Benign tumors from the actual bone tissue

Osteoblastoclastoma (giant cell tumor, osteoclastoma, gigantoma).
The term "osteoblastoclastoma" has become widespread in the Soviet Union over the past 15 years. First detailed description this tumor belongs to Nelaton (1860). Over the years, its teaching has undergone significant changes. In the second half of the 19th century, osteoblastoclastoma (giant cell tumor) was included in the group of fibrous osteodystrophies. In the works of S. A. Reinberg (1964), I. A. Lagunova (1962), S. A. Pokrovsky (1954), giant cell tumor is considered as local fibrous osteodystrophy. V. R. Braitsov (1959) expressed his view of a “giant cell tumor” of bones as a process of embryonic disorder of bone development, which, however, was not further confirmed. Currently, most researchers do not doubt the tumor nature of this process (A.V. Rusakov, 1959; A.M. Vakhurkina, 1962; T.P. Vinogradova, Bloodgood).
Osteoblastoclastoma is one of the most common bone tumors. There are no noticeable sex differences in the incidence of osteoblastoclastoma. Cases of familial and hereditary disease have been described.
The age range of patients with osteoblastoclastomas ranges from 1 year to 70 years. According to our data, 58% of cases of osteoblastoclastoma occur in the second and third decades of life.
Osteoblastoclastoma is usually a solitary tumor. Its double localization is rarely observed and mainly in adjacent bones. Long tubular bones are most often affected (74.2%), less often - flat and small bones.
In long tubular bones, the tumor is localized in the epimetaphyseal region (in children - in the metaphysis). It doesn't sprout articular cartilage and epiphyseal cartilage. IN in rare cases diaphyseal localization of osteoblastoclastoma is observed (according to our data, in 0.2% of cases).
Clinical manifestations osteoblastoclastomas largely depend on the location of the tumor. The first sign is pain in the affected area, bone deformation develops, and pathological fractures are possible.
X-ray picture osteoblastoclast of long tubular bones.
The affected bone segment appears asymmetrically swollen. The cortical layer is unevenly thinned, often wavy, and can be destroyed over a long area. At the site of the break, the cortical layer is disintegrated or sharpened in the form of a “sharpened pencil,” which in some cases imitates the “periosteal visor” in osteogenic sarcoma. The tumor, destroying the cortical layer, can extend beyond the bone in the form of a soft tissue shadow.
There are cellular-trabecular and lytic phases of osteoblastoclastoma. In the first case, foci of bone tissue destruction are identified, as if separated by partitions. The lytic phase is characterized by the presence of a focus of continuous destruction. The focus of destruction is located asymmetrically with respect to the central axis of the bone, but as it increases, it can occupy the entire diameter of the bone. Characteristic is a clear delineation of the focus of destruction from the intact bone. The medullary canal is separated from the tumor by the endplate.
The diagnosis of osteoblastoclastoma of long bones is sometimes difficult. The greatest difficulties arise in the radiological differential diagnosis of osteoblastoclast with osteogenic sarcoma, bone cyst and aneurysmal cyst.
Clinical and radiological indicators such as the patient’s age, medical history, and localization of the lesion become important in differential diagnosis.

table 2

Table 2 presents the main clinical and radiological symptoms characteristic of osteoblastoclastoma, osteogenic osteoclastic sarcoma and bone cyst.
An aneurysmal cyst in long bones, unlike osteoblastoclastoma, is localized in the diaphysis or metaphysis. With an eccentric location of an aneurysmal bone cyst, local swelling of the bone, thinning of the cortical layer, and sometimes the location of the bone crossbars perpendicular to the length of the cyst are determined. An aneurysmal bone cyst, unlike osteoblastoclastoma, in these cases is predominantly elongated along the length of the bone and may have calcareous inclusions (A. E. Rubasheva, 1961). With a central aneurysmal cyst, there is a symmetrical swelling of the metaphysis or diaphysis, which is not typical for osteoblastoclastoma.
The monoostotic form may be mistaken for osteoblastoclastoma fibrous osteodysplasia long tubular bone. However, fibrous osteodysplasia manifests itself, as a rule, in the first or early second decade of a child’s life (M.V. Volkov, L.I. Samoilova, 1966; Furst, Schapiro, 1964). Bone deformation manifests itself in the form of its curvature, shortening, less often lengthening, but not pronounced swelling, which occurs with osteoblastoclastoma. For fibrous osteodysplasia pathological process, as a rule, is localized in the metaphyses and diaphysis of tubular bones. There may be thickening of the cortical layer (compensatory), the presence of zones of sclerosis around the foci of destruction, which is not typical for osteoblastoclastoma. In addition, with fibrous osteodysplasia, the pronounced pain symptom, a rapid progression of the process with a growth inclination towards the joint, breakthrough of the cortical layer with the release of the tumor into the soft tissue. The main clinical and radiological symptoms characteristic of osteoblastoclastoma and fibrous dysplasia are presented in Table 3.
Table 3

