Parenchymal sialadenitis in children. Etiology, clinical picture, differential diagnosis, treatment

Benign tumors from the bone tissue itself

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 “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 frequent tumors bones. 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 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 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 of long osteoblastoclasts 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

Osteoblastoclastoma (lytic phase) Osteogenic osteoclastic sarcoma Bone cyst
Age 20-30 years Up to 20-26 years old 2 years -14 years
Localization Epimetaphysis Epimetaphysis Metadiaphysis
Bone Shape Pronounced asymmetric swelling Slight expansion in diameter Fusiform swelling
Contours of the focus of destruction Clear Fuzzy, blurry Clear
Condition of the bone marrow canal Closed by an endplate Open at the border with the tumor
Cortical layer Thinning, wavy, interrupted Thinned out, destroyed Thinned, smooth
Sclerosis Not typical Takes place Not typical
Periosteal reaction No Expressed mainly as a “periosteal visor” No
State of the pineal gland The epiphyseal plate is thinned, wavy IN initial stages the epiphysis remains intact Not changed
Adjacent diaphyseal bone Not changed Osteoporotic Not changed

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 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. 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, rapid progression of the process with a growth inclination towards the joint, breakthrough of the cortical layer with the tumor emerging into soft fabrics. The main clinical and radiological symptoms characteristic of osteoblastoclastoma and fibrous dysplasia are presented in Table 3.

Table 3

Osteoblastoclastoma Fibrous dysplasia
Age Mostly 20-30 years old Children's and youth
Localization Epimetaphysis Metadiaphysis, any
Prevalence of the process Solitary lesion Solitary and polyostotic
Deformation Club-shaped swelling Curvature, shortening, slight expansion
Nature of destruction Homogeneous, with bone bridges Ground glass symptom
Cortical layer Lumpy, wavy, may be interrupted The outer contour is smooth; internal - wavy, not interrupted
Sclerosis Not typical Areas of sclerosis in the area of ​​the bone marrow canal, in the cortical layer

X-ray picture of osteoblastoclastoma of flat bones.

Of the flat bones, changes are most often observed pelvic bones and shoulder blades. 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 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. 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.

Treatment of benign osteoblastoclastomas is carried out by two methods - surgical and radiation. Great value in the assessment of the treatment carried out belong to x-ray examination, 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 approximately 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 treatment of osteoblastoma 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. In first place in terms of the frequency of damage is 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 no changes. With cortical localization of the process, bone thickening can be determined by palpation. In some cases, laboratory tests show moderate leukocytosis and accelerated ESR in patients (Ponselti, Bartha). In our observations, laboratory parameters in patients with osteoid osteoma were without deviations from the norm.

X-ray picture of osteoid osteoma. Mostly in the diaphysis or metadiaphysis of a long tubular bone, an oval-shaped area with clear contours is identified as 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. Within the lesion, bone inclusions may be visible, which Walker (1952) calls “tiny round sequestra” and considers them typical of osteoid osteoma.

Rare cases of “giant osteoid osteoma” reaching 5-6 cm in diameter 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 even after radical surgery. surgical treatment, as a rule, does not recur.

Osteoma. A relatively rare, predominantly solitary, exophytically growing tumor consisting of bone tissue varying degrees maturity from fine-fibrous to lamellar. Is detected more often in childhood, sometimes an incidental radiological 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 of bone density, rounded in shape (rhinoliths).

Spongy osteoma is most often localized in short and long tubular bones and jaw bones.

Clinical course Osteoma 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. The cancellous osteoma of the tubular bone moves away from the joint as it grows, its contours are clear, the cortical layer can be traced throughout, it becomes thinner, but is not interrupted. Bone structure The tumor differs somewhat from the structure of the main bone by 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, the subperiosteal venous sinus of the skull - sinus pericranium - is mistaken for osteoma, which is a development option.

The prognosis for osteoma is favorable. Osteoma does not become malignant, but requires radical surgical treatment in avoiding possible tumor relapses.

