X-ray signs of bone and joint diseases

Radiodiagnosis of musculoskeletal diseases is a fascinating and at the same time very complex area of knowledge. Over 300 diseases and anomalies of bone and joint development have been described. Each disease is characterized by a certain dynamics - from initial manifestations, often elusive during radiological examination, to gross deformations and destruction. In addition, the pathological process can develop both in the entire skeleton and in almost any of the 206 bones that make it up. The symptoms of the disease are affected by age-related features of the skeleton, the properties of the pathogen, numerous regulatory, including endocrine, influences. In connection with the above, it is clear how heterogeneous the radiographs of each patient are, how thoughtfully the doctor must consider the totality of anamnestic, clinical, radiological and laboratory data in order to make the correct diagnosis.

Systemic and widespread lesions

Systemic and widespread lesions are based on one of 5 pathological conditions:

1. developmental anomalies of the musculoskeletal system;
2. disorder of protein, vitamin or phosphorus-calcium metabolism;
3. damage to other organs and systems (endocrine glands, blood system, liver, kidneys);
4. generalized tumor processes;
5. exogenous intoxications (including iatrogenic effects, such as treatment with steroid hormones).

Congenital developmental disorders occur in utero. After birth, they may progress, but mainly as long as the growth and differentiation of the musculoskeletal system continues. Some of these anomalies are latent and are accidentally detected during X-ray examination, while others cause significant skeletal dysfunction. Systemic anomalies affect the condition of the entire musculoskeletal system, but the damage to certain parts is most pronounced. If the developmental disorder occurs during the formation of the connective tissue skeleton, various types of fibrous dysplasia occur, and if during the formation of the cartilaginous skeleton, cartilaginous dysplasia (dyschondroplasia) occurs. Many anomalies are associated with disorders that occur during the replacement of the cartilaginous skeleton with bone (bone dysplasia). These include isolated and combined defects of enchondral, periosteal and endosteal ossification.

Radiographic symptoms of systemic and widespread anomalies are varied. Among them are changes in the size, shape and structure of bones. For example, such cartilaginous dysplasia as chondrodystrophy is characterized by disproportionately short and dense bones of the limbs with flared metaphyses and massive epiphyses. In such a defect as arachnodactyly, on the contrary, the tubular bones are excessively elongated and thin. In multiple cartilaginous exostoses, bizarre protrusions consisting of bone and cartilaginous tissue appear on the surface of the limb bones. In bone chondromatosis, radiographs show cartilaginous inclusions of various shapes in the expanded metaphyses of long tubular bones.

Anomalies of endosteal ossification often manifest themselves in compaction of bone tissue. The observer is struck by marble disease; in it, the bones of the skull, vertebrae, pelvic bones, proximal and distal femurs are very dense, in the images they seem to be made of ivory and structureless. And in such a defect as osteopoikilosis, multiple islands of compact bone substance are determined in almost all bones.

Endocrine and metabolic disorders manifest themselves in a delay or change in the normal growth of bones in length and systemic osteoporosis. Rickets is a classic example of such disorders. The bones are very sparse and often curved, since they cannot withstand normal loads. The metaphyseal sections of the bones are expanded in the form of a saucer, their ends facing the epiphysis have the appearance of a fringe. Between the metaphysis and the epiphysis there is a wide light stripe, which is the sum of the growth cartilage and osteoid substance, which was not calcified in time. Exogenous intoxications most often lead to systemic osteoporosis, but when salts of heavy metals enter the child's body, a transverse intense darkening strip is found in the distal part of the metaphyses. A peculiar picture can be observed with prolonged penetration of fluoride compounds into the body: the images show systemic sclerosis of the bones, reminiscent of marble disease. In clinical practice, systemic skeletal lesions are most often observed in tumor lesions: cancer metastases to bone, myeloma, leukemia, lymphoblastoma, including lymphogranulomatosis. In all these diseases, tumor foci can form in the bone marrow, which lead to the destruction of bone tissue. While the destruction is small, they can be detected mainly by osteoscintigraphy. When the foci increase, they are determined on radiographs as areas of destruction. Such foci are called osteolytic.