X-ray picture of osteoblastoclastoma of flat bones.
Of the flat bones, changes in the pelvic bones and scapula are most often observed. The lower jaw is affected in approximately 10% of cases. Solitary and isolated lesions are also characteristic. Bone swelling, thinning, waviness or destruction of the cortical layer and a clear delineation of the pathologically altered area of ​​​​the bone are determined. During the lytic phase, destruction of the cortical layer prevails; during the cellular-trabecular phase, thinning and waviness of the latter prevail.
(The greatest differential difficulties arise when osteoblastoclastoma is localized in the lower jaw. In these cases, osteoblastoclastoma is very similar to adamantinoma, odontoma, bone fibroma and true follicular cyst.
Benign osteoblastoclastoma can become malignant. The reasons for the malignancy of a benign tumor are not precisely understood, but there is reason to believe that trauma and pregnancy contribute to this. We observed cases of malignancy by osteoblastoclast of long bones after multiple series of remote radiation therapy.
Signs of malignancy of osteoblastoclastoma: rapid growth of the tumor, increasing pain, an increase in the diameter of the focus of destruction or the transition of the cellular-trabecular phase to the lytic phase, destruction of the cortical layer over a large area, unclear contours of the focus of destruction, destruction of the endplate that previously limited the entrance to the medullary canal, periosteal reaction.
The conclusion about the malignancy of osteoblastoclastoma based on clinical and radiological data must be confirmed by a morphological examination of the tumor.
In addition to the malignancy of the benign form of osteoblastoclastoma, there may also be primary malignancy of osteoblastoclastoma, which, essentially (T. P. Vinogradova) are a type of sarcoma of osteogenic origin. The localization of malignant osteoblastoclastomas is the same as that of benign tumors. At x-ray examination a focus of bone tissue destruction without clear contours is determined. The cortical layer is destroyed over a large area, the tumor often grows into the soft tissue. There are a number of features that distinguish malignant osteoblastoclastoma from osteogenic osteoclastic sarcoma: older age of patients, less pronounced clinical picture and more favorable long-term outcomes.
Treatment of benign osteoblastoclastomas is carried out by two methods - surgical and radiation. X-ray examination is of great importance in assessing the treatment, which makes it possible to establish anatomical and morphological changes in the affected part of the skeleton during therapy and in the long term after it. In these cases, in addition to multiaxial radiography, direct magnification radiography and tomography may be recommended. Certain structural features of osteoblastoclastoma are known in different terms after external beam radiation therapy. On average, after 3-4 months with favorable course process in place earlier
trabecular shadows appear in structureless areas of the tumor; gradually the trabeculae become more dense. The lesion acquires a fine-meshed or coarse-meshed structure. The thinned or destroyed cortical layer is restored; tumor size may decrease. The formation of a sclerotic shaft between the tumor and the unchanged part of the bone is noted. The duration of reparative bone formation varies from 2-3 months to 7-8 or more months. In cases of the development of the “paradoxical reaction” phenomenon, first described by Herendeen (1924), 2-8 weeks after radiation therapy, pain in the affected area increases, foci of destruction increase, trabeculae resolve, and the cortical layer becomes thinner. The paradoxical reaction subsides after about 3 months. However, a paradoxical reaction may not be observed during radiation therapy for osteoblastoclasts.
An important criterion for the effectiveness of osteoblastoclast therapy is the severity of remineralization of the former lesion. Relative concentration minerals at various times after radiation and surgical methods osteoblast treatment is determined by the method of relative symmetric photometry of radiographs. Our relative symmetrical photometry of radiographs allowed us to establish that in the group of patients with osteoblastoclastoma examined at various times after radiation therapy, remineralization of the lesions averaged 66.5+4.8% compared to the control area of ​​the skeleton Osteoid osteoma. A detailed study of this tumor by clinicians and radiologists began in 1935 after Jaffe identified it under the name “osteoid osteoma.” Five years earlier, Bergstrand presented a description of this pathological process, “osteoblastic disease,” as an embryonic malformation.
Currently, there are two opinions regarding the nature of osteoid osteoma. Some authors (S. A. Reinberg, I. G. Lagunova) consider osteoid osteoma to be an inflammatory process. S. A. Reinberg considered osteoid osteoma as a chronic focal necrotic non-purulent osteomyelitis, in which it is possible to bacteriologically isolate a common purulent pathogen.
Other authors (Jaffe, Lichtenstein, T.P. Vinogradova) classify osteoid osteoma as a tumor. T.P. Vinogradova considers one of the contradictions in the position of S. A. Reinberg to be the discrepancy between the presence of pyogenic microbes in the focus and the qualification of this focus as non-purulent osteomyelitis. According to T.P. Vinogradova, bacteriological and bacterioscopic studies of tissue from the lesion are negative.
It seems to us the most acceptable view of osteoid osteoma as a tumor.
Osteoid osteoma is predominantly observed in individuals young(11-20 years old). Males get sick twice as often as females. Osteoid osteoma is usually a solitary tumor localized in any part of the skeleton. The tumor is most often observed in long tubular bones. The first place in the frequency of lesions is the femur, then the tibia and humerus.
The clinical picture of osteoid osteoma is very characteristic. Patients are bothered by pain, especially severe at night. The pain is localized, sometimes aggravated by pressing on the lesion. The analgesic effect of aspirin is characteristic. Skin without changes. With cortical localization of the process, bone thickening can be determined by palpation. In some cases, when laboratory research patients experience moderate leukocytosis and accelerated ESR (Ponselti, Bartha). In our observations, laboratory parameters in patients with osteoid osteoma were without deviations from the norm.
X-ray picture of osteoid osteoma. Mainly in the diaphysis or metadiaphysis of a long tubular bone is determined oval shape with clear contours, a focus of bone tissue destruction, not exceeding 2 cm in diameter. Around the focus of destruction, a zone of osteosclerosis is determined, especially pronounced in cases of intracortical location of the focus of destruction. The sclerosis zone, due to periosteal and, to a lesser extent, endosteal changes, causes unilateral deformation of the long tubular bone. Massive bone growths interfere with identifying the focus of destruction on radiographs. Therefore, to clarify the nature of the lesion and more clearly identify the focus (“tumor nest”), tomography is indicated.
When the focus of destruction is localized in the spongy substance, a narrow rim of sclerosis is noted. Bone inclusions may be visible within the lesion, which Walker (1952) calls “tiny round sequestra” and considers them typical of osteoid osteoma.
Rare cases of “giant osteoid osteoma” reaching a diameter of 5-6 cm have been described (Dahlin). M.V. Volkov in his monograph provides an observation of a 12-year-old child with a giant form of osteoid osteoma of the spinous process of the third cervical vertebra.
Differential diagnosis of osteoid osteoma is carried out primarily with Brody's bone abscess. An isolated bone abscess occurs with less intense
pain. The radiograph reveals an elongated focus of destruction, surrounded by a less pronounced zone of sclerosis, sometimes with a periosteal reaction, in contrast to hyperostosis in osteoid osteoma. The lesion penetrates through the epiphyseal cartilage from the metaphysis into the epiphysis.
It should be noted that osteoid osteoma does not become malignant and, as a rule, does not recur after radical surgical treatment.
Osteoma. A relatively rare, predominantly solitary, exophytically growing tumor, consisting of bone tissue of varying degrees of maturity from fine-fibrous to lamellar. It is detected more often in childhood, sometimes it is an accidental x-ray finding. There are two types of osteomas: compact and spongy. On radiographs it is always a “plus shadow” additional education, connected to a bone by a wide base or pedicle. Compact osteoma is localized in the bones of the cranial vault, in paranasal sinuses, mainly in the frontal, less often - in the maxillary and ethmoid sinuses. In these cases, they are multiple, can be unlaced and lie in the cavities of the sinuses in the form of free bodies bone density, round shape(rhinolitis).
Spongy osteoma is most often localized in short and long tubular bones and jaw bones.
The clinical course of osteomas is favorable; tumor growth occurs slowly. Clinical manifestations largely depend on the location of osteomas.
Compact osteomas of the skull growing inward can cause serious complications.
X-ray diagnosis of osteomas is not difficult. Compact osteoma has the shape of a ball or hemisphere and gives a homogeneous, structureless, intense shadow. As it grows, the cancellous osteoma of the tubular bone moves away from the joint, its contours are clear, the cortical layer can be traced throughout, it becomes thinner, but is not interrupted. The bone structure of the tumor differs somewhat from the structure of the main bone due to the random arrangement of bone beams.
Differential X-ray diagnosis of osteomas of the extremities should be carried out mainly with myositis ossificans, subperiosteal hematoma, osteochondroma, and osteochondral exostoses. With myositis ossificans, there is pain, a lack of connection between the formation and the bone itself, and an irregular spotty, fibrous structure of the ossified muscle. The subperiosteal hematoma is a spindle-shaped shadow, the length of which merges with the long axis of the bone. In addition, it differs from osteoma in the absence of a structural bone pattern.
In children, subperiosteal osteoma is mistaken for osteoma. venous sinus skull - sinus pericranium, which is a development option.
The prognosis for osteoma is favorable. Osteoma does not become malignant, but requires radical surgical treatment in avoid possible relapses tumors.