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 “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 approximately 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:

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If you want to ask a doctor a question, use the online consultation section, perhaps you will find answers to your questions there and read

Differential diagnosis of cancer upper jaw with ameloblastoma(adamantinoma) is caused by the fact that when it is localized in the alveolar process, there is a thickening of this part of the maxillary bone. When ameloblastoma appears, its first clinical sign is

There is also swelling of the affected area of ​​the alveolar process of the upper jaw. From this moment, as N. M. Mikhelson and

L. O. Varshavsky (1955), there is a need to differentiate a malignant tumor from ameloblastoma.

The difference between cancer of this location and ameloblastoma is expressed in the rapid growth cancerous tumor, the presence of pain in the teeth and their looseness. Ameloblastoma grows extremely slowly and sometimes takes years to reach a large size. There are no pain symptoms with ameloblastoma. Loose teeth are observed extremely rarely, usually after tumor suppuration. When ameloblastoma is large, its bone wall becomes thinner and bends under finger pressure, which is accompanied by the appearance of a “parchment crunch.” There is no involvement of the lymph nodes. The X-ray picture of ameloblastoma is also significantly different from that of a cancerous lesion, as already mentioned earlier.

The need for differential diagnosis of alveolar cancer with osteoblastoclastoma is caused by the same general characteristics, i.e. the presence of deformation of the alveolar process.

The difference between alveolar cancer and osteoblastoclastoma is that, in addition to those already mentioned distinctive features with ameloblastoma, which is also characteristic of osteoblastoclastoma, localized in the alveolar process, it usually occurs in children and young people and much less often in older people.

At the same time, the long course of the disease, the absence of nasal discharge, and the absence of pain symptoms distinguish osteoblastoclastoma from a cancerous tumor. X-ray examination is important in differential diagnosis.

The final diagnosis is established based on the data

pathomorphological examination.

Differential diagnosis of cancer of the upper jaw with odontogenic cysts carried out due to the presence of them common feature- deformation of the alveolar process, which, as these formations grow and fill the maxillary sinus with them, can manifest themselves in protrusion of the anterior wall of the sinus and the corresponding lateral wall of the nose.

The difference between a cancerous tumor of the alveolar process and odontogenic cysts is that a cancerous tumor does not cause significant thickening of this part of the upper jaw, causes pain in the teeth, and quite quickly leads to the destruction of bone tissue and loose teeth with subsequent formation of ulcers. When spreading towards the orbit


the tumor causes exophthalmos and blurred vision. There is nasal discharge mixed with ichor.

Odontogenic cysts are manifested by a more distinct swelling of the alveolar process, which, when further development the cyst spreads to the anterior wall of the maxillary sinus and protrudes it. But even with a significant size, the cyst, as a rule, does not spread towards the orbit, does not cause exophthalmos and does not lead to visual impairment.

In addition, with an odontogenic cyst, there is no pain in the teeth, their looseness is not observed bloody discharge from the nose. The mucous membrane of the alveolar process has normal color. A test puncture through the anterior wall of the maxillary sinus in the area of ​​the transitional fold of the vestibule of the oral cavity with an odontogenic cyst allows one to obtain a viscous liquid amber color. If there is a cancerous tumor, the punctate will contain either blood or no contents.

On radiographs, both with a cyst and with cancer, shading of the maxillary sinus is noted, but with a cyst it will have clear boundaries and connection with the tooth - the presence of a tooth root facing the cyst (with a radicular cyst) or a crown (with follicular cyst). With cancer, the entire maxillary sinus is obscured, and destruction of its walls is revealed.

Differential diagnosis of cancer of the upper jaw from osteoma is carried out because the latter is often found on the upper jaw, localized on its anterior surface and on the zygomatic bone. Less commonly, it is located in the maxillary sinus. With the development of osteoma as a result of thickening of the affected part of the upper jaw, its deformation occurs.

Located in the maxillary sinus, with further growth towards the orbit it can cause displacement eyeball outward and impair vision, when growing towards the nose - lead to protrusion of its outer wall, and when growing towards the palatine processes - to protrusion hard palate. Symptoms mentioned also found in cancer

upper jaw.

The difference between cancer of the upper jaw and osteoma is the faster growth of the tumor, the absence of clear boundaries, the appearance of nasal discharge mixed with blood, and loose teeth. Osteoma grows extremely slowly.

