cartilage. All this contributes a fair amount of pessimism to the assessment of the possibility of recovery after any serious cartilage injury, but there are still reasons for optimism. The achievements of pharmacology and transplantology today are such that we can talk about the complete compensation of even very serious cartilage defects, no matter how laborious it may be.

The completeness of the restoration of damaged cartilage tissue largely depends on the quality of the post-traumatic period, when a hematoma is still being formed1. Then it is impregnated with a special kind of protein - fibrin, sweating from the blood plasma, and turns into scar tissue. And it, as we know, is a serious obstacle to the development of a full-fledged regenerate in this particular place. Therefore, immediately after an injury, everything must be done. possible measures to prevent the development of hematoma and soft tissue edema. Cool the injured area. To do this, it is covered with ice, irrigated with chlorethylene. If the joint of the limb is damaged, then it can simply be placed under the jet cold water. The timely assistance of a qualified traumatologist is very important. Local novocaine blockades not only anesthetize the injured area, but also prevent the development of edema and inflammation. Blockades can be repeated until the acute period has passed. If, as a result of a bruised joint, a hemorrhage occurred in its cavity - hemarthrosis, then it is necessary to pump out the blood from the joint as soon as possible. This is easy to do with a regular syringe. Sometimes it is necessary to pump out blood and transudate (fluid that leaks into the joint cavity from blood plasma) several times in a row. In no case should you wait until the blood "resolves itself." A blood clot as a result of the loss of a special kind of protein - fibrin, a large amount of scar tissue can develop. The damaged joint may remain deformed and enlarged. A sad example is the “kentus” of those who practice karate. Broken finger joints increase in size due to hemorrhages and remain enlarged due to the fact that blood is not pumped out of them in time. Despite their intimidating appearance, fists with broken joints are much weaker than normal fists and are very easily damaged by repeated injury.

In the subacute period, when soft tissue edema and pain are significantly reduced, care must be taken to resolve the damaged tissue as completely as possible. For this purpose, it uses proteolytic enzymes (trypsin, cheleotrypsin, papain, etc.), which are introduced into the damaged area using electrophoresis. A good effect is given by glucocorticoid hormones - hydrocortisone, prednisolone, etc. Like proteolytic enzymes, they are injected locally, into the affected area - whether it be the intervertebral disc or the joints of the extremities. Hydrocortisone is administered by ultrasound, and prednisolone is administered by electrophoresis. Sometimes injected glucocorticoid hormones into the cavity of the joints, for example, in the treatment of injuries of the knee joint. He has the most complex structure and it is very difficult to treat his injuries. Menisci - intra-articular cartilage in the knee joints with damage practically do not grow together. Therefore, if there are tears or tears of parts of the menisci, they must be removed as soon as possible. It is easier to “grow” a regenerate in place of the removed meniscus (and such a regenerate will definitely grow) than to achieve healing of the damaged meniscus. Fortunately, in last years arthroscopy has been widely developed and operations on the knee joint are becoming more and more sparing. The arthroscope allows using fiber optics to look inside the joint without opening it (only a few holes are made). Surgery is also performed through the arthroscope. Sometimes it happens that as a result of an injury, the meniscus remains intact, but breaks away from its place of attachment. If earlier such a meniscus was always removed, now more and more specialists appear who sew the torn meniscus back into place. After refreshing the edges of the wound, the sutured meniscus grows into place.

If arthroscopy reveals defibration of certain cartilaginous surfaces, then they are polished, “bitten” with special wire cutters, fibers and areas of deformed cartilage. If this is not done, then subsequent measures taken to enhance the regeneration of cartilage tissue can lead to the growth of deformed cartilage and disruption of its supporting functions.

With superficial injuries, complete restoration of the cartilage can be achieved using potent pharmacological agents. Over the past 40 years of experimental and clinical work, only one single drug has proved its high efficiency - somatotropic hormone (GH). It stimulates the growth of cartilage tissue 100 times stronger than the introduction of testosterone and insulin. An even greater effect is exerted by the combined administration of growth hormone and thyrocalcitonin, a special kind of thyroid hormone that enhances the repair of both bone and cartilage tissue. The exceptional effectiveness of the effect of growth hormone on cartilage repair is due to the fact that it directly stimulates the division of chondrocytes. Using STH, it is theoretically possible to bring the number of chondrocytes to any the right amount. They, in turn, restore the matrix to the required volume, synthesizing all its components, from collagen fibers to proteoglycans. The disadvantage of STH is that it cannot be applied topically, injected directly into the affected area of ​​cartilage tissue, since it acts indirectly. STH causes the formation of insulin-like growth factor (IGF-1) in the liver, which has the strongest anabolic effect. Its parenteral (injection) administration causes the growth of not only damaged cartilage, but also normal ones, and this is undesirable, because there are bones in the body in which cartilaginous growth zones do not close throughout life. Prolonged administration of large doses of growth hormone into a mature organism can cause skeletal imbalances. Although it should be noted that it acts more strongly on the affected cartilage, and there are no obvious skeletal deformities in the treatment of GH in the scientific literature.