Bone tissue sometimes responds to the formation of tumor nodules with a pronounced osteoblastic reaction. In other words, a zone of sclerosis forms around the cancer nodules. Such foci do not cause defects on radiographs, but foci of compaction in the bones, which are called osteoblastic metastases. They are easy to distinguish from developmental anomalies in which dense osteosclerotic islands form in bone tissue: the latter, in contrast to tumor metastases, do not concentrate the radiopharmaceutical during osteoscintigraphy.

It is worth mentioning another disease that often takes on a systemic character - deforming osteodystrophy (Paget's disease). Its characteristic manifestation is the reorganization of the bone structure, primarily a peculiar thickening and at the same time fraying of the cortical layer: it is as if divided into rough bone plates. The tubular bones are deformed, their medullary canal is blocked by the image of curved and thickened bone beams intersecting in different directions. In the bones of the cranial vault and pelvis, usually thickened, shapeless areas of sclerosis are observed, sometimes alternating with bone tissue defects. The cause of this disease has not been established, but its radiographic picture is typical and usually serves as a reliable basis for diagnosis.

Osteoporosis is one of the most common and at the same time important systemic diseases of the skeleton. Rotteg first described the clinical picture of osteoporosis and isolated it from osteomalacia in 1885. However, only in 1940, after the work of the famous American osteologist F. Albright and representatives of his school, this disease became known to a wide range of doctors. Osteoporosis acquired particular relevance in the 60s due to a significant increase in the number of elderly people and, no less importantly, due to the development of methods for radiological diagnostics of this disease. The social significance of osteoporosis is especially great, since it is the most common cause of fractures in middle-aged and especially elderly people. Thus, 17% of men and 32% of women aged 80 years experience hip fractures, 20% of them die, 25% become disabled.

Systemic osteoporosis is a skeletal condition characterized by decreased bone mass and microarchitectural abnormalities of bone tissue, leading to increased bone fragility and risk of fractures.

Most likely, osteoporosis should be considered not as a separate nosological form, but as a uniform response of the skeleton to the influence of various endogenous and exogenous factors.

First of all, it is necessary to clearly distinguish primary osteoporosis (it is also called senile or involutional). One of its varieties is postmenopausal (presenile) osteoporosis of women. Juvenile idiopathic osteoporosis (fish vertebrae disease) is rare. Secondary osteoporosis occurs as a consequence of various diseases or some types of drug therapy.

Osteoporosis, both primary and secondary, must be distinguished from osteomalacia (demineralization of the skeleton due to the influence of various factors with the preserved structure of the organic matrix of the bone), hypostasis (insufficient formation of bone tissue during skeletal development) and physiological age-related atrophy.

Risk factors for osteoporosis include a family history of the disease, female gender, late onset of menstruation, early or surgically induced menopause, lack of calcium in the diet, caffeine and alcohol use, smoking, treatment with corticosteroids, anticoagulants, anticonvulsants, methotrexate, repeated fasting to reduce body weight ("dietary weight loss"), and hypermobility. There is a special type of "osteoporotic people" - short, thin women with blue eyes and light hair, freckles, and hypermobility of the joints. Such women appear to have aged prematurely.

In understanding osteoporosis as a pathological condition of the skeleton, it is important to study the dynamics of bone mineralization throughout a person's life. As is known, in both sexes, bones are formed until approximately 25 years of age, but in women, the amount of bone mass is 13% less than in men. Starting from the age of 40, cortical bone mass decreases in men by an average of 0.4%, in women by 1% annually. Thus, the total loss of compact substance by the age of 90 reaches 19% in men and 32% in women. The dynamics of spongy substance is different: its loss begins much earlier than compact substance - from 25-30 years, at the same rate in men and women - on average 1% per year. The total loss of spongy substance by the age of 70 reaches 40%. Bone mass decreases especially quickly in women in the postmenopausal period.

X-ray diagnostics of osteoporosis includes a number of research methods. First of all, it is necessary to perform an X-ray of the spine in two projections, pelvic bones, skull and hands. X-ray signs of osteoporosis are increased transparency of bones and deformation of vertebrae, ranging from mild to severe ("fish vertebrae"). It should be noted, however, that visual assessment of bone transparency by X-ray is very subjective: the human eye is able to assess the change in transparency of the X-ray only when the bone mass decreases by at least 30-40%. In this regard, various quantitative methods for assessing the mineral density of bone tissue are more important.