Benign tumors of cartilage tissue

Chondroma. Chondromas, as S.A. Reinberg points out, are observed mainly in childhood and adolescence. According to T.P. Vinogradova, the age of patients varies with a predominance from the second to the fourth decade of life. Of the 52 chondroma patients we observed, more than half were aged 30-40 years. There is no predominance of any gender among patients. In most cases, the short tubular bones of the hand are affected (in about 70% of cases), less often the feet, then the pelvic bones, vertebral processes, and sternum. Long tubular bones are affected very rarely. In long tubular bones, chondroma is localized at the metaepiphyseal ends. According to I.G. Lagunova (1962), in middle and old age, chondroma in long tubular bones is located in the metaphysis, spreading to the epiphysis or diaphysis. In our observations, metaepiphyseal localization of chondromas prevailed. In childhood, chondromas in long tubular bones usually affect the metaphysis. In short tubular bones of the hand and foot, chondromas are often multiple, and bilateral lesions are noted. In flat bones, and especially in long tubular bones, solitary chondromas are observed. The joints, as a rule, are not changed. But with large tumor sizes, severe deformation of the bones occurs, mechanically preventing movements in the joints.
The X-ray picture of enchondromas is quite characteristic. Foci of bone tissue destruction are identified as round and oval in shape. These foci of destruction are located either centrally, causing swelling of the bone, or eccentrically. Single bone bridges and inclusions of lime may stand out against the cartilaginous background. In some cases, these calcareous inclusions are multiple, merge with each other and seem to fill the entire cartilaginous background (the site of destruction). The cortical layer is unevenly thinned, thickened in places, and is not interrupted. In long tubular bones, the focus of destruction, located in the metaepiphyseal region, causes moderate swelling of the bone. The thinned cortical layer, as a rule, has smooth contours. Possible club-shaped deformity affected part of the bone. Due to damage to the epiphyseal cartilages, children may experience inhibition of bone growth in length. Pathological fractures of the affected bone are observed.
Primary chondromas of bones can become malignant; chondromas of the pelvis and long tubular bones are more often malignant. The most dangerous in terms of malignancy are enchondromas with a predominance of calcifications (type 3 chondromas according to I.G. Lagunova). Malignancy of rib chondromas is also observed. There is an opinion that chondromas of the short tubular bones of the hand do not become malignant, although they have a less mature structure than chondromas of the pelvis. However, we observed in two cases malignancy of chondromas of the hand bones. Echondroma is observed in any part of the skeleton, more often it is localized in the pelvic bones. The tumor grows exophytically from the bone and in some cases reaches large sizes. The shape of the tumor can be very diverse. Echondromas are a collection of cartilaginous masses connected to the bone by a base of varying width and shape. The outer boundaries of the tumor are difficult to determine in cases of mild calcification of the ecchondroma. More often, calcifications are scattered throughout the tumor mass or merge into large conglomerates. In other cases, ossification predominates in the tumor. The contours of the tumor become clearer and a spotty-mesh pattern is detected on radiographs, with ossification more pronounced at the base of the tumor. Despite the diversity of the X-ray picture, diagnosing ecchondroma does not seem difficult and only in rare cases do they have to be distinguished from a calcified hematoma or myositis ossificans.
The signs of malignancy of chondromas are the same as those of other benign tumors: increasing pain, rapid growth, destruction of the cortical layer, extension of the soft tissue shadow beyond the bone, slightly pronounced periosteal reaction.
Diagnosis of chondromas does not present great difficulties, especially when they are localized in short tubular bones. When enchondromas are localized in long tubular bones, it may be necessary to conduct a differential diagnosis between a chondroma and a bone cyst. The chondroma is predominantly located in the metaepiphyseal region, while the bone cyst is localized in the metadiaphyseal region. The deformation of the bone with a bone cyst is close to fusiform, there are no inclusions of lime. Often the first symptom of a bone cyst is a pathological fracture, while an enchondroma due to pain is usually identified before a possible fracture. Differential diagnosis of centrally located enchondroma of long tubular bones with chondroblastoma, which is usually located in the end sections of the bones, can be difficult. Against the background of the focus of destruction, areas of calcification can also be traced. Unlike chondroma, around the focus of destruction in chondroblastoma there may be a narrow zone of sclerosis and in cases where the focus of destruction is located subcortically, periosteal layers appear.
The most difficult differential diagnosis for chondromas comes down to distinguishing between benign and malignant forms of tumors. This is complicated by the fact that chondrosarcomas in some cases are characterized by long course(in untreated cases, the tumor can exist for 4-5 years). Unlike chondroma, the focus of destruction in chondrosarcoma has unclear, uneven outlines. Chondrosarcoma grows beyond the bone and against the background of a soft tissue shadow that extends beyond the bone, mottling due to calcification is determined. The characteristic periostosis in the form of a “periosteal visor” also speaks in favor of chondrosarcoma.
In some cases, only a morphological study allows us to establish the true nature of the cartilage tumor.
Treatment of patients with chondroma is surgical. The extent of surgical intervention is decided individually in each specific case. For chondromas of long tubular bones, due to possible malignancy, it is recommended to perform bone resection with removal of the tumor within healthy tissue.
Chondroblastoma. In 1931, Codman described this bone neoplasm in detail under the name "epiphyseal chondromatous giant cell tumor." In the literature you can find a description of it under the name Codman's tumor. In 1942, Jaffe and Lichtenstein identified this tumor as a separate form called chondroblastoma, consisting mainly of chondroblasts.
Chondroblastoma is a rare tumor. Judging by the literature, it accounts for 1-1.8% of primary bone tumors. Persons of both genders are affected, but more often males. Chondroblastoma occurs at any age, but mainly in childhood and adolescence (10-25 years). Favorite localization is long tubular bones. Less commonly, chondroblastoma is located in the scapula, rib, calcaneus, bones of the hand and foot. In long tubular bones, hodroblastoma affects the epiphysis and metaphysis (proximal and distal parts femur, proximal - tibial and humerus, proximal part radius). Chondroblastoma spreads towards the joint and in some cases there is a reactive effusion in the joint. Pathological fractures are rarely observed.
The clinical picture is dominated by pain at the site of the lesion and in the adjacent joint. There is slight swelling, sometimes limited movement in the joint and atrophy of the muscles of the limb.
The X-ray picture has a number of features. A focus of destruction of a round or oval shape is determined. It is not homogeneous. Due to the presence of areas of calcification in the tumor, speckled shadows are visible on the radiograph. With a subcortical location of the lesion, a slight periosteal reaction is possible. The cortical layer can be thinned, sometimes its integrity is disrupted and the tumor extends beyond the bone, which, as with osteoblastoclastoma, is not a sign of its malignancy.
Differential diagnosis chondroblastoma is carried out with many bone tumors and primarily with solitary chondroma. Diagnosis of chondroblastoma and tuberculous osteitis is difficult. With loss of activity, the tuberculous focus is surrounded by a sclerotic border, which can mimic chondroblastoma. During the arthritic phase of tuberculous osteitis, pain and effusion in the joint are more pronounced. Radiographs show changes in the height of the joint space, thickening joint capsule, general osteoporosis of bones, which is not typical for chondroblastoma. The subsidence of clinical manifestations in tuberculous osteitis after the use of specific treatment, specific reactions and laboratory data resolve doubts about the diagnosis. Chondroblastoma is treated surgically. The prognosis for life is usually favorable.
Chondromyxoid fibroma. A rare tumor, isolated as an independent form in 1948 by Jaffe and Lichtenstein. The tumor is localized in the metaphyses or metadiaphyses of long tubular bones, mainly near knee joint. Chondromyxoid fibromas of small bones of the hand and feet, and pelvic bones have also been described. The clinical manifestations of the tumor are mild, sometimes it is quite long time is asymptomatic and is detected by chance on radiographs taken for another reason.
The X-ray picture is presented in the form of a focus of destruction, reaching a length of 4-5, 6-8 cm. Sometimes the focus of destruction is surrounded by a sclerotic rim; against the background of the focus of destruction, a trabecular pattern and inclusions of lime can be traced. With subperiosteal localization of the lesion, usuration of the cortical layer is detected, the tumor extends beyond the bone. Periosteal reaction is not typical.
The greatest difficulties arise when distinguishing a benign cartilaginous tumor from a malignant one. Jaffe notes that to diagnose chondromyxoid fibroma, one has to use a “sixth sense”, combining minimal impressions into one whole. Judging by the literature, diagnostic errors are still being made in the direction of overdiagnosis of sarcomas. All cases must be verified morphologically. Treatment is surgical.

