It should be noted that the process of weakening of bone tissue as the body ages is typical for both men and women, but in the latter this process is more pronounced. This is partly because women live longer, which means they take longer to lose bone tissue.
After 35 years, especially after the onset of menopause, the process of bone tissue resorption becomes gradually more pronounced than the process of formation of new tissue. Over the course of several years, this process gradually leads to a condition called osteopenia. If the process of leaching of bone tissue continues further, osteoporosis occurs. The severity of osteoporosis varies and is associated with the risk of fractures.
Osteoporosis can lead to decreased vertebral height and small fractures of the wrist bones. In addition, the likelihood of hip fractures increases. These are very serious fractures that affect the quality of life. In older women, there is an increased risk of complications, which is associated with prolonged bed rest after a hip fracture. Of these women, less than 20% return to their previous activities. In women over 75 years of age, the risk of mortality from complications such as vascular thrombosis due to a femur fracture is up to 30%. This is due to the fact that with prolonged bed rest and low physical activity, the speed of blood flow in the veins of the lower extremities slows down, which increases the risk of blood clots, which, if separated from the wall, can clog the lumen of the pulmonary artery.
What is osteoporosis
Osteoporosis, also known as bone loss, is a metabolic skeletal disease in which bones lose their strength.
They become porous and brittle. The disease is asymptomatic. The first symptom may be a fracture of the spine or femoral neck. According to the World Health Organization (WHO), osteoporosis is one of the most common diseases of our time. Osteoporosis affects approximately one in four women over 50 years of age. The incidence of osteoporosis exceeds the incidence of breast cancer, stroke and heart attack.1
The main task for doctors and patients is to identify the disease as quickly as possible. If osteoporosis is diagnosed at an early stage, its symptoms can be effectively treated, although a cure is not yet possible.
Exercise and a healthy diet (vitamin D and calcium) are effective measures. The precursor to osteoporosis is osteopenia (decreased bone density). With regular monitoring and following your doctor's recommendations, osteopenia may never develop into osteoporosis. In case of progression, osteoporosis occurs and the need to visit the doctor again so that he can prescribe appropriate therapy.
Methods for strengthening bone tissue
The most effective way to achieve this is a combination of lifestyle changes and the use of drug therapy.
Lifestyle changes concern those aspects that have a detrimental effect on the condition of bone tissue and the body as a whole: quitting smoking, physical exercise aimed at reducing excess weight.
A diet that should be rich in calcium and phosphorus (all dairy products, green vegetables (parsley, lettuce, onions), legumes, nuts, fish, citrus fruits), vitamin D and protein. Calcium is one of the hard-to-digest elements. Calcium absorption depends not only on its content in foods, but also on its ratio with other food components, primarily phosphorus, magnesium and proteins. Calcium absorption also worsens with a low-fat diet (milk fat, egg yolk, fish liver), i.e., those foods that contain vitamin D.
The main danger of osteoporosis is fractures, which usually occur due to a fall. In many cases, falls can be prevented by anticipating the situation in advance. Lifting weights with a tense, straight back and a raised chin will remove unwanted stress from the spine. The vertebrae are aligned in one line, the loads on the surface of the vertebral bodies and intervertebral discs are distributed evenly, which is extremely important for the safety of the back. When lifting an object from this position, the buttocks and leg muscles actively participate simultaneously with the back muscles. If you lift weights with your back bent and your head down, this leads to an uneven distribution of pressure on the intervertebral discs and back muscles. The discs are simultaneously compressed on one side and stretched on the other, with the main load falling on the lumbar region. It is important to create a safe environment at home with adequate lighting and no slippery floors or rugs. If you use stairs, check for broken railings or steps. Shoes should be comfortable. Drive carefully when outside, avoiding wet or icy sidewalks.
How does osteoporosis develop?
Some people believe that bones are durable structures that are not subject to change. In fact, this is not true. Bone is constantly renewed through the simultaneous destruction of bone substance and the formation of new one. Hormones, vitamins and other active substances control this process (bone remodeling). In adolescence and young adulthood, the process of bone formation prevails over destruction. As we age, bone formation slows down. After the balance shifts towards the destruction of bone tissue, the bone gradually loses its strength.
Bone density can be assessed using a special study called densitometry.
Osteoporosis is divided into two forms: primary
and
secondary
.
Primary osteoporosis
Primary osteoporosis
Approximately 95% of bone loss is due to primary osteoporosis.