In recent years, radionuclide and X-ray densitometric absorption methods for determining bone density have been introduced into clinical practice. Several key indicators are distinguished.

• Bone mineral content (BMC), measured in grams per 1 cm (g/cm).
• Bone mineral density (BMD), measured in grams per 1 cm ² (g/cm ² ).
• Bone mineral volume density (BMVD), measured in grams per 1 cm3 ⁽ g/ ^cm3 ).

The most accurate indicator is the BMV. However, the BMD index is more important, as it better matches the increase in fracture risk, therefore it has a greater prognostic value. The BMVD indicator is currently used relatively rarely, as its receipt requires computed tomography with a very complex and expensive data processing program.

In accordance with WHO recommendations, the following division of osteoporosis and osteopenia is adopted.

• Norm. The BMD and IUD values are not higher than 1 SD - the standard square deviation obtained during the examination of the reference group of young subjects.
• Decreased bone mass (osteopenia). BMC and BMD values are within 1 to 2.5 SD.
• Osteoporosis. BMD and BMC values exceed 2.5 SD.
• Severe (stable) osteoporosis. BMD and BMC values are greater than 2.5 SD, and there is a single fracture or multiple bone fractures.

Currently, there are several quantitative methods for determining skeletal mineralization. In single-photon absorptiometry, ^{125 I is used as a radiation source, which has a gamma-quantum energy of 27.3 keV, while for two-photon absorptiometry,153} Gd is used as a radiation source with a quantum energy of 44 and 100 keV. However, single-photon X-ray absorptiometry is the most popular. This study is carried out on special compact X-ray attachments: the distal part (cortical bone content 87%) and the epiphysis (trabecular bone content 63%) of the forearm bones are studied.

The most advanced and widespread method is dual-photon X-ray absorptiometry. The essence of the method is a comparative analysis of two peaks of X-ray radiation energy (usually 70 and 140 keV). Using a computer, the parameters of the IUD and BMD are determined in individual "zones of interest" - usually in the lumbar vertebrae, forearm bones and proximal femur. At present, this method is the main diagnostic test in organizing screening for the purpose of identifying involutional osteoporosis in the elderly and women in the pre- and postmenopausal period. Detection of reduced skeletal mineralization allows for timely therapy and reduces the risk of fractures.

Quantitative computed tomography is used to determine the mineralization of the skeleton, mainly the spine, forearm and tibia. The fundamental feature of the method is the ability to determine the mineralization of spongy bone, which is known to be the earliest to be absorbed in osteoporosis. A new direction in CT has become volumetric analysis of skeletal mineralization, using the most indicative index - BMVD (g/cm ³ ) as a unit of measurement. This has made it possible to significantly increase the accuracy of measurement, especially in the vertebrae and femoral neck.

Quantitative measurement of skeletal mineralization using ultrasound biolocation allows us to determine unique bone parameters, in particular its architectural properties, such as elasticity, trabecular fatigue, and bone structure anisotropy. New areas of MRI include obtaining high-resolution magnetic resonance images of bone trabecular structure. The main advantage of this study is the unique opportunity to study the architectonics of bone trabecular substance with the establishment of a number of important parameters: the ratio of trabeculae and bone marrow spaces, the total length of trabeculae per unit of bone surface, quantitative characteristics of the degree of bone pattern anisotropy, etc.

Focal bone lesions

A large group of focal lesions are local changes in bones caused by inflammatory processes of various natures. Among them, osteomyelitis and tuberculosis, as well as arthritis, are of particular practical importance.

Osteomyelitis is an inflammation of the bone marrow. However, having started in the bone marrow, the inflammatory process spreads to the surrounding bone tissue and periosteum, i.e. it includes both ostitis and periostitis. Depending on the origin of the disease, a distinction is made between hematogenous and traumatic (including gunshot) osteomyelitis.

