Treatment of fibrous bone dysplasia in Israel - accurate diagnosis and progressive methods of therapy

Pathology treatment methods

Fibrous dysplasia, or Braitsov's disease, usually manifests itself in pediatric patients and is very rarely first diagnosed in elderly patients. The pathology was first described about a hundred years ago, and over the ensuing years many studies have been carried out that have not provided specialists with information to determine the exact causes of its occurrence. Today, it is believed that hereditary predisposition plays a major role in the abnormal development of tissue that gives rise to bone in the prenatal period.

There is a monoosal form of dysplasia, in which only one bone is affected; painful symptoms debut in patients of any age; areas of skin pigmentation and endocrine disorders are not detected. The polyostotic form developing in children manifests itself in damage to several bones, accompanied by endocrine disorders and melanosis (the appearance of dark spots on the skin).

According to another classification, intraosseous, tumor, fibrocartilaginous and some other forms of fibrous dysplasia are distinguished. In some cases, total bone damage is observed.

Characteristic signs of the disease are the appearance in the patient of intense pain, pathological fractures and gradually progressive bone deformations. If the pathological focus is localized in the tubular bones of the legs, they become bent, shortened, and acquire a pathological shape. The patient also complains of lameness. The appearance of an area of ​​fibrous dysplasia in the spine is accompanied by the development of scoliosis or kyphosis, and postural disorders.

In many patients, the pathology, especially in the initial stages, occurs without clinical symptoms, so Israeli clinics tend not to prescribe specific treatment unless absolutely necessary. If there are no signs of disease progression, the patient is observed by the attending physician, and he must attend a preventive examination at least once every six months and undergo prescribed examinations.

The only effective treatment method is surgical removal of the pathological focus, for which progressive gentle surgical methods are used.

Surgery

Most often, to eliminate the affected area of ​​bone tissue, segmental resection is used, carried out within the boundaries of normal tissue. During this operation, the continuity of the bone is disrupted, as a result of which the defect is subsequently restored using a bone grafting procedure. The endoprosthesis replacement procedure involves the installation of endoprostheses, which are individually manufactured for each patient. An autograft can also replace the articular surface. Pathological fractures require placement of an Ilizarov apparatus on the patient.

Drug therapy

If, during the examination, multiple lesions are revealed in the patient, he is prescribed medications that prevent deficiency of bone tissue density, which is one of the main causes of pathological fractures, and its deformation. The prescribed drugs help strengthen bone tissue and prevent bone atrophy. In addition, the patient is prescribed vitamin D and calcium-containing medications. To eliminate severe pain, analgesics and other painkillers are indicated.

What is hip dysplasia?

Hip dysplasia is a severe pathology characterized by underdevelopment of all elements of the hip joint (bones, ligaments, joint capsule, muscles, blood vessels, nerves).

The modern name of this pathology is Developmental dysplasia of the hip, i.e. developmental dysplasia of the hip joint, which occurs during pre- and postnatal ontogenesis and may include neonatal instability, isolated underdevelopment of the acetabulum, subluxation and dislocation of the hip - the most severe degree of hip dysplasia, which is characterized by complete separation of the contact of the articular surfaces of the femoral head and acetabulum.

Modern methods of diagnosing the disease

Diagnosis of this disease, especially its monoosseous form, is difficult. Examination of the patient, consultation with an oncologist, therapist and TB specialist are necessary both to make a diagnosis and to determine the need for treatment or the possibility of replacing it with observation. In Israeli clinics, the stage of diagnosis and selection of the most effective methods of therapy takes about three days.

• Day 1
• Day 2
• Day 3

At the initial consultation with an orthopedist, which the patient must attend after admission to the medical center, the doctor performs a superficial examination, studies the results of previous studies, talks with the patient, collecting a detailed family history, clarifying the nature and duration of the symptoms.
At the final stage of the consultation, the orthopedist-traumatologist draws up a list of required examinations. The next day, the patient undergoes the types of diagnostic examinations indicated in the list of appointments:

- imaging studies (radiography, CT and MRI of the affected bone) - are intended to identify pathology at the earliest stages of development and establish its characteristics;

- bone scintigraphy;

- densitometry - an x-ray research technique that allows you to determine the mineral density of bone tissue, carried out to exclude the presence of multiple pathological foci;

— a biopsy with further morphological analysis is carried out in order to establish the form of the pathology, as well as to determine the exact cause of the disorders, in the absence of indicators sufficient to make a diagnosis after imaging studies.