Osteoporosis type I: The first type of osteoporosis develops in postmenopausal women (postmenopausal osteoporosis). With this type of osteoporosis, the vertebrae are most susceptible to fractures.
Osteoporosis type II: Osteoporosis type II usually occurs after age 70 (senile osteoporosis). With this type of osteoporosis, the most common fractures are the vertebrae, hip bones, and forearm bones.
Risk factors for primary osteoporosis:
- Aging
- Changes in hormonal levels (late menarche, early menopause)
- Physical inactivity
- Long period of immobilization
- Underweight
- A diet low in calcium or high in phosphate (fast food chains, sodas)
- Abuse of alcohol, coffee
- Smoking
Secondary osteoporosis
Secondary osteoporosis
Secondary osteoporosis occurs as a result of other diseases or is a side effect of certain medications:
- Anti-inflammatory hormonal drugs to treat asthma or rheumatism (cortisone)
- Hormonal imbalances, such as hyperthyroidism
- Tumor diseases
Risk factors for secondary osteoporosis:
- Long-term use of hormonal drugs (asthma, rheumatism)
- Long-term use of coumarin derivatives (Marcumar)
- Systematic disruption of the gastrointestinal tract, including diseases of the pancreas, intestines, and liver
- Chronic kidney disease
- Disorders of thyroid hormone metabolism (hypothyroidism) and pancreatic hormones (diabetes)
- Oncological diseases
Diagnosis of osteoporosis
A correct and prompt diagnosis is crucial for immediate initiation of treatment. Therefore, it is recommended to regularly visit a doctor and conduct screening tests (densitometry) if there are risk factors. This applies to postmenopausal women, as well as elderly and senile men. Whenever there is a suspicion of decreased bone mass, these suspicions must be confirmed or refuted by instrumental diagnostic methods. Symptoms that suggest osteoporosis are:
- decreased growth and formation of hyperkyphosis of the thoracic spine (hump)
- severe chronic pain in the back or sternum
- Bone fractures for no apparent reason, especially fractures of the spine due to one's own weight
Prevention of osteoporosis
There are various ways to slow down the process of bone destruction. Prevention of osteoporosis should begin in youth, when it is possible to form more massive bones, which will take additional time to weaken decades later. Preventive measures include:
- regular exercise and moderate muscle training (special exercises for training different muscle groups slow down bone loss),
- healthy and balanced diet with adequate intake of vitamins, proteins and calcium.
A combination of physical activity and proper nutrition can keep bones and muscles healthy for many years.
Why does the jawbone shrink?
When a person has all the teeth in the mouth, the chewing load is evenly distributed throughout the entire alveolar ridge (that is, pressure is received by the gums, ligamentous apparatus and directly the bone in which the tooth roots are located). This is a natural process through which bone cells receive nutrition and metabolic processes occur in them. And thus the bone maintains its volume.
In cases where a tooth is removed, the bone tissue no longer receives load. When chewing, all the pressure is redistributed between the remaining teeth. Therefore, the nutrition of tissue cells is disrupted, which leads to its resorption. And gradually atrophy of the jaw bone tissue occurs.
Bone loss is also affected by other dental problems, such as inflammatory processes (cysts, granulomas, periodontitis and periodontitis). In these cases, tissue resorption occurs as bone cells are replaced by others.
There are other reasons that lead to bone thinning:
- individual structural features of the maxillofacial apparatus,
- genetic predisposition,
- getting jaw injuries,
- age-related changes in humans and natural aging of all organs,
- prosthetics that rely only on the gums (removable) or on living teeth (bridge), due to which the bone again does not receive the necessary load,
- inflammation of the mucous membranes, periodontal tissue diseases.
Does all the bone atrophy?
Our jawbone consists of several sections: the central one is the spongy layer. It contains tooth roots. This section is the most porous, since it is in it that a large number of capillaries are concentrated, which means that it is the spongy section that undergoes atrophy first. Below it is the basal layer - it is already stronger, since it consists of bone partitions and there are several times fewer capillaries in it. Both layers are covered by a shell or cortical plate - it, like the basal layer, is very dense and does not undergo atrophy.
Further, already behind the basal section, on the upper jaw there is a zygomatic bone, as well as buttresses - these are lines of force that evenly distribute pressure on the jaw between all the bone tissues of the skull.
