Fibrous dysplasia of the leg bones: causes and symptoms of pathology, what treatment can be carried out using manual therapy methods

Fibrous dysplasia is a very serious pathology of bone tissue with partial replacement of it by connective fibers. Naturally, scar tissue does not have the properties of bone. Therefore, there is a violation of integrity, numerous fractures in the area of the replacement foci. With total destruction of the bone, its curvature can form.

Fibrous bone dysplasia mainly affects children and adolescents. This is due to the fact that the pathological changes are based on intrauterine developmental disorders. Primary signs can develop in the presence of associated risk factors. A sedentary lifestyle, insufficient development of muscle tissue of the lower extremities, nutritional deficiency of certain vitamins and minerals - all this is a trigger for the development of fibrous dysplasia of the leg bones.

It is important to understand that the disease, although in most cases has a congenital etiology, is easily correctable and preventable. Fibrous dysplasia of the leg often affects the long tubular bones: the femur, fibula, and tibia. With total destruction, a polyostotic form can be identified. The monoosal form is the localization of single foci of fibrous replacement of bone tissue in the cavity of one bone. Rarely does a two-way transformation occur. Usually only one limb is affected.

If you suspect that you or your child have such changes, we advise you to immediately seek medical help. To do this, you can make an appointment for a free appointment at our manual therapy clinic. An experienced orthopedist will conduct a thorough examination. He will make a diagnosis and tell you how treatment can be carried out to stop the pathological process and return the normal state of bone tissue.

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:

lack of sufficient care for the baby, including massage, gymnastics, air baths;
vitamin D deficiency, leading to the launch of the process of destruction of bone tissue against the background of rickets;
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.

Connective tissue dysplasia

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Fibrous dysplasia of the femur (hip)

Fibrous dysplasia of the femur can be congenital or acquired, single or multifocal, cystic or simple. The form of the pathology depends on the age of the patient. Multifocal fibrocystic fibrodysplasia occurs in elderly patients due to hormonal osteoporosis.

In children under 3 years of age, fibrous dysplasia of the hip most often manifests itself in the form of total replacement of bone tissue trabeculae with connective tissue scars. Curvature of the limb quickly occurs with a decrease in its length. Independent movement is impossible. Numerous fractures are recorded, the site of which does not heal in a typical manner through the formation of a bone callus.

In children aged 3 to 7-8 years, such a pathology can be the result of a gross violation of the diet and stress placed on the lower extremities. Recently, the so-called hypodynamic form of dysplasia has become widespread. It is worth understanding that for proper blood supply to the periosteum, good coordinated work of the muscles of the reed and lower leg is required. Well-trained muscles stimulate capillary blood supply and accelerate metabolic processes in bone tissue. If there is no regular and adequate physical activity on the lower extremities, then bone tissue may begin to deteriorate. In areas of dystrophic changes, scarring occurs with connective tissue.

Fibrous dysplasia of the hip is characterized by a rapidly progressive course. If your child has complaints of pain in the femur, hip or knee joint, immediately contact an experienced orthopedist. The doctor will prescribe treatment that will stop the progression of the dangerous pathology.

Fibrous dysplasia is a disease characterized by a developmental disorder (dysplasia) of the skeleton, in which normal bone is replaced by fibrous tissue with elements of dysplastic bone. There are monoostotic (about 85% of cases), monomelic (several adjacent bones of one limb, shoulder or pelvic girdle are affected) and polyostotic (about 5% of cases) forms. Fibrous dysplasia as a developmental anomaly is sometimes combined with extraskeletal disorders: 1) the polyostotic form of the lesion is combined with premature puberty and pigment spots on the skin in the form of coffee spots (Albright's syndrome); 2) a combination of fibrous dysplasia with soft tissue myxomas (Mazabraud's syndrome). Occurs at any age, most often in the first 3 decades of life (70% of patients). The monoosseous form is somewhat more common in males; with the polyostotic form, the ratio of males to females is 2:1. Any bone is affected, the most common location: the proximal part of the femur, tibia and humerus, ribs, skull bones, cervical spine. Spinal bones are affected only in 2.5% of cases.