The results are submitted for consideration to a medical council, which includes an orthopedist and highly specialized specialists. After analyzing the indicators, doctors collectively establish a diagnosis and build a treatment regimen.

results

The results of treatment were monitored over a period of 1 to 9 years. The effectiveness of treatment was assessed taking into account oncological and orthopedic criteria. The effectiveness criteria were the absence of complaints, relapse of the disease, signs of consolidation of the pathological fracture, and function of the operated limb.

All patients underwent safe osteoplastic surgery, only in 1 case no surgical treatment was performed, since repair of the pathological focus was recorded after healing of the fracture against the background of the cyst. The period of immobilization in a plaster cast was 6 weeks. In situations with other patients, surgical treatment was necessary. Considering the absence of displacement or the presence of slight displacement of bone fragments and the nosological affiliation of the underlying disease, fixation with plaster casts in 21 cases was the first stage of treatment. Fixation mainly lasted 1 month from the moment of injury, thereby consolidating the fracture, which ensured the creation of more favorable conditions for surgical treatment. In case of significant displacement, the first stage was trephine biopsy to verify the diagnosis and closed reposition to eliminate gross displacement. After which the affected limb was fixed with a plaster cast or a skeletal traction system was applied. After morphological verification of the diagnosis, patients underwent open reduction of the fracture, removal of pathological tissue, alloplasty and, if necessary, metal osteosynthesis. Patients operated on without metal osteosynthesis were treated with unloading and fixation of the affected limb with a plaster cast for 3 months from the date of surgery. Next, the plaster cast was removed and the development of movements in the joints of the operated limb began. Full weight-bearing was recommended 4 months after surgery. The use of bone osteosynthesis made it possible to abandon the use of external immobilization and begin early activation of the patient, to begin early development of movements in the joints of the operated limb, which in turn helped to reduce the length of hospital treatment and facilitate patient care.

In the presence of a metal fixator, the development of movements in the joints of the affected limb began 1 week after the operation, and full load - after 1 month. In the postoperative period, dynamic observation of all patients who received surgical treatment in the department was carried out. Control radiographs were taken 3, 6, 9 and 12 months after surgery. Consolidation of fractures was observed 2.5–3 months after surgery. The timing of non-organotypic reconstruction of grafts depended on a number of factors: the volume of the post-resection defect, the number, type and type of grafts and nosology of the disease. Autografts were reconstructed most quickly in a period of 8 to 12 months. With the isolated use of Perfoost grafts, the period of reconstruction took on average from 12 to 14 months. In cases of massive alloplasty with extensive bone resections, when superficially demineralized allo-implants were combined with cortical frozen implants, the reconstruction period increased to 18 months.

The timing of removal of metal structures depended on the nosology of the pathological process. In fibrous and osteofibrous dysplasia, taking into account the nature of the disease, metal structures were left in place to prevent the occurrence of deformities and pathological fractures in the long-term postoperative period. In other cases, the metal structures were removed 1.5–2 years after the operation.

The following complications were recorded between 3 and 6 months. In case of bone cysts: in 5 cases - relapse of the underlying disease, in 2 - shortening of the damaged segment, 1 case each - joint contractures and neurological disorders; with fibrous dysplasia: in 1 patient - shortening of the damaged segment; with non-osteogenic fibroma: 2 – joint contractures. In the long-term postoperative period (9–18 months) with fibrous dysplasia, migration of metal structures was noted in 2 cases.

Advantages of treatment in Israel

• International level of specialist training.
• Modern material and technical base of clinics
• Performing surgical interventions using progressive methods.
• Comfortable conditions for treatment.
• Loyal prices.

Carrying out therapy at the initial stages of the disease allows most patients to forget about the disease and quickly restore lost functions. Do not hesitate, contact an Israeli clinic and undergo a full course of treatment and rehabilitation.

1. 5
2. 4
3. 3
4. 2
5. 1

(0 votes, average: 5 out of 5)

Causes of fibrous dysplasia

Knowing the causes of fibrous bone dysplasia is necessary in order to be able to exclude them and thus carry out effective prevention of the disease.

You should start with exposure factors at the stage of intrauterine development. A high risk of developing pathology in the fetus may occur if a woman during pregnancy:

• did not follow the doctor’s recommendations;
• did not take vitamin-mineral complexes;
• used hormonal medications as prescribed by a doctor to maintain pregnancy;
• suffered from acute viral and bacterial infections;
• was treated with antibacterial and antiviral agents.

After birth, the following triad of negative factors comes into play:

1. lack of sufficient care for the baby, including massage, gymnastics, air baths;
2. vitamin D deficiency, leading to the launch of the process of destruction of bone tissue against the background of rickets;
3. decreased level of immune defense in the absence of a long period of breastfeeding.

Thus, we can conclude that the risk group for developing fibrous dysplasia of the leg bones includes infants from socially disadvantaged families, premature babies and those who are bottle-fed. Prevention of rickets is important, especially in northern regions where there is a shortage of sunny days.