Located at a wide base on the surface of the bone, it is clearly demarcated from the surrounding bone tissue. Bloody-purulent discharge is not observed with it. There is no looseness of the teeth. Even with a significant size of osteoma, the mucous membrane of the upper jaw does not change, does not grow with a tumor and does not ulcerate.

An x-ray of osteoma reveals newly formed bone tissue that has a homogeneous structure with clear contours.

The need for differential diagnosis of cancer of the upper jaw with fibroma sometimes occurs due to the presence of such general symptoms as deformation of the upper jaw, impaired nasal breathing, copious discharge from the nose.

The difference between cancer of the upper jaw and fibromatous growths of the nasal cavity and maxillary sinus is that with cancer of the upper jaw, spontaneous pain and loosening of the teeth are usually observed, and nasal discharge is purulent in nature. X-ray reveals

intense shading of the maxillary sinus without clear boundaries and destruction of bone tissue. With fibromatous growths in the nasal cavity and in the maxillary sinus, pain and loose teeth are not observed. Discharge from the nose is mucopurulent in nature without admixture of blood. The x-ray shows a smooth, clearly defined border of the tumor, separating it from the walls of the maxillary sinus.

In difficult cases, the question of the nature of the tumor is decided on the basis of biopsy data.

Differential diagnosis of cancer of the upper jaw with chronic inflammation of the maxillary sinus is determined by the following general symptoms: duration of the disease, presence in the upper jaw aching pain, difficulty in nasal breathing, purulent discharge from the nose.

The difference between cancer of the upper jaw and chronic inflammation maxillary sinus is that with cancer there is deformation of the upper jaw as a result of protrusion of the anterior wall of the maxillary sinus, loose teeth, and discharge of pus from the nose mixed with ichor.

With chronic inflammation of the maxillary sinus, there is no deformation of the upper jaw, no loose teeth are noted, pus is released in greater quantities than with cancer and without the admixture of ichor. A test puncture indicates the presence of pus in the sinus. The x-ray shows no signs of destruction of the bone walls of the maxillary sinus, which is usually observed with cancer.

The need for differential diagnosis of hard palate cancer with syphilitic gumma determined by the presence of a number of similar characteristics. Thus, with an infiltrative form of cancer emanating from the mucous membrane of the hard palate, the neoplasm initially appears in the form of a painless infiltrate, covered with normal mucous membrane. With gummous lesions of the hard palate, a limited painless infiltrate of bluish-red color is also initially noted. Subsequently, both with cancer and with tertiary syphilis, the infiltrates disintegrate with the formation of ulcers. Moreover, the edges of the ulcers in both cases are dense.

The difference between a cancerous ulcer of the hard palate and a syphilitic gumma is that a cancerous ulcer, as already indicated, has crater-shaped, torn edges, covered with granular, easily bleeding tissue. It quickly spreads along its length, capturing the soft palate and alveolar process, causing loosening of the teeth.

A gummous ulcer has a regular round or oval shape, surrounded by a ridge of bluish-red infiltrate. Its bottom is covered with a yellow-gray coating. Probing reveals necrotic bone, which is subsequently sequestered to form a perforation opening connecting the oral cavity with the nasal cavity.

A gummous ulcer does not tend to spread along its length and does not cause loosening of the teeth. There is usually no nasal discharge. The x-ray shows signs of thickening and compaction of bone tissue due to periosteal layers.

They appear unexpectedly for the patient.

The causes may be bruises or fractures, but in most cases, experts cannot name the exact prerequisites that could lead to the presented troubles.

Depending on the substance that provoked the growth, benign and malignant tumors bones.

Treatment is carried out according to the same principle: some tumors are not affected throughout life if they do not cause harm to the human body, while others must be immediately removed.

Giant cell tumors of the bone are removed almost immediately after detection. surgical method. In some cases, the tumor is removed along with the limb.

Concept and statistics

Giant cell tumor of bone (has official name– osteoblastoclastoma) – benign tumor bone, consisting of an accumulation of layers of ovoid-shaped mononuclear cells and osteoclast-like giant multinucleated cells.

The presented disease accounts for approximately 20% of all cases of formation.

Giant cell tumor of bone began to be studied in more detail in the 19th century, although it was known about it in ancient times. Until recently, this neoplasm was considered a disease of young people, in most cases boys.