Benign tumor of bone and cartilage tissue

Osteochondroma. Osteochondroma is a single, or in rare cases, multiple tumor, consisting of bone and cartilage tissue. M.V. Volkov notes that the difference between chondroma and osteochondroma is quantitative in terms of the degree of ossification of the tumor.
M.V. Volkov believes that osteochondromas refer to calcified chondromas. “When we talk about osteochondroma, most often we mean ossifying chondroma, chondroma with calcareous inclusions.” We cannot agree with such a point of view. The morphological picture of true osteochondromas was described by T. P. Vinogradova. Our clinical and radiological observations revealed certain differences in the picture of chondromas and osteochondromas. Osteochondromas, unlike chondromas, are predominantly localized in long tubular bones (the medial surface of the proximal metaphysis of the humerus, distal metaphysis, femoral epiphysis, proximal metaphysis of the tibia and proximal metaphysis, epiphysis of the fibula, etc.) and are connected to the main bone by a pedicle. Of the flat bones, the scapula, ribs, and pelvic bones are most often affected. Osteochondroma can arise from the processes of the vertebrae and small bones.
Our data confirm the information available in the literature about the predominant localization of osteochondromas in long tubular bones and the scapula. These locations for chondromas are rare.
The X-ray picture of osteochondromas is quite typical. However, we cannot completely agree with the description of osteochondroma presented in the manual by S. A. Reinberg “Osteochondroma is only slightly different from osteoma: in addition to bone, it also contains cartilaginous tissue covering the surface of the tumor in the form of a cap.” A similar description characterizes juvenile osteochondral exostoses (dysplasia).
Osteochondroma on a radiograph is presented in the form of an additional shadow connected to the bone by a stalk or, less commonly, by a wide base. Grows away from the joint, slowly, but can reach large sizes. The contours of osteochondroma are lumpy and uneven. The cortical layer in the form of a thin bordering plate can be traced throughout the entire length of the tumor. Sometimes the cortex is directed towards the surface of the tumor in a radial manner. Noteworthy is the combination of small areas of destruction ( cartilage tissue) with the presence of a trabecular pattern and massive inclusions of calcareous shadows. With large osteochondromas, deformations of adjacent bones are observed. For example, pronounced curvature and deformation of the cortical layer of the fibula with large osteochondroma tibia. We also observed spreading and deformation of the ribs due to osteochondroma of the rib in an 11-year-old child.
Osteochondroma must be differentiated from single and multiple osteochondral exostoses, which are related to dysplasia. In long tubular bones, osteochondral exostoses are located in the area of ​​the metaphyses, and as they grow, they seem to move toward the diaphysis. Osteochondral exostoses have a varied shape and are surrounded by a compact bone plate that passes from the main bone. The structure of exostoses resembles the structure of tubular bone. In linear exostoses with a pronounced stalk, a cartilaginous “cap” is defined at its apex; with a spherical form of exostosis, the cartilage is located over the entire spherical surface. It can become calcified, and radiographs reveal calcareous inclusions, often less pronounced than with osteochondroma. Polyosseousness should be considered in favor of osteochondral exostoses. lesions and abnormalities of bone development, often observed with dysplasia.
Osteochondroma can become malignant. Malignancies of osteochondromas of the scapula and pelvic bones, and osteochondromas of long tubular bones are known. We observed malignancy of osteochondromas of the rib (I), humerus (I), and short tubular bone of the foot (I). These changes are characterized by the appearance severe pain, destruction of the cortical layer, pronounced destruction and additional soft tissue shadow outside the osteochondroma. Treatment of osteochondroma is surgical.

Benign tumors of types of connective tissue

This group of benign tumors includes rare neoplasms - fibroma, lipoma and myxoma.
Fibroma is detected in people of any age, but mainly in childhood and in the second to fourth decades of life. Fibromas of the upper and lower jaw, long tubular bones, and scapula have been described. Clinically, fibroma is manifested by pain and some bone deformation in the area where the tumor is located. The X-ray picture of fibroma is not typical. A slight swelling of the bone is determined due to a centrally, less often - eccentrically located focus of destruction of bone tissue with a thin pattern of trabeculae. The cortical layer is thinned, but not interrupted. Sometimes the tumor spreads along the entire length of the diaphysis, causing a fusiform deformity. We observed three cases of bone fibroma (confirmed by histological examination) localized in the proximal metadiaphysis of the femur. In all cases, bone deformation of the “shepherd’s stick” type occurred. There was moderate swelling of the metadiaphysis due to foci of destruction of a confluent nature with the presence of trabeculae. The cortical layer is unevenly thinned.
Differential diagnosis of bone fibromas with monoosseous forms of fibrous dysplasia is difficult due to the commonality of a number of radiological signs.
The X-ray picture of the monoosseous form of fibrous dysplasia is very diverse. The process is localized mainly in the metaphyses and diaphyses of tubular bones. The bone may be swollen, widened in diameter, or curved. Areas of rarefaction of bone tissue of various sizes and shapes, sometimes with a cellular structure, are usually located eccentrically in the cortical layer; subcortical and subperiosteal localization of lesions are also described. Areas of bone compaction are often found. The cortex may be compensatory thickened, but usually becomes thinner. Characteristic features are waviness, scalloping of the internal contour of the cortical layer and the “ground glass” symptom (structure of the lesion). The course of fibroids is benign. Possible pathological fracture.
Bone lipoma is a very rare tumor localized in long tubular bones juxtacortically and parostally. Bone lipoma does not have any characteristic clinical or radiological signs. On radiographs, “gentle enlightenment” is determined, in the words of S. A. Reinberg. Decisive diagnostic value acquires a morphological study.
Bone myxoma is a rare tumor, the existence of which is denied by a number of authors. Myxomas have been described in the jaw bones, long and short tubular bones. When interpreting radiographs of bone myxoma, the impression is of chondromyxoid fibroma or chondroblastoma.