On the upper jaw, the sinuses are located close to the jawbone. They have a rather thin shell, which can be easily damaged if implants are too long1. There are no sinuses on the lower jaw - the chin and jaw bone go under the alveolar process. They are very durable, so tissue atrophy below is less common, and implantation is easier.
Treatment of osteoporosis
Treatment of osteoporosis is aimed at improving the quality of life of patients. Therapy consists of combining several approaches, which are combined by specialized specialists into clinical recommendations for osteoporosis. Effective therapy for osteoporosis must be multicomponent:
Drug therapy
The following groups of drugs are used to treat osteoporosis:
SMRE
SERMs (selective estrogen receptor modulators) are chemically similar to the hormone estrogen, whose production declines after menopause. SERMs activate estrogen receptors and increase bone formation. However, this group of drugs, unlike estrogen, does not increase the risk of breast cancer and cardiovascular diseases.
Bisphosphonates
Bisphosphonates slow down the degradation of bone tissue and thus slow down the process of bone loss.
Calcium and vitamin D
Calcium and vitamin D. Calcium is the main element of the mineral component of bone tissue. It must be supplied to the body in sufficient quantities through diet. If calcium intake is insufficient, it is recommended to take calcium supplements. Vitamin D facilitates the absorption of calcium from the gastrointestinal tract and the integration of the element into the bone structure.
Parathyroid hormone/teriparatide
Parathyroid hormone/teriparatide stimulates the formation of osteoblasts and increases their activity. Osteoblasts are specialized cells responsible for bone formation and bone remodeling.
Analgesics
Painkillers reduce pain immediately after fractures (acutely) and relieve chronic pain resulting from vertebral fractures. Pain is known to limit activity, so patients with osteoporosis must receive adequate pain therapy.
Motor mode
Exercise is a treatment for osteoporosis. Special physical exercises developed by physical therapy specialists and doctors increase motor activity, improve the functional state of muscles and coordination, and have a positive effect on the general emotional state.
Therapeutic exercises, especially exercises to train the strength of the trunk muscles, should be performed constantly.
A special simulator-corrector, working on the principle of biofeedback, maintains the spine in a physiological position and trains the abdominal and back muscles. In addition to physical therapy, the following types of physical activity are recommended for patients with osteoporosis:
- Walking
- Nordic walking
- Skiing
- Swimming
- Dancing
The ideal combination is a combination of strength and endurance training. The greater the muscle mass, the better the prognosis for bone quality. Exercising outdoors is especially effective as sunlight stimulates the natural production of vitamin D in the skin.
Important information:
Patients with osteoporosis should always discuss their level of physical activity and physical therapy exercises with their doctor.
Strength training helps build bone tissue
Strength training creates biomechanical and biochemical stimuli for bone formation. At the same time, these exercises contribute to the formation of good posture. Strong muscles work harmoniously and coordinated.
When used correctly, the Spinomed corrective trainer also trains muscles. The belt system and aluminum tire create a force that stimulates your own muscles. Thus, the product works almost on a subconscious level. The use of Spinomed is consistent with clinical guidelines for the treatment of osteoporosis.3
Training planning
The ideal is a combination of different types of sports activity. The result is increased muscle mass, improved bone quality, overall health and a sense of balance. Your attending physician or physical therapy doctor will help you choose the types of sports and physical exercises that suit you.
Functional orthotics
The functioning of the skeletal and muscular systems is closely related, so simultaneous loss of bone and muscle mass usually occurs.
For this reason, treatment of spinal fractures should be functional, and not just medicinal. A vertebral fracture dramatically increases the likelihood of a subsequent fracture and is a cause of chronic pain, physical inactivity, and associated muscle loss. Modern means of rehabilitation for spinal fractures simultaneously train muscles and correct posture at the same time.
In the past, immobilization after spinal fractures in rigid corsets was practiced, but this only led to the progression of osteoporosis. Currently, an increasing number of doctors are refusing to use rigid corsets for spinal fractures due to osteoporosis, because there are modern means, for example, the Spinomed corrector simulator.
medi products: orthotics for osteoporosis
Vertebral fractures in osteoporosis are accompanied by chronic back pain, which severely limits the motor activity of patients and leads to even greater progression of the disease. The Spinomed corrector exercise machine trains muscles and reduces pain, which has been confirmed in clinical studies.4,5
The effectiveness of Spinomed and Spinomed active has been confirmed in several clinical studies 5,6:
- the strength of the abdominal and torso muscles increases by 73 and 56%, respectively,
- the deviation of the body from the vertical axis is reduced by 25%,
- the angle of thoracic hyperkyphosis decreases by 11%,
- pain intensity decreases by 47%,
- physical activity becomes more comfortable - by 18%,
- respiratory function of the lungs improves by 19%.