But recent statistics have shown that the growths occur in people between 15 and 30 years of age.

Reasons for the manifestation of education

To date, the exact causes of the manifestation of the neoplasm have not been established. Some of the supposed factors are still subject to debate among scientists.

Experts agreed that the following factors can influence the formation of a giant cell tumor:

  • inflammatory processes of bones and periosteum;
  • and bruises that were received repeatedly in one place;
  • injuries can also “convert” an existing benign tumor to malignant status;
  • The “transition” is sometimes influenced by a woman’s pregnancy.

Of course, when diagnosing a bone tumor, the causes of such a disease fade into the background. But people who fall into the risk group according to the list above should be careful and attentive.

Tumor symptoms

Symptoms of the described neoplasm include:

  • pain in the affected area, manifested by movement or palpation;
  • a skin vascular pattern is observed over the affected area;
  • during the process of enlargement, the patient notices a deformation of the affected area, which upon palpation causes excruciating suffering;
  • there is a dysfunction of the joint adjacent to the affected area or the entire limb;
  • Palpation of the tumor causes not only pain, but also a characteristic crunching sound.

Doctors should be contacted at the first manifestation of the listed symptoms.

Diagnostic approach

The photo shows osteoblastoclastoma of the jaw

Diagnosis of osteoblastoclastoma begins with general examination specialist.

Accurate diagnosis of a neoplasm occurs through the following studies:

  1. X-ray examination– allows you to quickly determine the nature of changes in bone surfaces, and sometimes determine the structure of the neoplasm.
  2. MRI and CT– intended to study the depth of the lesion and its composition.
  3. Tumor biopsy– used to identify the composition of the tumor if specialists have any questions. It is also often performed before surgery. Represents the removal of part of the tumor for laboratory research its composition and structure.

Based on the diagnosis, specialists determine the method and treatment regimen (if possible).

How are tumor formations removed?

Typically, giant cell tumors will not go away on their own. Therefore, only a few methods are used here to remove the affected area:

  1. Surgical intervention– marginal resection of the affected area. Requires reconstruction of the removed part, since in some cases a giant cell tumor of the bone is removed along with the entire bone (sometimes with the joint). Surgeons and oncologists make such a decision to prevent recurrence of the disease. The resulting defect is restored using a special implant. If a growth is removed from a child, the implant has the technical ability to increase, as a result of which the operated child undergoes surgical intervention every 2-3 years.
  2. Limb amputation– is carried out extremely rarely. The reason for such removal is suppuration of the affected area or soft tissues due to infection entering the body. Sometimes amputation of a limb is performed in the presence of a huge tumor.
  3. Radiation therapy– the method is used quite rarely and only in the case of a small tumor, that is, on initial stage progression of the disease. Under the influence of rays, the tumor decreases in size.
  4. R radiation exposure– used extremely rarely and only in cases of “difficult access” of the affected area. Attracts many unpleasant consequences in the form of diseases of internal organs. It is carried out in a course and does not always contribute to the complete elimination of the tumor.

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The treatment method directly depends on the course of the disease and other factors that were identified at the diagnostic stage.

It should be noted that giant cell tumor has the characteristic of rapid growth, so diagnosis and treatment must be resorted to immediately.

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Complications and prognosis

Complications of the disease can result from untimely treatment or infection.

Also, complications of an existing neoplasm are affected by all of the above reasons for the manifestation of the presented disease.

Complications include its transition from a benign tumor to a malignant one, as well as the formation of metastases in internal organs person. The lungs and other respiratory organs are more vulnerable in this regard.

Therefore, surgery to remove a tumor can often be postponed due to the minimal likelihood of a favorable outcome.

As for prognosis, a benign giant cell tumor of the bone, despite its size, can be removed by any given treatment method.

Relapses are quite rare. They are provoked by the same causes of manifestation that led to the formation of the first neoplasm.

If a person consults a doctor in time, namely at the stage of manifestation pain with movement or palpation, a favorable outcome of events has an almost 100% probability.

Monitor your condition carefully and at the first symptoms, consult a doctor for a diagnosis.