Benign tumor of chordal tissue - chordoma

Chordoma develops from persistent remnants of the notochord. The predominant localization of chordoma is the area of ​​the sphenooccipital joint and the sacrococcygeal spine. Frequency information separate forms chordomas are very controversial.
Jaffe provides the following data: cranial chordomas - 35%, vertebral - 10%, caudal - 55%. According to S. A. Reinberg, 60% of all chordomas are located in the sacral region, in particular, 40% at the base of the coccyx, and only a small percentage of chordomas are localized in the base of the skull.
The age of patients is varied: rarely - in children and young men; more often - in mature age. Men get sick more often than women. Clinically, chordoma can be benign or malignant. Some authors (S.A. Reinberg) classify chordoma as a malignant neoplasm.
Chordomas can reach large sizes, especially when they are localized in the caudal spine. The clinical picture largely depends on the direction of chordoma growth. When a tumor grows into the spinal canal, it causes symptoms of compression spinal cord, cauda equina and nerve roots.
The X-ray picture of chordomas is characterized by the presence of a focus of destruction involving a number of vertebrae. The bone defect appears homogeneous or large-chambered due to thin bone strips. Lateral radiographs of the sacrum are shown, on which, in case of chordoma, an increase in the anteroposterior size of the sacrum is determined due to the expansive growth of the tumor. In some cases, small bone inclusions can be traced in the tumor, which can serve as a reason for the erroneous diagnosis of teratomas, especially in childhood. (In childhood, teratomas are common; their ratio to chordomas, according to M.V. Volkov, is 60:2).
Treatment of chordomas is surgical. In cases of non-radical surgical intervention, tumor recurrences may occur.

Benign bone tumors from vascular tissue

Angioma. Vascular tumors bones were described in Russian literature at the end of the last century (M. F. Matveev, 1886 and P. I. Dyakonov, 1889). There are capillary and venous angiomas. The macroscopic appearance of the tumor varies depending on its type, which to a certain extent affects the variety of X-ray morphological variants of angiomas.
Most often, angiomas are localized in the vertebrae and bones of the cranial vault. Non-vertebral localizations of angiomas are rare (long tubular bones; bones of the pelvis, foot, scapula, jaw). Angioma can be solitary and multiple. Multiple angiomas are usually localized in the vertebrae. Combinations of bone angiomas with skin angiomas and, less commonly, liver angiomas have been described. The age of patients at which the tumor is detected is 35-45 years. At the same time, rare cases of angiomas in childhood and old age have been described. In people's vertebrae old age During autopsy, angiomatous nodules are often found against the background of osteoporosis, but they are not, as T. P. Vinogradova points out, angiomas.
The clinic depends on the location and its prevalence. With vertebral angioma, patients are worried local pain, fatigue when walking. In cases of significant vertebral destruction and compression, radicular or spinal symptoms may develop. We observed patients with T7_8 angiomas who complained of chest pain and were examined in therapeutic clinics about angina pectoris. Angiomas of the calvarial bones cause headache in cases of bone deformation inward. If the underlying bone is affected, exophthalmos may occur. The X-ray picture of vertebral angiomas is very characteristic. The cortical layer is preserved intervertebral discs are not damaged. The structure of the vertebra in angioma is represented by vertically extending thickened trabeculae with clearing between them. This is the most common option for restructuring the bone structure of the vertebral body in case of angioma. In some cases, osteoporosis or fine-cell restructuring may be observed. The affected vertebra in some cases appears deformed like a “barrel”. With vertebral angioma, the process may also involve the arches, which appear somewhat thickened on radiographs; the same structural changes, as in the vertebral body.
When the vertebral body is compressed, its height decreases, the structure becomes denser, and in these cases, diagnosing angiomas presents certain difficulties. There is a need for differential diagnosis of vertebral angioma and tuberculous spondylitis, as well as cancer metastasis. Similar symptoms of these diseases are pain, a picture of a compression fracture, and osteoporosis. However, with tuberculous spondylitis, a focus of destruction is determined, a breakthrough of the focus of necrosis through the cranial or caudal plate with the involvement of the adjacent vertebra in the process and deformation of the intervertebral disc. With metastatic lesions of the vertebra, in addition to osteoporosis, foci of bone tissue destruction with uneven contours, the cortical layer is damaged, but the intervertebral discs, as with angioma, are not damaged.
In the bones of the calvarium, angioma is represented by a clearly demarcated area of ​​reorganization of the bone structure according to the fine-mesh type. More often there is a slight swelling of the bone, thinning and partial destruction of the outer or inner bone plate and a characteristic radial structural pattern due to the different thickness of the bone crossbars.
Less commonly, hemangioma can be localized in the ribs. As a rule, one rib is affected, but hemangiomas of two ribs and a combination of hemangiomas of the ribs and vertebrae are described. In the vast majority of cases, damage to the vertebral segment of the rib is observed over a length of 5-10 cm. The affected area of ​​the rib is slightly fusiform thickened or sharply swollen. The cortical layer is thinned. The bone structure is rebuilt according to the fine-cellular type. The size and shape of the cells vary significantly. Between the cells, the bone crossbars have different thicknesses. They, like the cells, are predominantly located in the longitudinal direction, which creates longitudinal striations on radiographs. Angioma in long tubular bones is localized in the metaphysis and diaphysis. The entire length of the diaphysis may be affected, which appears unevenly expanded. The cortical layer is not visible in some areas, the contours of the bone are uneven due to the pronounced reaction of the periosteum. The bone structure is rebuilt according to a fine-cellular type with a longitudinal arrangement of foci of destruction with individual linear areas of sclerosis.
For angiomas of the vertebrae and calvarial bones, radiation therapy is effective. During dynamic X-ray observations, especially after the second course of radiation therapy, some compaction of the bone structure is noted. For angiomas of long tubular bones, surgical treatment is used.