The Spinomed corrector trainer and Spinomed active were developed by Professor Helmut W. Minne in collaboration with the company medi. Spinomed is similar in design to a backpack. Spinomed active is designed as a bodysuit and can be used under outerwear. All Spinomed models operate on the principle of biological feedback.
Sources
1 Epidemiologie der Osteoporose: Bone Evaluation Study, Deutsches Ärzteblatt 2013,4, 52 ff. 2 Hadji P et al. Dtsch Arztebl Int 2013;110(4):52–57. 3 Lesnyak O.M., Benevolenskaya L.I. Osteoporosis. Diagnosis, prevention and treatment. Clinical recommendations. Ed. 2nd. - M.: "GEOTAR-MED", 2010. 4 Pfeifer M et al. Die Wirkungen einer neu entwickelten Rückenorthese auf Körperhaltung, Rumpfmuskelkraft und Lebensqualität bei Frauen mit postmenopausaler Osteoporose. Eine randomisierte Studie. Am J Phys Med Rehabil 2004;83(3):177-186. 5 Pfeifer M et al. Die Wirkungen von zwei neu entwickelten Rückenorthesen auf Rumpfmuskelkraft, Körperhaltung und Lebensqualität bei Frauen mit postmenopausaler Osteoporose. Eine randomisierte Studie. Am J Phys Med Rehabil 2011;90(5):805-815.
The human body
Human back
A stronger back means an easier life
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Exercise machine-corrector for the treatment of osteoporosis
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Issues of differential diagnosis of osteoarticular pathology.
Diseases of the osteoarticular system and connective tissue represent an urgent medical and social problem of not only national but also global significance. They occupy one of the leading places in the structure of primary and general morbidity of the population. They are the most common cause of long-term pain and disability.
Structure of osteoarticular pathology.
- dystrophic diseases
- dysplastic diseases
- metabolic diseases
- injury
- inflammatory diseases
- neoplastic diseases
Questions that a radiologist should answer when a bone mass is detected.
1 - neoplastic, infectious formation or the result of dystrophic (dysplastic) changes or metabolic disorders 2 - benign or malignant 3 - primary or secondary formation It is necessary to use not skialological, but morphological language of description.
The purpose of radiation studies.
• Localization • Quantitative assessment: number of infestation formations.
• Qualitative assessment: malignant or benign, presumptive histological type
• Probable diagnosis: normal variant dystrophic/dysplastic changes metabolic disorders (metabolic) trauma inflammation tumor
Important.
Referral diagnosis • Age • Evaluation of results of previous studies, tests • Symptoms and results of physical examination • Mono - or polishing lesion
Assessing changes in tests • Osteomyelitis - increased ESR, leukocytosis • Benign tumors - no changes in tests • Ewing's sarcoma - leukocytosis • Osteosarcoma - increased alkaline phosphatase • Metastases, myeloma - anemia, increased calcium in the blood • Myeloma - Bence-Johnson protein in urine
Grade.
• Localization of formation • Number of formations • Destruction/sclerotic changes of bone • Presence of hyperostosis • Type of periosteal reaction • Changes in surrounding tissues
Quantitative assessment. • Primary tumors – often solitary • Metastases and myeloma – multiple
Groups of main changes: • changes in the shape and size of the bone • changes in the contours of the bone • changes in the bone structure • changes in the periosteum, cartilage • changes in the surrounding soft tissues
Groups of main changes. • Bone curvature (arched, angular, S-shaped) • Change in bone length (shortening, elongation) • Change in bone volume (thickening (hyperostosis, hypertrophy), thinning, swelling) • Change in bone structure osteolysis (destruction, osteoporosis, osteonecrosis, sequestration ) – well differentiated, poorly differentiated • osteosclerosis
Destruction of bone tissue.
• Benign - due to expansive growth, increased pressure, periosteum is preserved (for a long time), benign personal reaction • Malignant - invasive growth, poor differentiation of edges, soft tissue component, malignant periosteal reaction, periosteal hyperplasia, moth-eaten pattern
Cortical destruction.