Acute hematogenous osteomyelitis begins suddenly. The patient has a high body temperature, chills, rapid pulse, headache and vague pain in the area of the affected bone. The clinical picture is supplemented by neutrophilic leukocytosis in the peripheral blood and an increase in ESR. Despite the pronounced clinical picture, no changes in the bones are determined on radiographs during this period. Other radiation methods must be used to confirm clinical data and initiate treatment in a timely manner. In the first hours of the disease, radionuclide examination of the skeleton reveals increased accumulation of RFP in the affected area. Sonography can detect the presence of fluid (pus) under the periosteum relatively early, and later - an abscess in soft tissues. Clinical and radiological data are the basis for early antibiotic therapy in large doses. MRI opens new prospects in the diagnosis of osteomyelitis. Tomograms directly detect bone marrow damage.

With successful treatment, bone changes may not appear on radiographs at all and the process ends with recovery. However, in most cases, hematogenous osteomyelitis is accompanied by pronounced radiographic symptoms, which are detected mainly by the end of the 2nd week after the acute onset of the disease (in children - by the end of the 1st week). If the area of inflammation is located deep in the bone, the earliest radiographic signs are local osteoporosis and small foci of bone tissue destruction (destructive foci). Initially, they can be detected on CT and MRI scans. On radiographs, enlightenment, a kind of "porosity" with vague uneven outlines are determined in the spongy bone tissue of the metaphysis of a tubular bone or in a flat bone.

If the inflammation is localized subperiosteally, the first radiographic symptom is periosteal stratification. A narrow strip of calcified periosteum appears along the bone edge at a distance of 1-2 mm from its surface. The outer contour of the cortical layer in this area becomes uneven, as if eaten away.

Subsequently, small destructive foci merge into larger ones. In this case, bone fragments of different sizes and shapes separate from the edges of the deteriorating bone, float in pus, become necrotic and turn into sequesters, which in turn support inflammation. Periosteal layers grow, their outlines become uneven (fringed periostitis). Consequently, in the acute phase of the disease, the processes of destruction, necrosis and purulent inflammation of tissues predominate. Their radiographic reflection is destructive foci, sequesters and periosteal layers.

Gradually, signs of reactive inflammation around the necrotic areas, delimitation of inflammation foci and symptoms of the reparative osteoblastic process appear in the X-ray picture. Bone destruction stops, the edges of destructive foci become sharper, and an osteosclerosis zone appears around them. Periosteal layers merge with the bone surface (these layers are assimilated by the cortical layer). The course of osteomyelitis becomes chronic.

Purulent masses often find an outlet on the body surface - a fistula is formed. The best way to examine a fistula is its artificial contrasting - fistulography. A contrast agent is introduced into the external fistula opening, after which X-rays are taken in two mutually perpendicular projections, and, if necessary, CT scans. Fistulography allows you to determine the direction and course of the fistula, the source of its formation (sequester, purulent cavity, foreign body), the presence of branches and purulent leaks.

Unfortunately, chronic osteomyelitis cannot always be cured by a single surgical intervention. The disease is prone to relapses. They are signaled by recurring pain, increased body temperature, and changes in the blood. Radionuclide examination is an effective method for detecting relapses. Radiographs reveal new destructive foci and “fresh” periosteal layers.

The radiographic picture of gunshot osteomyelitis is more varied and difficult to interpret. Radiographs taken after the injury show a gunshot fracture of the bone. Within 10 days after the injury, the fracture gap increases, regional osteoporosis is noted, but these symptoms are observed after any fracture and cannot be used as a basis for diagnosing osteomyelitis. Only at the beginning of the 3rd week and especially towards the end of it, small foci of destruction appear at the edges of the fragments, which can be distinguished from local osteoporosis due to their uneven distribution, blurred outlines, and the presence of small sequesters in the center of the foci. Purulent inflammation leads to necrosis and separation of bone sections. The size and shape of the sequesters vary: small pieces of spongy bone tissue, oblong plates of compact bone substance, part of the epiphysis or diaphysis may separate. Against the background of osteoporosis, sequesters stand out as denser areas that have lost their connection with the surrounding bone.

In the first weeks of the disease, as in hematogenous osteomyelitis, the processes of necrosis, destruction and melting of tissues predominate. The formation of bone callus is sharply impaired, as a result of which the consolidation of fragments is delayed, and under unfavorable circumstances a false joint may form. However, timely antibiotic therapy and surgical intervention prevent such an outcome. When acute inflammatory phenomena subside, proliferative processes intensify. Destructive foci gradually decrease and disappear, and areas of sclerosis are found in their place. Periosteal layers become smooth, and gaps in them are eliminated. Eventually, these layers merge with the bone, which as a result thickens. The ends of the fragments are fixed with bone callus. Usually, radiographs can detect clearings in the sclerotic bone. Some of them are bordered by a thin closing plate and represent fibrous-osteoid fields, others are surrounded by sclerotic bone and are residual cavities walled up in the sclerotic zone. They can be the cause of recurrent osteomyelitis.