In recent years, a dosage form of IGF-1 has been synthesized, which is increasingly being used by injection instead of somatotropin. Since IGF-1 acts directly on tissues (including cartilage), there is a tempting prospect of using it for local administration (electrophoresis, ultrasound, etc.). Such use of IGF-1 would allow to localize its action at the site of the affected cartilage and exclude the effect on healthy cartilage of the body.
Anabolic steroids (AS) have a good effect on the restoration of cartilage and the surrounding connective tissue. In terms of efficiency, they are in second place after IGF-1 and somatotropic hormone, although they do not directly cause chondrocyte division. Anabolic steroids, however, accelerate physiological regeneration and potentiate the anabolic action of insulin and other endogenous anabolic factors, block the action of catabolic hormones (glucocorticoids). The practical use of AS in surgical and traumatological practice has proved their high efficiency. It is a pity that it has not yet been developed dosage forms AC for local use. This would make it possible to create high concentrations of the drug exactly at the site of damage and prevent systemic (at the level of the whole organism) side effects. Unfortunately, research in this area is not funded by anyone due to the inclusion of AS among doping drugs in sports.

Some researchers in the field of molecular biology have presented very convincing material proving that stimulants (2-adrenergic receptors) are able to simulate the anabolic effects of somatomedins and, in particular, in relation to cartilage tissue. The mechanism of this action is not entirely clear. It is possible that it simply increases the sensitivity liver to endogenous somatotropic hormone and increases the synthesis in the liver of IGF-1. One of the most powerful selective stimulants (2-adrenergic receptors is clenbuterol. This drug does not have hormonal effects and, at the same time, has a good anabolic effect. Like IGF-1 it stimulates the growth of cartilaginous tissue and can be successfully used in the post-traumatic recovery period.There are many stimulating drugs (2-adrenergic receptors, but I would especially like to note such an old and proven remedy as adrenaline. Adrenaline, the hormone of the adrenal medulla, does not cause addiction. In high doses, adrenaline acts mainly on a-adrenergic receptors. There is a narrowing of the vessels of the skin, an increase in blood pressure, an increase in blood sugar levels. Small doses of adrenaline do not affect a-adrenergic receptors, stimulate (2-adrenergic receptors. Muscle vessels expand, blood sugar levels decrease and arterial pressure. A general anabolic effect develops and, in particular, in relation to cartilage tissue. The daily administration of small (precisely small!) doses of adrenaline has proven itself as a means of promoting regeneration.

Some vitamins in large pharmacological dosages can significantly increase the release of endogenous somatotropin into the blood. The palm here is held by nicotinic acid (vitamin PP). Intravenous administration of relatively small doses of nicotinic acid can increase the basal secretion of growth hormone by 2-3 times. Increases the secretion of growth hormone vitamin K, only it must be used in moderate doses so as not to increase excessive blood clotting.

Despite the fact that the cartilage matrix is ​​a derivative of chondrocytes, changing its state can improve their activity. The state of the matrix can be improved by using large doses of ascorbic acid in combination with vitamin P. Ascorbic acid has a particularly strong effect on the state of collagen structures. Therefore, it is traditionally used to enhance collagen synthesis, especially in combination with glycine and anabolic steroids. A combination of large doses of ascorbic acid with lysine, alanine and proline is also used.
The state of the cartilage matrix of the intra-articular cartilage can be temporarily improved with the help of substances introduced into the synovial fluid. In recent years, the introduction of a 15% solution of polyvinylpyrrolidone into the joint has been especially widely used, where it stays for about 5-6 days, then the procedure is repeated, sometimes several times. Polyvinylpyrrolidone serves as a kind of temporary "prosthesis" of the intraarticular fluid. It improves the friction of the intra-articular surfaces, temporarily relieving the load from the articular cartilage. In cases of severe, irreversible damage to the cartilage tissue, prosthetics are used, which, with the development of operational technology, gives more and more encouraging results. You will not surprise anyone with intervertebral disc prostheses. Unsuccessful attempts are being made to replace intra-articular cartilage (menisci) knee joints.
A very promising direction is the introduction of chondrocyte suspensions into damaged areas. Weak regeneration of cartilage tissue, as we remember, is due to a small number of cartilage cells (chondrocytes) per unit mass of cartilage tissue. Alien chondrocytes, being introduced, say, into the joint cavity do not cause a rejection reaction, because have weak immunogenic activity. They are able to multiply and form new cartilage tissue. Apply a suspension of chondrocytes obtained from the cartilage of cattle, dead people. The most promising is the use of embryonic (germ) cartilage cells. They do not cause an immune response at all and, multiplying, cause the formation of new cartilage tissue. Unfortunately, all work with germ cells is still experimental in nature and has not entered into widespread practice. But this is a matter of the near future. The problem of cartilage tissue repair should soon be solved. There are already all the prerequisites for this.