Eosinophilic granuloma

Described by N.I. Taratynov in 1913. It is classified as X reticulosis (Lichtenstein), but there is every reason to consider it in the group of tumors. Mostly children get sick school age. But we had to observe this disease in 2-3 year old children, as well as in middle-aged people.
The clinical course of the process is characterized by the presence of a painful tumor formation in the soft tissues, quite dense to the touch, immobile, associated with the bone. In rare cases, there may be low-grade fever body and moderate eosinophilia. The disease can last for months. In some cases, bone damage is combined with simultaneous damage to the lungs or skin, which aggravates clinical course diseases. The localization of the process is varied. Flat bones are most often affected - the bones of the cranial vault, pelvis, and ribs. In the pelvic bones, eosinophilic granuloma can be located in upper branch pubic bone and in the symphysis area. Long tubular bones and literally all parts of the skeleton can be affected.
Localization of the focus of destruction in the diaphysis of long tubular bones may result in a periosteal reaction.
The X-ray picture is very characteristic. Bone destruction is determined. Foci of destruction are single and multiple, often confluent. One bone or several bones may be affected at the same time. The shape of the foci of destruction is varied - round, irregularly oval, but more often card-shaped. The diameter of the foci of destruction is from 0.5 to 5 or more cm. In cases of the confluent nature of the foci of destruction, bone bridges can be traced. The contours of the foci of destruction are usually clear. Foci of destruction in some cases may be surrounded by a rim of sclerosis. Foci of destruction originate from the bone marrow, but compact tissue quickly grows from within. The cortical layer thins unevenly.
The morpho-radiological dynamics of eosinophilic granuloma can be presented in the following way: initially, in the area of ​​the bone marrow canal or diploe, an area of ​​osteoporosis is determined - a rarefaction of the bone structure with fairly clear contours. These changes are asymptomatic. During this period, patients do not yet seek help. Over time, the area of ​​osteoporosis replaces the developed area of ​​destruction.
After radiation therapy, he begins to recover bone structure and in favorable cases, 12-13 months after remote gamma therapy, the focus of destruction is completely replaced by bone tissue. In the differential diagnosis of eosinophilic granuloma, the greatest practical significance have inflammatory processes- primary chronic osteomyelitis (See Chapter II).
At bone form xanthomatosis is a triad of symptoms. In addition to foci of bone tissue destruction in flat bones, it is noted diabetes insipidus and bulging eyes. Foci of destruction in flat bones extend to both the outer and inner plates. Foci of destruction are usually multiple with clear contours.

Osteoblastoclastoma(osteoblastoclastoma, giant cell tumor, osteoclastoma, gigantoma).

The term "osteoblastoclastoma" has become widespread in the Soviet Union over the past 15 years. The first detailed description of this tumor belongs to Nelaton (1860). Over the years, its teaching has undergone significant changes. In the second half of the 19th century, osteoblastoclastoma (giant cell tumor) was included in the group of fibrous osteodystrophies. In the works of S. A. Reinberg (1964), I. A. Lagunova (1962), S. A. Pokrovsky (1954), giant cell tumor is considered as local fibrous osteodystrophy. V. R. Braitsov (1959) expressed his view of a “giant cell tumor” of bones as a process of embryonic disorder of bone development, which, however, was not further confirmed. Currently, most researchers do not doubt the tumor nature of this process (A.V. Rusakov, 1959; A.M. Vakhurkina, 1962; T.P. Vinogradova, Bloodgood).

Osteoblastoclastoma is one of the most common bone tumors. There are no noticeable sex differences in the incidence of osteoblastoclastoma. Cases of familial and hereditary disease have been described.

The age range of patients with osteoblastoclastomas ranges from 1 year to 70 years. According to our data, 58% of cases of osteoblastoclastoma occur in the second and third decades of life.

Symptoms of Osteoblastoclastoma:

Osteoblastoclastoma is usually a solitary tumor. Its double localization is rarely observed and mainly in adjacent bones. Long tubular bones are most often affected (74.2%), less often - flat and small bones.

In long tubular bones, the tumor is localized in the epimetaphyseal region (in children - in the metaphysis). It does not grow into articular cartilage and epiphyseal cartilage. In rare cases, diaphyseal localization of osteoblastoclastoma is observed (according to our data, in 0.2% of cases).

Clinical manifestations of osteoblastoclastoma largely depend on the location of the tumor. The first sign is pain in the affected area, bone deformation develops, and pathological fractures are possible.

Benign osteoblastoclastoma can become malignant.

Causes of malignancy A benign tumor has not been precisely determined, but there is reason to believe that trauma and pregnancy contribute to this. We observed cases of osteoblastoclast malignancy of long bones after multiple series of external beam radiation therapy.

Signs of malignancy of osteoblastoclastoma: rapid growth of the tumor, increasing pain, an increase in the diameter of the focus of destruction or the transition of the cellular-trabecular phase to the lytic phase, destruction of the cortical layer over a large area, unclear contours of the focus of destruction, destruction of the endplate that previously limited the entrance to the medullary canal, periosteal reaction.

The conclusion about the malignancy of osteoblastoclastoma based on clinical and radiological data must be confirmed by a morphological examination of the tumor.

In addition to malignancy, the benign form of osteoblastoclastoma can also be primary malignant osteoblastoclastomas, which, essentially (T.P. Vinogradova) are a type of sarcoma of osteogenic origin.

The localization of malignant osteoblastoclastomas is the same as that of benign tumors. An X-ray examination reveals a focus of bone tissue destruction without clear contours. The cortical layer is destroyed over a large area, the tumor often grows into the soft tissue. There are a number of features that distinguish malignant osteoblastoclastoma from osteogenic osteoclastic sarcoma: older age of patients, less pronounced clinical picture and more favorable long-term outcomes.

Diagnosis of Osteoblastoclastoma:

X-ray picture of osteoblastoclastoma of long bones.
The affected bone segment appears asymmetrically swollen. The cortical layer is unevenly thinned, often wavy, and can be destroyed over a long area. At the site of the break, the cortical layer is disintegrated or sharpened in the form of a “sharpened pencil,” which in some cases imitates the “periosteal visor” in osteogenic sarcoma. The tumor, destroying the cortical layer, can extend beyond the bone in the form of a soft tissue shadow.

There are cellular-trabecular and lytic phases of osteoblastoclastoma. In the first case, foci of bone tissue destruction are identified, as if separated by partitions. The lytic phase is characterized by the presence of a focus of continuous destruction. The focus of destruction is located asymmetrically with respect to the central axis of the bone, but as it increases, it can occupy the entire diameter of the bone. Characteristic is a clear delineation of the focus of destruction from the intact bone. The medullary canal is separated from the tumor by the endplate.

Diagnosis of osteoblastoclastoma long tubular bones sometimes seems difficult. The greatest difficulties arise in the radiological differential diagnosis of osteoblastoclastoma with osteogenic sarcoma, bone cyst and aneurysmal cyst.

Clinical and radiological indicators such as the patient’s age, medical history, and localization of the lesion become important in differential diagnosis.

An aneurysmal cyst in long bones, unlike osteoblastoclastoma, is localized in the diaphysis or metaphysis. With an eccentric location of an aneurysmal bone cyst, local swelling of the bone, thinning of the cortical layer, and sometimes the location of the bone crossbars perpendicular to the length of the cyst are determined. An aneurysmal bone cyst, unlike osteoblastoclastoma, in these cases is predominantly elongated along the length of the bone and may have calcareous inclusions (A. E. Rubasheva, 1961). With a central aneurysmal cyst, there is a symmetrical swelling of the metaphysis or diaphysis, which is not typical for osteoblastoclastoma.