Tuberculous bone lesions occur as a result of the transfer of Mycobacterium tuberculosis from a primary focus in the lung or, less commonly, in the intestine to the bone marrow. A tuberculous granuloma forms in the bone marrow, which leads to the resorption and destruction of bone trabeculae. Such a granulation focus forms in the epiphysis and is usually not clinically manifested or its symptoms are weakly expressed. On radiographs, it causes a single area of enlightenment or a group of adjacent foci with uneven outlines. With a favorable course, the granulation tissue turns into fibrous and is subsequently replaced by bone. In caseous necrosis with calcification of the bone, a compacted focus can be detected.

Under less favorable circumstances, the growing granulation tissue replaces the bone beams, and one or more large destructive foci are determined. In the center of such a focus, a spongy bone sequestrum often appears. Gradually, the edges of the foci become denser, and they turn into bone caverns. Unlike hematogenous osteomyelitis caused by staphylococcus or streptococcus, in tuberculous osteomyelitis, reparative phenomena develop slowly. This is explained, in particular, by the location of the focus in the epiphysis. Periosteal layers are weakly expressed, since the periosteum in this area is thin and weak.

Due to localization in the epiphysis, the tuberculous process very often moves to the joint. Up to this point, the disease is in the so-called prearthritic phase, but the spread of granulation tissue along the synovial membrane steadily leads to the development of tuberculous arthritis (arthritic phase of the disease), undoubtedly the main stage of tuberculous damage.

Clinically, the onset of the arthritic phase is marked by a gradual impairment of joint function, the appearance or increase of pain, and slowly progressing muscle atrophy. Osteoscintigraphy and thermography allow us to establish the involvement of the joint in the pathological process even before the appearance of radiographic symptoms. The first of these is osteoporosis. If in tuberculous osteomyelitis osteoporosis is local and is determined only in the area of developing tuberculous foci, then in arthritis it becomes regional. This means that osteoporosis affects an entire anatomical area - the joint ends and adjacent bone sections.

Direct signs of arthritis include narrowing of the X-ray joint space and destructive foci. The latter are often detected as small erosions in the places where the joint capsule and ligaments attach to the bony part of the epiphysis. The contours of the end plates of both epiphyses become uneven, thinning in places, and becoming sclerotic in places. The foci of destruction cause a disruption in the nutrition of the epiphysis areas, which become necrotic (necrotic) and separate.

The attenuation of tuberculous arthritis is reflected on radiographs by the replacement of small destructive foci with bone tissue, compaction and sclerotic delimitation of large foci. The X-ray joint space remains narrowed, but the contours of the end plates of the epiphyses are restored and become continuous. Gradually, the disease passes into the postarthritic phase (metuberculosis osteoarthrosis), when stabilization of the altered tissues occurs. It can be stable for many years. Osteoporosis remains, but acquires new features: in accordance with the new load conditions, the longitudinal bone beams thicken in the bones. They stand out sharply against the background of sparse bone. Such osteoporosis is called reparative. The cortical layer of the bones thickens.

Among focal inflammatory lesions, one cannot ignore panaritiums - acute purulent inflammatory processes in the tissues of the fingers. Radiographs are extremely important to exclude or confirm the development of a bone or osteoarticular panaritium and to distinguish it from an isolated lesion of soft tissues. With a bone panaritium, osteoporosis of the bone phalanx is determined already 5-8 days after the onset of the disease and small destructive foci begin to appear. Small sequesters may join this. A narrow strip of exfoliated periostitis appears along the edges of the affected phalanx. The foci of destruction develop mainly at the attachment sites of the joint capsule, which is why the process often spreads to the interphalangeal joint. Its gap narrows, and foci of bone tissue destruction also appear at the other end of the joint.