Osteoblastoclastoma (osteoblastoclastoma)- a tumor originating from bone tissue. It is also called gigantoma, brown, or giant cell tumor. The name of the tumor is due to the composition of its cells: giant multinucleated cells that take part in bone resorption (osteoclasts), and mononuclear cells that restore the latter - osteoblasts. Morphologically, there is no difference between the peripheral and central forms of osteoblastoclastoma. If a giant cell tumor is localized on the gums, then it is a peripheral form. A central tumor develops in the bone and differs from the peripheral one in the presence of many hemorrhagic foci, which is why it is also called a brown tumor. Since blood circulates slowly in the cavity, sedimentation of erythrocytes begins, disintegrating with the formation of hemosiderin, which determines brown color tumors. If the cysts are connected into one cystic cavity, most often they grow with fibrous tissue.

Osteoblastoclastoma central shape develops as a solitary formation, that is, it is represented by one conglomerate. Bone trauma or infection plays a significant role in the etiology.

Complaints. At the beginning of the development of the tumor there are few complaints; it grows slowly, without causing any sensations. Sometimes pain may appear early in the teeth located in the affected area, or disruption of the eruption of permanent teeth may occur. As the tumor grows, pain appears when chewing.

Children or their parents turn to a doctor when a jaw deformity appears or a tumor is found by chance when an X-ray examination is performed for another purpose (jaw injury, dental disease or temporomandibular joint disease). If not large sizes tumor, facial asymmetry is not determined. A large tumor causes jaw deformation, often fusiform, and as a consequence, asymmetry.

Clinic. Mouth opening is free, but may be limited as the tumor grows if it is localized in the ramus of the mandible. The mucous membrane over the tumor does not change color for a long time.

Osteoblastoclastoma often spreads to the outer surface of the lower jaw, and over time can involve the entire body of it. When osteoblastoclastoma reaches a large size and thins bottom edge the jaw is in danger of breaking. Inflammation periodically develops in the tumor


Section 7


Benign neoplasms bones maxillofacial area

body process, which can result in the formation of fistulas on the mucous membrane.

According to radiographic and morphological studies, the central form of osteoblastoclastoma is divided into cystic, cellular and lytic.

Cystic form is observed in children in approximately 60% of cases of osteoblastoclastoma. The tumor grows slowly. X-ray reveals a focus of bone loss with a zone of sclerosis around it, clearly separating the tumor from healthy tissue. Usually there is horizontal resorption of tooth roots in the tumor area, which is a pathognomonic sign cystic form(Fig. 211). It is necessary to distinguish horizontal resorption of tooth roots in osteoblastoclastoma from unformed apexes of teeth and physiological resorption of temporary teeth.

Cellular This form of tumor is very rare in children. Clinically, it resembles a cystic form, but the surface of the jaw is often tuberous. Radiologically, the cellular form is characterized by small cavities separated by partitions (Figure " soap bubbles") and clearly demarcated from healthy tissue.

The lytic form is the most aggressive, found in 10-15 % cases of osteoblastoclastoma in children early age and teenagers. It is characterized by rapid expansive growth. When localized on the upper jaw, it can grow into maxillary sinus And nasal cavity, and in some cases - to go beyond the cortical layer of the affected bone. The tumor often leads to severe facial asymmetry. Pain in the jaw, displacement and mobility of teeth are observed. X-rays reveal unclear contours of bone tissue (in contrast to cystic and cellular forms).

For staging final diagnosis it is necessary to apply additional methods - puncture and histological examination of the tumor. Tumor puncture should be performed under local anesthesia with a thick needle in the area of ​​its greatest protrusion in the lower pole. For osteoblastoclastoma, a brown-cherry-colored punctate containing hemosiderin, without cholesterol crystals, is obtained, or blood can be obtained (circulatory features, which have already been mentioned).

At peripheral form of osteoblastoclastoma (giant cell epu-lid) complaints the child will be diagnosed with a painless neoplasm, which is located on the alveolar ridge and interferes with eating. When injured (eating, brushing teeth), the neoplasm bleeds.

Clinic. Upon examination, a bright red tumor is revealed, which is located on both sides of the alveolar ridge, like a rider on a horse. The neoplasm has wide base, densely elastic consistency, covered with a mucous membrane with areas of ulceration resulting from frequent trauma to it. The giant cell epulid covers several teeth (Fig. 212-214). The latter may acquire mobility, the degree of which depends on the size of the tumor and the changes that have occurred in the bone.