1 The cessation of the growth of most bones in length can be an indication that treatment is already possible, for example, with anabolic steroids, which lead to premature closure of the growth zone of the cartilage, if the growth zones of the node are closed, (which is clear from the x-ray of the radius of a young man), then there is no longer a danger of closing the growth zones of steroid use too quickly, which means that their use can begin.

1 Literally, this means “blood tumor”, but the term does not quite correspond to the essence of the phenomenon. A hematoma is a diffusely damaged tissue swollen with blood.

From Muscle Nutrition Review #8

Cartilaginous tissue (textus cartilaginus) forms articular cartilages, intervertebral discs, cartilages of the larynx, trachea, bronchi, external nose. Cartilage tissue consists of cartilage cells (chondroblasts and chondrocytes) and a dense, elastic intercellular substance.

Cartilage contains about 70-80% water, 10-15% organic matter, 4-7% salts. About 50-70% of the dry matter of cartilage tissue is collagen. The intercellular substance (matrix) produced by cartilage cells consists of complex compounds, which include proteoglycans. hyaluronic acid, glycosaminoglycan molecules. There are two types of cells in the cartilaginous tissue: chondroblasts (from the Greek chondros - cartilage) and chondrocytes.

Chondroblasts are young, capable of mitotic division, rounded or ovoid cells. They produce components of the intercellular substance of cartilage: proteoglycans, glycoproteins, collagen, elastin. The cytolemma of chondroblasts forms many microvilli. The cytoplasm is rich in RNA, a well-developed endoplasmic reticulum (granular and non-granular), the Golgi complex, mitochondria, lysosomes, and glycogen granules. The chondroblast nucleus, rich in active chromatin, has 1-2 nucleoli.

Chondrocytes are mature large cartilage cells. They are round, oval or polygonal, with processes, developed organelles. Chondrocytes are located in cavities - lacunae, surrounded by intercellular substance. If there is one cell in the gap, then such a gap is called primary. Most often, the cells are located in the form of isogenic groups (2-3 cells) occupying the cavity of the secondary lacuna. The walls of the lacunae consist of two layers: the outer one, formed by collagen fibers, and the inner one, consisting of aggregates of proteoglycans that come into contact with the glycocalyx of cartilage cells.

The structural and functional unit of cartilage is the chondron, formed by a cell or an isogenic group of cells, a pericellular matrix, and a lacuna capsule.

Cartilage tissue is nourished by diffusion of substances from the blood vessels of the perichondrium. In the tissue of the articular cartilage, nutrients penetrate from the synovial fluid or from the vessels of the adjacent bone. Nerve fibers are also localized in the perichondrium, from where individual branches of amyopiatic nerve fibers can penetrate into the cartilaginous tissue.

In accordance with the structural features of the cartilage tissue, there are three types of cartilage: hyaline, fibrous and elastic cartilage.

hyaline cartilage, from which the cartilages of the respiratory tract, the thoracic ends of the ribs and the articular surfaces of the bones are formed in humans. In a light microscope, its main substance appears to be homogeneous. Cartilage cells or their isogenic groups are surrounded by an oxyphilic capsule. In differentiated areas of cartilage, a basophilic zone adjacent to the capsule and an oxyphilic zone located outside of it are distinguished; Together, these zones form a cellular territory, or chondrin ball. A complex of chondrocytes with a chondrin ball is usually taken as a functional unit of cartilage tissue - a chondron. The ground substance between chondrons is called interterritorial spaces.
Elastic cartilage(synonym: mesh, elastic) differs from hyaline by the presence of branching networks of elastic fibers in the main substance. The cartilage of the auricle, epiglottis, vrisberg and santorin cartilages of the larynx are built from it.
fibrocartilage(a synonym for connective tissue) is located at the transition points of dense fibrous connective tissue into hyaline cartilage and differs from the latter by the presence of real collagen fibers in the ground substance.

7. Bone tissue - location, structure, functions

Bone tissue is a type of connective tissue and consists of cells and intercellular substance, which contains a large amount of mineral salts, mainly calcium phosphate. Minerals make up 70% of bone tissue, organic - 30%.