Osteoarticular panaritium is an example of how any purulent arthritis looks in typical cases. It is characterized by the following radiographic signs: narrowing of the X-ray joint space (uneven and rapidly progressing), destructive foci in the articular surfaces of the articulating bones, regional osteoporosis, an increase in the volume of the joint. An increased concentration of radiopharmaceuticals in osteoscintigraphy, signs of destruction of articular cartilage in sonography and CT complement this picture.

In recent decades, rheumatoid arthritis has become widespread - a chronic relapsing systemic disease that occurs with predominant damage to the joints. It is characterized by a progressive course and disorders in the body's immune system. A special immunoglobulin, the rheumatoid factor, is found in the blood of patients. Rheumatoid arthritis can only be conditionally classified as a focal lesion, since radiographic changes can be determined in several joints.

In the initial period of the disease, radiographs of impeccable quality are indistinguishable from those in the norm, so other radiation methods of examination have a clear advantage. Osteoscintigrams demonstrate increased accumulation of radiopharmaceuticals in the area of the affected joints. Sonograms reflect thickening of the synovial membrane, the appearance of fluid in the joint, changes in the articular cartilage, the development of synovial cysts, the degree of periarticular edema.

Later, radiographic symptoms of rheumatoid arthritis appear. First of all, this is swelling of the soft tissues of the joint, osteoporosis and a slight narrowing of the joint space. Then, erosions (small marginal defects in the articular ends of the bones) and rounded racemose enlightenments in the epiphyses are added to this. These defects, as well as the violation of the integrity of the end plate, are revealed earlier and more clearly using radiography with direct magnification of the image. As the process progresses, further narrowing of the joint space, a significant increase in the severity of osteoporosis and new foci of destruction in the bone tissue of the epiphyses are observed, as a result of which severe destruction with subluxations and ugly deformation of the articular ends of the bones can develop.

In the absence of a rheumatoid factor, we speak of seronegative arthritis, which includes many joint lesions. Some of them arise as a local manifestation of a systemic disease of connective tissue (systemic lupus erythematosus, periarteritis nodosa, scleroderma, etc.), a complication of liver and intestinal diseases, uric acid diathesis (gout). Others are special nosological forms: Reiter's syndrome, psoriatic arthritis, ankylosing spondylitis (Bechterew's disease). Their recognition and sometimes difficult differential diagnosis are based on a combination of clinical, laboratory and radiological data. It is important to note that most often the most significant symptoms are detected during radiography of the affected joint, as well as small joints of the hands and feet, sacroiliac joints and spine.

It is advisable to pay attention to the very frequently observed lesions of ligaments and tendons. They are divided into fibroostoses (tendinoses) and fibroostitis (tendinitis). In fibroostosis, there is no increased accumulation of RFP in the affected area, and radiographs may show ossification of the ligament attachment sites and bone protrusions (osteophytes). These protrusions have smooth contours and a bone structure. Fibroostitis is an inflammatory process. It often accompanies rheumatic diseases and seronegative spondylitis. The protrusions on the bones have an irregular shape, sometimes not clearly outlined. A marginal defect may be determined at the ligament attachment site. RFP is intensely concentrated in the affected area. Typical examples of tendinitis are scapulohumeral periarthritis and Achilles bursitis, as well as calcaneal fibroostitis of rheumatic origin.

Another large group of focal lesions of bones and joints are dystrophic processes and aseptic necrosis. Dystrophic changes develop mainly in the joints and essentially represent premature wear of the articular cartilage (in the spine - intervertebral cartilage). Cartilage particles that lose their normal state and die have antigenic properties and cause immunopathological changes in the synovial membrane. Joint overload leads to secondary, including compensatory, reactions in the bone tissue of the epiphyses.

The radiographic picture of dystrophic joint damage is quite stereotypical. It consists of the following main symptoms: narrowing of the radiographic joint space, compaction and expansion of the end plate of the epiphyses, sclerosis of the subchondral layer of bone tissue (i.e. the layer lying under the end plate), bone growths along the edges of the articular surfaces. In general, this process is called "deforming osteoarthrosis".

Deforming osteoarthrosis is observed very often and can affect any joint. The most widespread are degenerative-dystrophic diseases of the spine, and among them - osteochondrosis. The radiation semiotics of this condition was described above. A large group of patients are people with deforming arthrosis of the hip and knee joints, interphalangeal joints of the hand and the 1st metatarsophalangeal joint. In recent years, surgical methods of treating osteoarthrosis have been widely used, in particular, replacing the deformed articular end of the bone with a prosthesis.