Clinical picture. Pain of varying intensity, curvature and deformation of bones, pathological fractures. X-ray: lytic lesion with clear contours and sclerotic edges; there may be swelling of the bone, a pathological fracture.

Pathomorphology. Macroscopically - dense white-gray tissue with small inclusions of bone density; pathological tissue is almost always located only inside the medullary canal.

Microscopy. Connective tissue stroma with bone trabeculae of a primitive structure, myxoid changes, sometimes cementum-type structures, foci of chondroid tissue, and cysts are formed. Bone trabeculae are only occasionally limited by osteoblasts. Cytological atypia and mitoses are not typical. In very rare cases, cell atypia associated with degenerative or regressive changes may be observed.

Differential diagnosis. Osteofibrous dysplasia, giant cell reparative granuloma of bone, Paget's disease, well-differentiated central osteosarcoma, parosteal osteosarcoma.

Treatment. Marginal resection of the bone followed by plastic surgery of the defect. In case of severe bone deformities, marginal resection should be combined with corrective osteotomies with extraosseous or intraosseous osteosynthesis.

The outcome is favorable; malignancy of fibrous dysplasia is observed in 0.4% of cases, with Albright's syndrome - in 4% of cases, more often at the age of 30–40 years. Mostly, fibrous dysplasia is malignant, localized in the bones of the facial skeleton (lower and upper jaws), then the femur and pelvic bones.

Fibrous dysplasia of the knee

Fibrous dysplasia of the knee joint is a pathology in which the heads of the articulation of the bones (femur and tibia) are affected. The rest of the tubular structure may remain unchanged. Numerous foci of fibrous filling are formed in the area of the heads. This pathology requires careful diagnosis using radiographic images. They clearly show delimited lesions, in the cavity of which there is not bone tissue, but scar tissue. It gives a darkening effect. Differential diagnosis is required to exclude osteosarcoma and other types of malignant neoplasms.

Pathology of the knee joint is manifested by the following symptoms:

constant dull pain that intensifies after physical activity;
clicks and crunches when moving in the plane of a given bone articulation;
cramps in the thigh and lower leg;
shortening of the limb by 3-5 cm;
lameness and waddling gait;
permanent fractures, dislocations, sprains in the knee joint.

If you experience any discomfort, you should seek medical help. Timely prevention and treatment can stop negative manifestations.

Non-ossifying fibroma (fibrous cortical defect)

Non-ossifying fibroma is the most common non-neoplastic fibrous bone lesion. This is a larger type of fibrous cortical defect (< 3 cm); both conditions reflect the term fibroxanthoma or metaphyseal fibrous defect .

Epidemiology

Non-ossifying fibroma is very common in children and adolescents and is the most common fibrous bone lesion in this age group, with a peak incidence of 10-15 years [4]. The prevalence is up to 30-40% among healthy children. It occurs twice as often in boys as in girls [6]. It usually does not occur after 30 years, since it spontaneously heals on its own, gradually being replaced by bone tissue.

Clinical picture

Most nonossifying fibromas are asymptomatic. Large lesions can be painful and, by weakening the bone, predispose the patient to a pathological fracture. Multiple nonossifying fibromas are associated with neurofibromatosis type I, fibrous dysplasia, and Jaffe-Campanacci syndrome. Rarely, non-ossifying fibroma can cause hypophosphatemic vitamin D-resistant rickets [5].

Pathology

Non-ossifying fibroma is macroscopically a fleshy, fibrous, yellow or tan lesion with areas of hemorrhage [3]. Microscopically, the lesion is characterized by high cellularity, with the presence of spindle cells, against the background of the stroma, forming a so-called “moiré” pattern. Foamy histiocytes and multinucleated giant cells are found. Mitotic figures and/or dysplasia are not typical for fibroxanthoma [3]. Bone islands are thought to be self-healing fibroxanthomas.