The monoosseous form of fibrous osteodysplasia of the long tubular bone may be mistaken for osteoblastoclastoma. However, fibrous osteodysplasia manifests itself, as a rule, in the first or early second decade of a child’s life (M.V. Volkov, L.I. Samoilova, 1966; Furst, Schapiro, 1964). Bone deformation manifests itself in the form of its curvature, shortening, less often lengthening, but not pronounced swelling, which occurs with osteoblastoclastoma. With fibrous osteodysplasia, the pathological process is usually localized in the metaphyses and diaphyses of tubular bones. There may be thickening of the cortical layer (compensatory), the presence of zones of sclerosis around the foci of destruction, which is not typical for osteoblastoclastoma. In addition, with fibrous osteodysplasia, there is no pronounced pain symptom inherent in osteoblastoclastoma, a rapid progression of the process with a growth inclination towards the joint, or a breakthrough of the cortical layer with the tumor emerging into the soft tissue.

Of the flat bones, changes in the pelvic bones and scapula are most often observed. The lower jaw is affected in approximately 10% of cases. Solitary and isolated lesions are also characteristic. Bone swelling, thinning, waviness or destruction of the cortical layer and a clear delineation of the pathologically altered area of ​​​​the bone are determined. During the lytic phase, destruction of the cortical layer prevails, during the cellular-trabecular phase - thinning and waviness of the latter.

The greatest differential difficulties arise when osteoblastoclastoma is localized in the lower jaw. In these cases, osteoblastoclastoma is very similar to adamantinoma, odontoma, bone fibroma and true follicular cyst.

Treatment of Osteoblastoclastoma:

Treatment of benign osteoblastoclastomas carried out by two methods - surgical and radiation. X-ray examination is of great importance in assessing the treatment, which makes it possible to establish anatomical and morphological changes in the affected part of the skeleton during therapy and in the long term after it. In these cases, in addition to multiaxial radiography, direct magnification radiography and tomography may be recommended. Certain structural features of osteoblastoclastoma are known at various times after external beam radiation therapy. On average, after 3-4 months, with a favorable course of the process, trabecular shadows appear in place of previously structureless areas of the tumor; gradually the trabeculae become more dense. The lesion acquires a fine-meshed or coarse-meshed structure. The thinned or destroyed cortical layer is restored; tumor size may decrease. The formation of a sclerotic shaft between the tumor and the unchanged part of the bone is noted. The duration of reparative bone formation varies from 2-3 months to 7-8 or more months. In cases of the development of the “paradoxical reaction” phenomenon, first described by Herendeen (1924), 2-8 weeks after radiation therapy, pain in the affected area increases, foci of destruction increase, trabeculae resolve, and the cortical layer becomes thinner. The paradoxical reaction subsides after about 3 months. However, a paradoxical reaction may not be observed during radiation therapy for osteoblastoclasts.

An important criterion for the effectiveness of osteoblastoclast therapy is the severity of remineralization of the former lesion. The relative concentration of mineral substances at various times after radiation and surgical treatment of osteoblastomas is determined by the method of relative symmetric photometry of radiographs.

Which doctors should you contact if you have Osteoblastoclastoma:

Is something bothering you? Do you want to know more detailed information about Osteoblastoclastoma, its causes, symptoms, methods of treatment and prevention, the course of the disease and diet after it? Or do you need an inspection? You can make an appointment with a doctor– clinic Eurolab always at your service! The best doctors they will examine you and study you external signs and will help you identify the disease by symptoms, advise you and provide the necessary assistance and make a diagnosis. you also can call a doctor at home. Clinic Eurolab open for you around the clock.

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You? It is necessary to take a very careful approach to your overall health. People don't pay enough attention symptoms of diseases and do not realize that these diseases can be life-threatening. There are many diseases that at first do not manifest themselves in our body, but in the end it turns out that, unfortunately, it is too late to treat them. Each disease has its own specific symptoms, characteristic external manifestations- so called symptoms of the disease. Identifying symptoms is the first step in diagnosing diseases in general. To do this, you just need to do it several times a year. be examined by a doctor to not only prevent a terrible disease, but also maintain healthy mind in the body and the organism as a whole.

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Benign course (rarely malignant in the initial appearance). Despite its benign quality, it, in fact, occupies an intermediate place, since it grows quickly and can metastasize.

Osteoblastoclastoma statistics

Shows that the disease accounts for 20% of cancer diseases And affects children and adults aged 15-30 years(about 58% of cases).

Statistics also show that the tumor most often affects long bones (in approximately 74% of cases).

Classification

There is an x-ray division of tumors, highlighting:

• Cellular. The neoplasm has a cellular structure and is formed from incomplete bone bridges.
• Cystic. Appears from a cavity formed in the bone. The cavity fills with brown fluid, causing it to look like a cyst.
• Lytic. The bone pattern cannot be determined because the tumor destroys the bone tissue.

Depending on the type of tumor, patient survival may vary.

Localization

There are 2 types of location of osteoblastoclasts relative to bone structures:

1. central, growing from the thickness of the bones;
2. peripheral, affecting the periosteum and superficial bone tissue;

In this case, the tumor can be localized to:

• bones and soft tissues;
• tendons;
• sacrum;
• lower jaw;
• tibia;
• humerus;
• spine;
• femur;

Causes of giant cell tumor of bone

Despite the fact that osteoblastoclastoma began to be studied back in the 19th century, its causes could not be fully elucidated. Scientists have come to a consensus that the conditioning factors include:

• inflammation affecting the periosteum and bone;
• permanent bone injury, mostly limbs;

Bone tissue can grow uncontrollably if it is not formed correctly during the formation of the baby’s body. This can also be affected by repeated radiation therapy.

Clinical manifestations

The symptoms of osteoblastoclastoma are sparse and similar to some diseases of bone tissue. Before other symptoms, constant aching, rarely turning into acute, pain at the site of the lesion makes itself felt. The affected bone is deformed, and a pathological fracture is often observed.

Signs and causes of tumor malignancy

The reasons why benign osteoblastoclastoma becomes malignant are not fully understood.

There is a connection between malignancy of the neoplasm and pregnancy, which is associated with hormonal levels women. The process can also be affected by injury to the affected limb. Malignancy can occur due to repeated radiation therapy.

Signs that the tumor has become malignant are:

• The tumor is growing rapidly.
• The diameter of the focus of bone tissue destruction increased.
• The tumor passed from cellular-trabecular to lytic.
• The endplate has collapsed.
• The contours of the source of destruction become unclear.

Patients also experience a multiple increase in pain.

Diagnostics

Accurate diagnosis of osteoblastoclastoma is only possible using X-ray equipment. However, this is preceded by collecting the patient’s medical history and analyzing symptoms.