It is determined in a wide range of pathologies, inflammatory changes in benign and malignant tumors. Complete destruction can occur with highly differentiated malignant tumors, with local aggressive benign formations, such as eosinophilic granuloma, with osteomyelitis. Partial destruction can occur in benign and poorly differentiated malignant tumors. Scalloping along the inner surface (endosteal) can occur with a fibrous cortical defect and poorly differentiated chondrosarcomas. Bone swelling is also a variant of cortical destruction - endosteal resorption occurs and bone formation occurs due to the periosteum; the “neocortex” can be smooth, continuous and with areas of discontinuity.
According to radiography, in malignant small round cell tumors (Ewing's sarcoma, small cell osteosacroma, lymphoma, mesenchymal chondrosarcoma), the integrity of the cortical plate can be preserved, but, spreading through the Haversian canals, they can form a massive soft tissue component.
Types of personal reaction.
- Solid – linear, exfoliated periostitis
- “Bulbous” - layered periostitis
- Spiculous – needle-shaped periostitis
- Codman's visor - periostitis in the form of a visor
- In domestic practice, the division into benign and aggressive types is not used and is contradictory.
- Types of periosteal reaction Linear periostitis (left) Bulbous periostitis (right)
- Types of periosteal reaction Spiculous periostitis (left) Codman's visor (right)
Matrix calcification.
• Calcification of the chondroid matrix in cartilaginous tumors. “Popcorn” symptom, calcification like flakes, like rings and arcs. • Calcification of the osteoid matrix in osteogenic tumors. Trabecular ossification. Can be found in benign (osteoid osteoma) and malignant tumors (osteogenic sarcoma)
Osteomyelitis.
- bacterial inflammation of the bone marrow after metal osteosynthesis (more often in adults) - limited purulent focus with the formation of destruction (focal osteomyelitis) - superficial form - affects the cortical layer of the bone and surrounding soft tissues - a common type of osteomyelitis - extensive bone damage against the background of the previous process - chronic osteomyelitis – layered periosteal layers, the process of periosteal bone formation (periostosis) alternates with the formation of new bone
- bone marrow edema (X-ray negative phase, up to 4 weeks, method of choice - MRI) - infiltration of parasotal soft tissues - purulent inflammation of the bone marrow - necrotization of the bone marrow - foci of destruction - formation of sequestration - spread of pus along muscle structures, formation of fistulas
Comparative image of osteomyelitis 1) osteogenic sarcoma 2) osteomyelitis 3) eosinophilic granuloma.
Bone marrow edema.
Cerebral edema is visualized in 15 different pathologies.
- On the left - swelling due to rheumatoid arthritis
- In the center - edema due to thalassemia
- On the right - enchondroma
Osteoarthritis.
Stage 1 - subchondral sclerosis - marginal bone growths Stage 2 subchondral cysts (geodes) - reaching the edge - erosion, narrowing of the joint space Stage 3 - defiguration of the articular surfaces, disruption of the relationship in the joint - chondromalacia, subchondral edema (MRI) - effusion in the joint (reactive synovitis, MRI) - vacuum phenomenon (CT)
Geodes occur in: - osteoarthrosis - rheumatoid arthritis (also erosion) - diseases with impaired calcium deposition (pyrophosphate arthropathy, chondrocalcinosis, hyperparathyroidism) - avascular necrosis
Geodes. Erosion.
Hyperparathyroidism.
• subperiosteal resorption in the tubular bones of the hands (radial part), femoral neck, proximal tibia, ribs • tunneling of the cortical layer • Brown's tumor (brown tumors) – lytic lesion with clear, smooth edges, swells the periosteum, m.b. hemorrhage (pelvic bones, ribs, femur, facial bones). More often in women, age 30-60 years. Develop in 20% of patients with hyperaparathyroidism. Heterogeneous signal in MRI sequence • chondrocalcinosis

Brown's tumor in hyperparathyroidism
Age distribution of bone formations.
Localization of bone formations FD - fibrous dysplasia Ewing - Ewing's sarcoma EG - ephosinof. granuloma Osteoidosteoma - osteoid osteoma NOF - not ossific. Fibroma SBC - simple bone cyst CMF - chondromyxoid fibroma ABC - anerismatic bone cyst Osteosarcoma - osteogenic sarcoma Chondroblastoma - chondroblastoma Osteohondroma - osteochondroma Enchondroma-enchondroma Chondrosarcoma - chondrosarcoma Infection - infection Geode (geodes) - subchondral cyst Giant CT (G CT) – giant cell tumor Metastasis – Myeloma metastasis – Lymphoma myeloma – HPT lymphoma – hyperparathyroidism
Location.