Diagnostics

X-ray / Computed tomography

Non-ossifying fibroma is characterized by a lobular shape and usually has a sclerotic rim. They are localized eccentrically, in the metaphysis adjacent to the growth plate. As the patient grows, it shifts and moves away from the growth plate. It is not combined with a periosteal reaction, a violation of the integrity of the cortical plate and does not have a soft-tissue component.

Magnetic resonance imaging

The MR picture is varied and depends on the duration of the disease and the reparative phase at which the images were obtained. Early in the disease, the lesion is characterized by high or intermediate signal on T2-weighted images, surrounded peripherally by a low-intensity rim reflecting the sclerotic border. With the onset of ossification, the signal becomes low-intensity on all sequences [2]. Contrast enhancement varies.

Scintigraphy

Scintigraphy data depend on the phase of the lesion. In general they are negative; however, during the repair processes, moderate hyperemia and moderate uptake are present. If there is significant uptake or hyperemia, an alternative diagnosis should be considered or a fracture should be suspected [3].

Treatment and prognosis

Non-ossifying fibroma falls into the category of “ leave me alone and leave me alone ” lesions. In the vast majority of cases, no biopsy or treatment is required. When more than half the bone diameter is involved in the process, curettage with graphite/bone replacement is performed to prevent pathological fracture [1].

Differential diagnosis

aneurysmal bone cyst eccentric lytic metaphyseal defect
fluid levels during MR examination

chondromyxoid fibroma

fibrous dysplasia

desmoplastic fibroma

Synonyms

non-ossifying fibroma
unossified bone fibroma
fibrous cortical defect
fibroxanthoma
metaphyseal fibrous defect

Fibrous dysplasia of the tibia and fibula

Developing fibrous dysplasia of the tibia in the initial stages causes incorrect positioning of the foot. The leg at the ankle turns inward or outward. Depending on this, a valgus or varus deformity of the tibia is formed. If only one bone is affected, then gait disturbance occurs, but in general the ability to move independently is not lost.

Fibrous dysplasia of the tibia poses a great danger in terms of future prognosis, since in this variant there is a high probability of disability at an early stage. In most cases, fibrous dysplasia of the tibia is accompanied by severe pain and lack of ability for prolonged physical activity. rapid fatigue of the lower leg muscles is the first sign of trouble. If a child complains of pain in the lower leg when climbing stairs, he should be immediately seen by an orthopedist.

Fibrous dysplasia of the fibula rarely causes permanent disability. It collapses more slowly due to the fact that less stress is placed on it. Usually the disease is detected by a random X-ray for a suspected fracture of the fibula.

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.

Treatment of fibrous bone dysplasia

Official medicine treats fibrous bone dysplasia with surgery. A special structural composition, reminiscent of bone tissue in properties, is introduced into the foci of pathologically altered tissue. This gives a positive result only for an extremely limited period. The rapid destruction of bone tissue located next to the filled areas begins due to an even greater deterioration in the blood supply.

The only effective treatment for fibrous dysplasia is to completely eliminate the cause of this pathology. Manual therapy allows you to solve this problem in a radical way. Osteopathy eliminates disturbances in the movement of lymphatic fluid and blood. Massage accelerates microcirculation processes. Kinesitherapy and therapeutic exercises strengthen the muscles and restore the natural nutrition of the periosteum.

Reflexology launches metabolic and restoration processes. In combination with the recommendations of a nutritionist and chiropractor, these techniques give positive and long-term results.

It is important to start treatment early. The sooner you see a doctor, the higher the chances of recovery.

Depending on the stage of the disease, we choose one or more treatment methods:

Therapeutic massage, osteopathy, manual therapy

Helps bones and joints take the correct physiological position, relieves pain and spasms, relaxes muscles.

Acupuncture

Work on biologically active points. It affects the affected area and the body as a whole. Eliminates the cause of the disease and removes the symptoms.

In addition, according to indications, the following are used: taping, pharmacopuncture, FormTotix insoles, exercise therapy with an instructor and other methods. The choice of procedures depends on the current condition; taken together, they act faster and give a more lasting result.

chiropractor appointment