After making the presumptive diagnosis, the patient is prescribed:

• Blood chemistry. Shows the patient’s health status and the presence of bone tissue resorption markers in the blood.
• X-ray. Allows you to assess the condition of bone tissue. The good thing about this method is that every hospital has equipment for the study, however, MRI and CT are more accurate and efficient.
• MRI or . Studies allow you to obtain a layer-by-layer image of the tumor, assess its depth and condition.
• . It is a sampling of a tumor area, allowing to assess its malignancy and finally establish a diagnosis.

If necessary, the doctor will prescribe additional tests of the blood and the affected area of ​​the body.

Treatment

The main treatment for osteoblastoclastoma is resection of the area of ​​bone affected by the disease. In this case, the removed part is replaced by an explant.

The photo shows surgery to remove osteoblastoclastoma

Sometimes a standard operation can be performed using cryosurgical equipment. If tumor metastases penetrate into the area, partial resection of the organ is indicated. Very rarely, the tumor can become infected or bleed heavily, which is why it is necessary to amputate the affected limb.

Radiation therapy is prescribed to patients if surgery is not possible due to the location of the tumor, for example, on the spine, pelvic bones, base of the skull, and other awkward areas. Also, the reason for radiation therapy may be the patient’s refusal to undergo surgery.

Radiation therapy uses:

1. orthovoltage radiotherapy;
2. remote gamma therapy;
3. Bremsstrahlung and electron radiation;

Doctors say that the optimal dose is 3-5 thousand rads per month of course.

Complications and prognosis

If you consult a doctor in a timely manner, the patient has a 95-100% chance of cure. Relapses, which are extremely rare, occur for a reason similar to the primary tumor. Therefore, with proper prevention, they can be avoided in most cases.

Factors influencing complications include:

• Untimely or illiterate treatment of the disease.
• Injury to bone tissue.
• Infection.

As a result of complications, a benign tumor can develop into malignant form, metastasize, which complicates its treatment.

Osteoblastoclastoma(osteoblastoclastoma, giant cell tumor, osteoclastoma, gigantoma).
The first detailed description of this tumor belongs to Nelaton (1860). Over the years, its teaching has undergone significant changes. In the second half of the 19th century, osteoblastoclastoma (giant cell tumor) was included in the group of fibrous osteodystrophies. In the works of S.A. Reinberg (1964), I.A. Lagunova (1962), S.A. Pokrovsky (1954) giant cell tumor is considered as local fibrous osteodystrophy. V.R. Braitsov (1959) expressed a view on the “giant cell tumor” of bones as a process of embryonic disorder of bone development, which, however, was not further confirmed. Currently, most researchers do not doubt the tumor nature of this process (A.V. Rusakov, 1959; A.M. Vakhurkina, 1962; T.P. Vinogradova, Bloodgood).

Osteoblastoclastoma is one of the most common bone tumors. There are no noticeable sex differences in the incidence of osteoblastoclastoma. Cases of familial and hereditary disease have been described.

The age range of patients with osteoblastoclastomas ranges from 1 year to 70 years. According to our data, 58% of cases of osteoblastoclastoma occur in the second and third decades of life.

Osteoblastoclastoma is usually a solitary tumor. Its double localization is rarely observed and mainly in adjacent bones. Long tubular bones are most often affected (74.2%), less often flat and small bones are affected.

In long tubular bones, the tumor is localized in the epimetaphyseal region (in children - in the metaphysis). It does not grow into articular cartilage and epiphyseal cartilage. In rare cases, diaphyseal localization of osteoblastoclastoma is observed.

Clinical manifestations of osteoblastoclastoma largely depend on the location of the tumor. The first sign is pain in the affected area, bone deformation develops, and pathological fractures are possible.

Benign osteoblastoclastoma can become malignant.

Causes of malignancy A benign tumor has not been precisely determined, but there is reason to believe that trauma and pregnancy contribute to this.

Signs of malignancy of osteoblastoclastoma: rapid growth of the tumor, increasing pain, an increase in the diameter of the focus of destruction or the transition of the cellular-trabecular phase to the lytic phase, destruction of the cortical layer over a large area, unclear contours of the focus of destruction, destruction of the endplate that previously limited the entrance to the medullary canal, periosteal reaction.

The conclusion about the malignancy of osteoblastoclastoma based on clinical and radiological data must be confirmed by a morphological examination of the tumor.

In addition to the malignancy of the benign form of osteoblastoclastoma, there may also be primary malignancy of osteoblastoclastoma, which, essentially (T. P. Vinogradova) are a type of sarcoma of osteogenic origin.

The localization of malignant osteoblastoclastomas is the same as that of benign tumors. An X-ray examination reveals a focus of bone tissue destruction without clear contours. The cortical layer is destroyed over a large area, the tumor often grows into the soft tissue. There are a number of features that distinguish malignant osteoblastoclastoma from osteogenic osteoclastic sarcoma: older age of patients, less pronounced clinical picture and more favorable long-term outcomes.

Diagnostics: X-ray picture of osteoblastoclastoma of long bones.
The affected bone segment appears asymmetrically swollen. The cortical layer is unevenly thinned, often wavy, and can be destroyed over a long area. At the site of the break, the cortical layer is disintegrated or sharpened in the form of a “sharpened pencil,” which in some cases imitates the “periosteal visor” in osteogenic sarcoma. The tumor, destroying the cortical layer, can extend beyond the bone in the form of a soft tissue shadow.

There are cellular-trabecular and lytic phases of osteoblastoclastoma. In the first case, foci of bone tissue destruction are identified, as if separated by partitions. The lytic phase is characterized by the presence of a focus of continuous destruction. The focus of destruction is located asymmetrically with respect to the central axis of the bone, but as it increases, it can occupy the entire diameter of the bone. Characteristic is a clear delineation of the focus of destruction from the intact bone. The medullary canal is separated from the tumor by the endplate.

Differential diagnosis osteoblastoclastoma is carried out with osteogenic sarcoma, chondroblastoma, monoosseous form of fibrous dysplasia, bone cyst and aneurysmal bone cyst.

Of the flat bones, damage to the pelvic bones and scapula is most often observed. The lower jaw is affected in approximately 10% of cases. Solitary and isolated lesions are also characteristic. Bone swelling, thinning, waviness or destruction of the cortical layer and a clear delineation of the pathologically altered area of ​​​​the bone are determined. During the lytic phase, destruction of the cortical layer prevails; during the cellular-trabecular phase, thinning and waviness of the latter prevails.

The greatest differential difficulties arise when osteoblastoclastoma is localized in the lower jaw. In these cases, osteoblastoclastoma is very similar to adamantinoma, odontoma, bone fibroma and true follicular cyst.

Treatment: carried out by two methods - surgical and radiation. A marginal bone resection is performed with auto- and/or alloplasty of the defect.
For large tumors with destruction of the cortical bone layer or for recurrent tumors, resection of the articular end of a long tubular bone with auto- or alloplasty of the defect is indicated; endoprosthetics is also possible.