• Central: simple bone cyst, aneurysmal bone cyst, eosinophilic granuloma, fibrous dysplasia, enchondroma. • Eccentric: osteosarcoma, non-ossifying fibroma, chondroblastoma, chondromyxoid fibroma, osteoblastoma, giant cell tumors. • Cortical: osteoid osteoma. • Juxtacortical: osteochondroma, paradoxical osteosarcoma
Principle of radiographic evaluation.
Relationship between age and the most common pathology.
FD - fibrous dysplasia Ewing - Ewing's sarcoma EG - ephosinof.granuloma Osteoidosteoma - osteoid osteoma NOF - non-ossifying. Fibroma SBC - simple bone cyst CMF - chondromyxoid fibroma ABC - anerismatic bone cyst Osteosarcoma - osteogenic sarcoma Chondroblastoma - chondroblastoma Osteohondroma - osteochondroma Enchondroma-enchondroma Chondrosarcoma - chondrosarcoma Infection - infection Geode (geodes) - subchondral cyst Giant CT (GCT) ) – giant cell tumor Metastasis – metastasis Myeloma – myeloma Lymphoma – lymphoma HPT- hyperparathyroidism Leukemia – leukemia Bone island – bone islands Low grade – poorly differentiated High grade – highly differentiated Parosteal Osteosar – paraosteal osteosarcoma
Key points of differential diagnosis.
• The bulk of bone tumors are osteolytic. • In patients under 30 years of age, the presence of growth plates is normal • Metastases and myeloma are always included in the differential for multiple lytic lesions in lesions in patients over 40 years of age • Ostemyelitis (infection) and eosinophilic granulomas can simulate a malignant tumor (aggressive type of periosteal reaction, destruction cortical plate, poor margin differentiation) • Malignant tumors cannot cause a benign periosteal reaction • The presence of a periosteal reaction excludes fibrous dysplasia, enchondroma, non-ossifying fibroma, simple bone cyst.

Localization of bone tumors.
FD-fibrous dysplasia Ewing - Ewing's sarcoma EG-efosinof. granuloma Osteoidosteoma - osteoid-osteoma NOF - not ossified. Fibroma SBC - simple bone cyst CMF - chondromyxoid fibroma ABC - anerismatic bone cyst Osteosarcoma - osteogenic sarcoma Chondroblastoma - chondroblastoma Osteohondroma - osteochondroma Enchondroma-enchondroma Chondrosarcoma - chondrosarcoma Infection - infection Geode (geodes) - subchondral cyst Giant CT (GCT) ) – giant cell tumor Metastasis – metastasis Myeloma – myeloma Lymphoma – lymphoma HPT- hyperparathyroidism Leukemia – leukemia Bone island – bone islands Low grade – poorly differentiated High grade – highly differentiated Parosteal Osteosar – paraosteal osteosarcoma

Specific localization of a number of bone formations.
Formations with multiple lytic changes of the “moth-eaten” type
Changes that can form sequestration
Formations with multiple lytic changes of the “soap bubble” type
The most common spinal lytic lesions.
1- hemangioma 2- metastasis 3- multiple myeloma 4 - plasmacytoma

Other variants of spinal lytic lesions.
Paget's disease.
Bedget's disease (BD) is a fairly common disease in many European countries and the USA. Prevalence estimates in people over 55 years of age ranged from 2% to 5%. It is a fact that a significant proportion of patients remain asymptomatic throughout their lives. PD should always be considered in the differential diagnosis of osteosclerotic as well as osteolytic skeletal lesions. Stage I (lytic) - acute stage, destruction of the cortical layer is determined in the form of foci of flame or in the shape of a wedge. Stage II (transitional) – mixed lesion (osteolysis + sclerosis). Stage III (sclerotic) – predominance of sclerosis with possible bone deformation In monoosseous cases, the frequency of which, according to publications, starts from 10-20% reaching almost 50%, the differential diagnosis can be much more difficult. In the vast majority of cases of PD, the presence of patchy areas of bone sclerosis or osteolysis with distortion of trabecular architecture in combination with cortical thickening and focal thickening of the bone is almost pathognomonic for the disease. The femur is the second most common monoosseous site after the pelvis. In cases where there is distal involvement, radiological signs characteristic of PD are detected with less frequency or are less pronounced, so differentiation from other processes, in particular tumors, may be difficult.