The group of aseptic necroses includes various pathological processes. They are brought together by three common features:

1. development of aseptic necrosis of bone matter and bone marrow;
2. chronic benign course;
3. natural clinical and morphological evolution with a relatively favorable outcome.

An overload of a particular section of the skeleton plays a major role in the genesis of the disease. If the overload concerns the entire bone, then aseptic necrosis of the entire bone develops (for example, the navicular bone of the foot). If the entire epiphysis is overloaded, then necrosis of this epiphysis or its part occurs. An example is the most frequently observed type of aseptic necrosis - damage to the head of the femur. Overload of a part of the diaphysis leads to the formation of the so-called remodeling zone, and overload of the apophysis - to its necrosis.

The radiographic picture of aseptic necrosis can be conveniently described using the example of the head of the femur of a child (this type of aseptic necrosis is called osteochondropathy of the femoral head or Legg-Calve-Perthes disease). The child complains of mild pain. Limited joint function is noted. Early diagnosis is extremely important, but pathological changes are not visible on radiographs. The main thing during this period is to use special techniques. Osteoscintigraphy allows us to detect increased accumulation of radiopharmaceuticals in the head of the femur, and CT and MRI make it possible to directly detect the area of necrosis of the bone substance and bone marrow.

Later, radiographic symptoms appear. The affected bone area is distinguished on the images as a denser lesion, devoid of bone structure. This is mainly due to multiple fractures and compression of bone beams, which leads to deformation of the epiphysis - its flattening and unevenness of outlines.

In this phase, differential diagnostics of aseptic necrosis and tuberculosis of the joint plays an extremely important role, since in the latter, necrosis of the bone substance also occurs in the joint end. However, the reference points for differentiation are quite solid: in tuberculosis, the joint space narrows, and in aseptic necrosis in a child, it widens. In tuberculosis, the second joint end is also affected (in our example, the acetabulum), and in aseptic necrosis, it remains intact for a long time. Later, the differentiation becomes even simpler. In aseptic necrosis, the dead area is broken up into several dense bone islands (fragmentation), the epiphysis flattens even more, the joint space widens and a slight subluxation is observed.

The earlier the disease is recognized, the more favorable its consequences. The bone structure of the epiphysis is restored, it remains only slightly deformed. The joint space is slightly widened. However, if the disease is detected late, the joint remains defective due to the deformations that occur in it.

In adults, aseptic necrosis of the part of the head that is usually most heavily loaded, i.e. the upper-outer part of the epiphysis, is observed. In these cases, the joint space does not widen, subluxation does not occur, arthrosis always develops, and fragments of dead cartilage or bone can penetrate into the joint cavity, turning into joint "mice". Frequently observed focal skeletal lesions include bone tumors. They are conventionally divided into benign and malignant, although benign neoplasms are almost always not true tumors, but local developmental defects.

Depending on the structure and tissue composition, benign tumors include formations from bone tissue (osteomas), connective tissue (fibromas), cartilage (chondromas), cartilage and bone tissue (osteochondromas), and blood vessels (hemangiomas, lymphangiomas).

Common features of all these tumors are their slow development, relatively sharp contours and clear demarcation from surrounding tissues (absence of infiltrative growth), correct structural pattern. The tumor does not destroy, but replaces bone substance. It can lead to bone deformation with an increase in its volume.

Radiographic recognition of benign tumors rarely encounters serious obstacles. Compact osteoma clearly stands out on images as a dense structureless formation. Spongy osteoma preserves the structure of lamellar bone. Osteoma can be located deep in the bone or on its surface. Fibromas and chondromas cause a defect in the bone - a light area with sharp outlines, and in the case of chondroma, speckled shadows of calcareous and bone inclusions can be seen against the background of the defect. Osteochondroma is perhaps the most demonstrative: it has a wide base or pedicle and grows away from the bone. Cartilaginous areas are visible as clearings in the tumor image, and bone beams form diverging rafters. Hemangioma also causes a bone defect, but it often shows a lacy bone pattern or radially diverging bone plates. Hemangiomas are quite common in the cranial vault. The tumor causes a round defect, delimited from the surrounding bone by a narrow strip of sclerosis. The edges of the defect are clear and may be slightly wavy. In the vertebral body, hemangiomas cause numerous clearings separated by rough vertical bone beams. The vertebral body is swollen. Small clearings and serpentine stripes can also be determined in the arch of the affected vertebra. In these cases, computer and magnetic resonance tomograms are very important, since they make it possible to detect extraosseous development of the vascular network (in particular, in the spinal canal).