Rice. 211. X-ray of the right half Rice. 212. Giant cell epulidus of the left

ns of the lower jaw of a child with osteoblast - the upper jaw in the premolar area

toclastoma (cystic form)

Rice. 213. Giant cell epulide upper- Fig.214. Giant cell epulidus right

of the lower jaw in the area of ​​25, 26 teeth of the half of the lower jaw in the area of ​​the molar

Central osteoblastoclastoma should be differentiated from solid or cystic ameloblastoma, chronic destructive-productive osteomyelitis, fibrous dysplasia, intraosseous hemangioma, and sarcoma.

The peripheral form of osteoblastoclastoma is easily distinguished from the banal epulid and local form fibromatosis.

Treatment osteoblastoclastoma surgical. Excochleation of small cystic tumors is supplemented with curettage of the underlying bone. For the lytic form, the method of resection of a section of the jaw within healthy tissue is used. For large osteoblastoclastomas, especially lytic ones, subperiosteal resection of the mandible along with the tumor is performed, preserving the mandibular margin.

The most likely consequences with adequate treatment may be different types deformations of the jaws, teeth, bite, and if inadequate - tumor recurrence, inflammation, jaw fracture.

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OSTEOMA

Osteoma is a rare benign tumor of bone tissue, mainly in children of middle school age.

Diagnosis this tumor is diagnosed based on following signs: clinically - painless, slowly increasing deformation of the jaw; X-ray: a neoplasm is determined, delimited by a cortical plate, its structure is somewhat denser than normal bone tissue. The histological structure of osteoma is characterized by a violation of the architectonics of compact bone, narrowing of vascular canals, and an almost complete absence of osteon canals.

Differential diagnosis. Particular difficulties may arise in the differential diagnosis of osteomas with osteodysplasias. Often the diagnosis can be established only on the basis of pathohistological examination data.

Osteoma is also differentiated from exostoses resulting from traumatic irritation or chronic inflammation of the periosteum, which can be learned from the child or his parents when collecting anamnesis.

Treatment. Surgery is indicated when the tumor causes discomfort, functional or aesthetic disorders, and consists of leveling (that is, giving the bone the correct shape) of the affected area of ​​the jaw.

STE0ID-0STE0MA

Osteoid osteoma is a benign tumor of the cortical bone layer, consisting of osteoid structures, connective tissue and newly formed bone. It is observed very rarely in children, mainly in boys 5-15 years old. It is most often located on the lower jaw (in its lateral sections). It can be localized in the cortical, spongy layer or subperiosteal.

Complaints. A typical complaint of a child is the presence of pain, which has a local constant or paroxysmal character, most intense at night, often reminiscent of neuralgia trigeminal nerve. If the tumor is localized in the alveolar process of the lower jaw, the pain may intensify while eating.

Clinic. In most cases, osteoid osteoma does not manifest itself in any way, especially on early stages development. There may be swelling of the surrounding tissues, an increase in local temperature, pain on palpation of the affected area, and if the tumor is localized subperiosteally, the phenomenon of periostitis.

Clinical signs do not allow an immediate diagnosis to be made, so it is necessary to carry out additional methods research. The most informative of them are radiological and pathohistological. The latter becomes decisive.

At the onset of the disease, the tumor is detected as a rounded focus of bone destruction with unclear boundaries, surrounded by sclerotic bone (Fig. 215). The width of the sclerosis zone depends on the duration of the disease. On late stages the focus of destruction is performed by the newly formed bone tissue and on X-ray


frame looks darker. With cortical localization of osteoid osteoma, a thick zone of sclerosis (periosteal growths) is detected on the radiograph. The X-ray picture of the tumor corresponds to chronic inflammatory process bones.

Differential diagnosis carried out with osteosarcoma, osteoma, productive form of chronic osteomyelitis, fibrous dysplasia.

Treatment osteoid osteoma is partial resection jaw within healthy tissues, preserving its lower edge. The tumor recurs very rarely. The consequences of the disease can be deformations of the jaws, teeth and bite.