Functions of bone tissue:

1) support;

2) mechanical;

3) protective (mechanical protection);

4) participation in the mineral metabolism of the body (depot of calcium and phosphorus).

Bone cells - osteoblasts, osteocytes, osteoclasts. The main cells in the formed bone tissue are osteocytes. These are process-shaped cells with a large nucleus and weakly expressed cytoplasm (nuclear-type cells). The cell bodies are localized in the bone cavities (lacunae), and the processes are located in the bone tubules. Numerous bone tubules, anastomosing with each other, penetrate the bone tissue, communicating with the perivascular space, form the drainage system of the bone tissue. This drainage system contains tissue fluid, through which the exchange of substances is ensured not only between cells and tissue fluid, but also in the intercellular substance.

Osteocytes are definitive forms of cells and do not divide. They are formed from osteoblasts.

osteoblasts found only in developing bone tissue. In the formed bone tissue, they are usually contained in an inactive form in the periosteum. In developing bone tissue, osteoblasts surround each bone plate along the periphery, tightly adhering to each other.

The shape of these cells can be cubic, prismatic and angular. The cytoplasm of osteoblasts contains a well-developed endoplasmic reticulum, the Golgi lamellar complex, many mitochondria, which indicates a high synthetic activity these cells. Osteoblasts synthesize collagen and glycosaminoglycans, which are then released into the extracellular space. Due to these components, an organic matrix of bone tissue is formed.

These cells provide mineralization of the intercellular substance through the release of calcium salts. Gradually releasing the intercellular substance, they seem to be walled up and turn into osteocytes. At the same time, intracellular organelles are significantly reduced, synthetic and secretory activity is reduced, and the functional activity characteristic of osteocytes is preserved. Osteoblasts localized in the cambial layer of the periosteum are in an inactive state; synthetic and transport organelles are poorly developed in them. When these cells are irritated (in case of injuries, bone fractures, etc.), a granular EPS and a lamellar complex rapidly develop in the cytoplasm, active synthesis and release of collagen and glycosaminoglycans, the formation of an organic matrix (bone callus), and then the formation of a definitive bone fabrics. In this way, due to the activity of osteoblasts of the periosteum, bones regenerate when they are damaged.

osteoclasts- bone-destroying cells are absent in the formed bone tissue, but are contained in the periosteum and in places of destruction and restructuring of bone tissue. Since local processes of bone tissue restructuring are continuously carried out in ontogeny, osteoclasts are also necessarily present in these places. In the process of embryonic osteohistogenesis, these cells play a very important role and are present in in large numbers. Osteoclasts have a characteristic morphology: these cells are multinucleated (3-5 or more nuclei), have a rather large size (about 90 microns) and a characteristic shape - oval, but the part of the cell adjacent to the bone tissue has a flat shape. In the flat part, two zones can be distinguished: the central (corrugated part, containing numerous folds and processes), and the peripheral part (transparent) in close contact with the bone tissue. In the cytoplasm of the cell, under the nuclei, there are numerous lysosomes and vacuoles of various sizes.

The functional activity of the osteoclast is manifested as follows: in the central (corrugated) zone of the cell base, carbonic acid and proteolytic enzymes are released from the cytoplasm. The released carbonic acid causes demineralization of bone tissue, and proteolytic enzymes destroy the organic matrix of the intercellular substance. Fragments of collagen fibers are phagocytosed by osteoclasts and destroyed intracellularly. Through these mechanisms, resorption (destruction) of bone tissue occurs, and therefore osteoclasts are usually localized in the depressions of bone tissue. After the destruction of bone tissue due to the activity of osteoblasts, which are evicted from the connective tissue of the vessels, a new bone tissue is built.

intercellular substance bone tissue consists of the main (amorphous) substance and fibers, which contain calcium salts. The fibers consist of collagen and are folded into bundles, which can be arranged in parallel (orderly) or randomly, on the basis of which the histological classification of bone tissues is built. The main substance of bone tissue, as well as other types of connective tissues, consists of glycosamino- and proteoglycans.

The bone tissue contains less chondroitin sulfuric acids, but more citric and others, which form complexes with calcium salts. In the process of bone tissue development, an organic matrix is ​​first formed - the main substance and collagen fibers, and then calcium salts are deposited in them. They form crystals - hydroxyapatites, which are deposited both in an amorphous substance and in fibers. Providing bone strength, calcium phosphate salts are also both a depot of calcium and phosphorus in the body. Thus, bone tissue takes part in the mineral metabolism of the body.

When studying bone tissue, one should also clearly separate the concepts of “bone tissue” and “bone”.

Bone is an organ whose main structural component is bone tissue.

Classification of bone tissue