Aneurysmal bone cysts.
• Intramedullary eccentric metaepiseal multilocular cystic formation • Multiple levels of fluid containing blood are detected in the cavities • Bounded by a membrane of varying thickness, consisting of bone trabeculae and osteoclasts • In 70% - primary, without obvious causes • In 30% - secondary, as a result of trauma • Etiology unknown, suspected neoplastic nature • No gender predisposition, at any age • Most often located in long bones and spine Aneurysmal bone cysts • Multilocular cysts with septations • Multiple levels of fluid • Sclerotic ring along the periphery • When localized in the vertebrae – affects more than one segment • Rarely located bone, causes destruction of bone beams, compact substance • Can spread to adjacent bone elements
Another case of ACC
Simple bone cyst.
Intramedullary, usually unilateral cavities, with serous or serous-hemorrhagic contents, separated by a membrane of varying thickness • More common in men (2/3:1) Found in the first two decades of life in 80% • In 50% - the proximal half of the humerus • In 25% - proximal half of the femur • The third most common location is the proximal half of the fibula • In elderly patients, it is more common in the talus and calcaneus • Well demarcated, symmetrical • Does not extend above the epiphyseal plate • Located in the metaepiphysis, with growth into the diaphysis The compact lamina is deformed and thinned • There is no periosteal reaction • Fractures are possible, against the background of cysts • There are practically no septa • On T2W, stir, PDFS there is a high homogeneous signal, low on T1W, without a solid component. Signs of a high protein component (blood, increased signal on T1W) possible with fractures
Juxtaarticular bone cyst.
• Non-neoplatic subchondral cystic formation, develops as a result of mucoid degeneration of connective tissue • Not associated with dystrophic processes • Contains mucinous fluid and is delimited by fibrous tissue with myxoid properties • If degenerative changes are detected in the joint, this change is interpreted as a degenerative subchondral pseudocyst (often multiple in nature ) • Men predominate • 80% - between 30 and 60 years • Most often located in the hip, knee, ankle, wrist and shoulder joints
Juxtaarticular bone cyst • Defined as a well-demarcated oval or round cystic formation • Eccentric • Located subchondral, in the epiphyses • Bounded by a connective tissue membrane with fibroblasts, collagen, synovial cells • Synonyms – intraosseous ganglion, intraosseous mucoid cyst. • They can deform the periosteum • They are delimited by a sclerotic rim • Most often 1-2 cm, rarely up to 5 cm • Dystrophic changes in the joint are not expressed
- Uniform low signal on T1W, high on T2W
- Low signal in all sequences in the sclerotic rim
- There may be swelling (high signal on stir) in the adjacent bone marrow
Metaepiphyseal fibrous defect (fibrous cortical defect).
• Synonym – non-ossifying fibroma (not to be confused with fibrous dsyplasia), used for formations larger than 3 cm • Non-neoplastic formation • Consists of fibrous tissue with multinucleated giant cells, hemosiderin, inflammatory elements, histiocytes with adipose tissue • One of the most common tumor-like formations of bone tissue • 60% - men, 40% - women • 67% - in the second decade of life, 20% - in the first • Most often it affects the distal metaepiphysis of the femur and the proximal metaepiphysis of the tibia. Account for 80% of cases
• The length is located along the axis of the bone • 2-4 cm, rarely up to 7 cm or more • Cystic formation in the metaepiphysis, always closely adjacent to the endosteal surface of the compact plate, often along the periphery there is sclerosis, clearly demarcated from the surrounding bone marrow • Can cause destruction of the cortical plate, complicated by a fracture • Wider in the distal part • No growth through the metaepiphyseal plate, spreads towards the diaphysis • There may be hemorrhagic changes • No periosteal reaction, no changes in the adjacent soft tissues • Reduced signal on T1W, variable on T2W, stir more often - high
Periosteal desmoid.
• A variant of a fibrous cortical defect, localized along the dorsal surface of the distal third of the femur • Semiotics similar to a fibrous cortical defect, only the process is limited to the cortical plate
Fibrous dysplasia.