At the age of over 3 years, risk factors for the development of dysplasia are supplemented by a deficiency of certain elements in the daily diet. It is known that children of toddler and preschool age are particularly picky in choosing foods for their diet. For the most part, they categorically refuse milk and dairy products. This leads to inevitable calcium deficiency. Total destruction of tooth enamel begins. Following persistent and invincible caries comes bone dysplasia. Calcium is washed out of it in large quantities. In conditions of total deficiency of this microelement in the blood, the lesions are replaced by fibrous connective fibers.

Thus, if your child aged 4–7 years has a serious problem with his teeth, you constantly visit the dentist and still this does not help cure caries, you should not think that the baby just eats a lot of sweets. Most likely he has a calcium deficiency. We urgently need to do a biochemical blood test to determine this microelement. If a deficiency is indeed present, then it is important to carry out specific prevention and look for the cause of the pathology.

In an adult, fibrous dysplasia of the leg bones can be caused by the following pathologies:

• osteoporosis, including those caused by hormonal disorders and intestinal diseases;
• excess body weight with increased physical stress on the periosteum, which loses its ability to provide blood supply to the bone;
• incorrect foot placement;
• sedentary lifestyle and predominantly sedentary work;
• total dystrophy of the sciatic nerve against the background of long-term osteochondrosis of the lumbosacral spine with impaired innervation of all tissues of the lower limb on one or both sides;
• endocrine diseases of the adrenal glands and thyroid gland;
• destruction of large joints of the lower limb and, as a result, weakening of the muscle tissue that ensures normal blood supply.

general characteristics

Jaw dysplasia is the replacement of the jaw bone with connective tissue containing elements of cement-like calcifications. The fibrous mass consists of cells responsible for the synthesis of collagen, elastin and other components.

The affected jaw bones lose their normal structure, strength, and their composition and morphology change. The pathological process leads to the emergence of factors:

• Changes in bone shape.
• Facial asymmetry.
• Fractures.
• Destruction of surrounding areas.
• The appearance of inflammation, pain and other clinical signs.

In most cases, the disease is asymptomatic.

The first case of pathology was described by Recklinghausen, a pathologist from Germany in 1891.

There is no consensus among doctors regarding the classification, stages and types of this anomaly. The article describes generally accepted formulations and characteristics.

The localization of foci and the prevalence of the disease are determined by its type. Women are more susceptible to this anomaly compared to men. The average incidence rate is 1-6%.

The key cause is non-hereditary gene mutations that disrupt the normal process of bone formation.

Before treating fibrous dysplasia

It is important to understand that such symptoms, especially in children, can manifest a huge number of dystrophic, endocrine and metabolic diseases. Therefore, before treating fibrous dysplasia of the lower extremities, it is necessary to conduct a thorough differential diagnosis.

To get started, you can make an appointment with an experienced podiatrist at our chiropractic clinic. During the first examination, an experienced doctor will be able to make a correct preliminary diagnosis. If necessary, additional examination measures will be recommended to you. Usually, MRI is used, during which diagnostics makes it possible to exclude all malignant neoplasms. You will also need to do a biochemical blood test to exclude endocrine and metabolic pathologies.

Sign up for a free initial consultation. in our clinic. You can visit the doctor at any time convenient for you.

Clinical manifestations

Symptoms of the disease are determined by its form, stage, location.

CDD is characterized by an asymptomatic course. The defect is detected randomly during an x-ray diagnosis for another reason. Less common symptoms:

• Soreness in the affected area.
• Chronic osteomyelitis.
• Fistulas on the alveolar process, exposure of avascular tissue.
• Death of pathological areas of tissue.

With the fibrous type of defect, the clinical manifestations are pronounced:

• Facial deformation.
• Damage to dental elements and eyeball.
• Disturbance of the nasal passages.
• Headache.
• Damage to the ossicles of the middle ear, optic and cranial nerves.
• Loss of hearing and vision.
• Fractures of pathologically altered jaws.

Malignancy is rare.

Diagnostics

An experienced dentist can identify the disease. The following types of diagnostics are used:

• Clinical examination of the patient. Assessment of facial symmetry. Study of anamnesis and complaints.
• Radiography.
• CT, MRI.
• Puncture with histology.

Laboratory studies are not informative.

Treatment process

Surgical treatment with excision of pathological tissue is carried out in the presence of pronounced symptoms. In case of an asymptomatic course of the disease, a wait-and-see approach with regular doctor’s examinations is chosen. Maintaining oral hygiene and taking measures to prevent tooth loss are required. The inflammatory process is controlled by antibiotic therapy.