There are many different malignant tumors of bones and joints. Some of them are characterized by rapid growth and significant destruction of bone tissue, others develop relatively slowly and rather press on surrounding tissues than infiltrate them. However, all malignant tumors are characterized by a progressive course, increasing pain, changes in the peripheral blood (anemia, increased ESR), the appearance of regional or distant metastases.

A classic sign of a malignant tumor is the destruction of bone tissue. On radiographs, a defect is determined in it, most often with uneven and unclear contours. At the same time, which is very important for distinguishing from inflammatory lesions, no sequesters or exfoliated or fringed periostitis occur.

A peculiar form of bone tumor is osteoblastoclastoma (also called giant cell tumor). It develops in flat bones, vertebrae or epimetaphysis of tubular bones, characterized by a relatively regular shape and sharp demarcation from the surrounding bone tissue. In many osteoblastoclastomas, a large-cell bone pattern is determined, which allows this tumor to be differentiated from other malignant neoplasms.

The most well-known malignant bone tumor is osteogenic sarcoma. It grows rapidly and infiltrates the bone, and on radiographs it appears as an area of bone destruction with uneven and unclear outlines. At the edges of the tumor, where it disturbs the periosteum, calcified protrusions are formed - periosteal visors. This tumor is characterized by needle-like periostitis, in which multiple bone needles - spicules - are located perpendicular to the surface of the cortical layer that has been eaten away.

Osteogenic sarcoma cells are capable of producing bone substance, so often chaotically scattered foci of ossification are found in the tumor. Sometimes they obscure the area of destruction with their shadow. This type of sarcoma is called osteoblastic, as opposed to the first - osteolytic. However, at the border of the area darkened by bone masses, it is possible to discern the destruction of the cortical layer, periosteal visors and spicules. Sarcoma tends to give early metastases to the lungs, so patients need to be prescribed an X-ray examination of the chest organs.

One of the relatively frequently observed variants of malignant tumors is Ewing's sarcoma, originating from bone marrow cells. In the images, it causes a group of destructive foci, mainly in the diaphyseal part of the bone. Incidentally, we emphasize that the localization of the tumor has a certain differential diagnostic value. If osteoblastoclastoma is characterized by spreading to the epiphysis of the tubular bone, then osteogenic sarcoma is localized in the metaphysis and adjacent part of the diaphysis, and Ewing's sarcoma is localized in the diaphysis. The insidiousness of the latter is that the clinical symptoms and destructive foci can be similar to those in hematogenous osteomyelitis. Patients experience fever, leukocytosis, pain in the limb. However, with the tumor, there is no bone sequestration and exfoliated periostitis. Changes in the periosteum in Ewing's tumor are called bulbous or layered periostitis, in which strips of calcified periosteum are located in several rows along the surface of the affected bone.

The radiographic picture of generalized metastatic tumor lesion of the skeleton was described above. However, single or few metastases are often encountered. They also come in two types: osteolytic and osteoblastic.

The first ones cause destructive foci in the bone. In the second ones, the destruction may be unnoticeable, since the surrounding osteosclerosis of the bone tissue only shows up as compacted foci on the images. The nature of the lesion is easy to establish if the patient has a history of malignant tumor or one is detected simultaneously with a metastasis in the bone. If there is no relevant data, then they are guided by radiation symptoms. The presence of metastases is indicated by the multiplicity of foci, their destructive nature, the absence of sequesters and periosteal reaction.

Osteoscintigraphy has acquired special significance. Increased accumulation of phosphorus compounds 99mTc in the lesion, indicating the activity of metabolic processes, is characteristic of malignant neoplasms. It is important that radionuclide signs are detected long before, sometimes several months before, clear radiological symptoms of bone destruction.

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