• Benign intramedullary fibro-osseous dysplastic acquired formation • May be mono- and polyostotic lesion • Mono-osseous form – 75% • Women predominate slightly (F-54%, M-46%)
• Age characteristics are presented on the next slide • 3% of patients with the polyostotic form develop McCune-Albright syndrome (café-au-lait spots + endocrine disorders, most often gonadotropin-dependent precocious puberty) Localization Long bones - proximal third of the femur, humerus, tibia • Flat bones - ribs, maxillofacial region - upper and lower jaw • In tubular bones it is localized in the metaepiphyses and diaphyses In open growth zones - localization in the epiphyses is rare • Histologically consists of fibroblasts, dense collagen, richly vascularized matrix, bone trabeculae, immature osteoids, osteoblasts are present • Possible pathological fractures, perpendicular to the long axis
A pathognomonic sign is the “ground glass” pattern according to CT and radiography; less often, a pattern of lytic changes can be observed, depending on the degree of predominance of the fibrous component • Expansive growth • Clear contours • High density figures, in comparison with the spongy substance, but less than compact • Deforms, “inflates” the bone • In tubular bones a “shepherd’s crook” deformation is formed • Periosteal reaction, soft tissue component is not expressed, destruction of the cortical plate is not determined Mass with expansive growth can form • Rarely cartilaginous component • High signal on T2W , the ground glass symptom is defined as a lightly mineralized formation. CT picture is more specific and indicative • MRI can detect cysts, clearly demarcated, homogeneously high signal on T2W • Scalloped edge of the inner surface of the cortical plate

Osteofibrous dysplasia.
• Benign fibro-osseous formation • Synonym – ossifying fibroma • More often in children, boys predominate • The first two decades of life • The most common localization is the anterior cortical plate of the tibia, less commonly the fibula • It is a multifocal cystic formation, the main mass limited to the anterior cortical plate and sclerosis along the periphery
• Deforms, inflates the bone anteriorly and laterally • High signal on T2W, low on T1W • No periosteal reaction • Unlike fibrous dysplasia – extramedullary, cortical formation

Myositis ossificans (heterotopic ossification).
Rare, benign formation • Local, well-circumscribed, fibro-osseous • Localized in muscles or other soft tissues, tendons • Males predominate • Can occur at any age, predominates in adolescence or young adulthood • Lower extremity (quadriceps and gluteal muscles) is more often involved • At an early stage, compaction of soft tissues is determined • From 4 to 6 weeks - patchy calcification of the “veil” type • The cortical plate is not involved There is no bone marrow invasion • There is no periosteal reaction, in close proximity it may seem that it is a false affiliation with the bone • By 3- 4 months mineralizes, less pronounced mineralization in the center, peripheral calcification is often observed, like a shell, or blocky calcification may persist. • On MRI in the form of an inhomogeneous mass (high signal on T2W, stir, low on T1W) areas of low signal on T1W, T2W, PDFS due to calcification, for accurate visualization it is better to perform T2* (GRE) • Does not contain cartilage tissue, which is good visible on T2* and PDFS • CT is more informative

Langerhans cell histiocytosis.
Forms: - eosinophilic granuloma - Hand-Schuller-Christian disease (disseminated form) - Letterer-Siwe disease disease (disseminated form) Etiology is unknown. Less than 1% of all bone formations. More often the monoostotic form than the polyostotic form. It can happen at any age, but is more common in children. Cranial vault, lower jaw, vertebrae, valley bones of the lower extremities - rarely. Ribs - most often affected in adults
“hole in the hole” - flat bones (cranial vault), sclerosis along the periphery - “vertebra plana” - with damage to long tubular bones - lytic intramedullary lesion in the metaepiphysis or diaphysis - there may be cortical destruction, periosteal reaction - very rarely fluid level - low signal on T1W, high on T2W, stir, accumulate HF
Metastatic breast cancer
Osteoid osteoma
Conclusions
1. Differential diagnosis in osteoarticular pathology is complex and extensive.
2. It is advisable and justified to use a multimodal approach, using X-ray data, CT, MRI, and ultrasound diagnostics. 3. It is necessary to take into account the data of laboratory research methods and the clinical picture when building a differential series. 4. Strictly follow the methodology and fully use all the capabilities of radiation diagnostic methods (polypositional, comparative radiography, bone mode for CT ABP, DWI sequences for any focal process, etc.) Material taken from the lecture:
- Issues of differential diagnosis of osteoarticular pathology. What should a radiologist know? Ekaterinburg 2015
- Meshkov A.V. Tsoriev A.E.