Osteoporosis is a systemic disease of the skeleton, characterized by a decrease in bone mass per unit volume and a disorder of bone microarchitecture, leading to an increase in bone fragility and a high risk of fractures.
This definition is now generally accepted, although from a clinical point of view it is obvious that osteoporosis is in most cases secondary to a particular disease and, strictly speaking, is a syndrome.
Along with the term “osteoporosis,” the term osteopenia, which has a dual meaning, is used in assessing skeletal diseases. As it is used to refer to the concept of “decrease in bone mineral density”.
According to the WHO, osteoporosis as a cause of disability and mortality of patients with bone fractures takes the 4th place among non-communicable diseases, being second only to diseases of the cardiovascular system, oncological pathology and diabetes mellitus. This is due to the wide prevalence of osteoporosis, its multifactorial nature, late diagnosis and late initiation of treatment.
Osteoporosis is one of the most well-known metabolic diseases of the skeleton, whose density increases with age. Every third woman after menopause and more than half of all people aged 75-80 years have osteoporosis, the consequences of which are fractures of the vertebral bodies and tubular bones, which determines a significant interest in morbidity, disability and mortality among elderly people. . About 20% of patients with hip fractures die within 6 months after the fracture, and of the remaining 50%, they become disabled. The frequency of hip fractures is one measure of the prevalence of osteoporosis.
Etiology and pathogenesis
Most forms of osteoporosis should be considered symptomatic in a number of diseases. Thus, in ICD-10, osteoporosis is distinguished with abnormal bone fractures and without abnormal fractures.
According to morphological features, trabecular, cortical, and mixed osteoporosis are distinguished; by metabolic activity, osteoporosis with increased bone metabolism, with a low degree of bone tissue metabolism, and with normal bone metabolism indices. The rate of loss of bone matter may depend on many factors. With any pathophysiological mechanism, the bone mass will decrease, reaching a certain threshold value, after which the fracture stage begins.
In osteoporosis with high bone metabolism, high bone resorption is not compensated by normal or increased bone formation, and in osteoporosis with low bone exchange, the rate of bone resorption is normal or reduced, and the bone formation rate is slowed. Both forms can be detected as different stages of the osteoporotic process in one patient.
In the pathogenesis of postmenopausal osteoporosis, the triggering factor is estrogen deficiency, which sharply accelerates bone loss. The presence of estrogen receptors on osteoblasts has been proven, and the estrogen deficiency contributes to the production of osteoblasts by a factor that stimulates both differentiation and osteoclast activity, which leads to increased bone resorption. The lack of estrogen contributes to a decrease in calcitonin release and increased bone sensitivity to the resorptive effect of parathyroid hormone, as well as secondary vitamin D deficiency and a decrease in calcium absorption in the intestine.
In the pathogenesis of senile osteoporosis, along with the deficiency of sex steroids and calcitonin, great importance is attached to the negative calcium balance due to vitamin D deficiency and reduced calcium absorption in the intestine, which results in the formation of repeated hyperparathyroidism and increased bone resorption tissue. Violation of vitamin D is explained by both a decrease in insolation due to a decrease in exposure to the street, and a violation of the formation of active forms due to a deficiency of sex hormones. Excessive or insufficient secretion of more hormones at any age leads to osteoporosis. Examples of the dramatic prevalence of bone resorption are the bone form of primary hyperparathyroidism and the pathology of bone tissue metabolism in severe recurrent thyrotoxicosis.
Excess glucocorticoids with Cushing’s syndrome suppresses bone formation, while calcium absorption in the intestine decreases and kidney excretion increases, which creates a negative calcium balance, leading to secondary hyperparathyroidism and increased bone resorption.
The mechanism of osteoporosis in hypogonadism in women in the reproductive period is similar to that in postmenopausal women. Decreased androgenic function in men leads to reduced bone formation and the formation of osteoporosis with low bone metabolism.
Fractures of the proximal femur may be characteristic fractures for osteoporosis.He eats the vertebrae and distal parts of the forearm bones, although fractures of any localization may occur. Fractures of the vertebral bodies are one of the classic signs of osteoporosis, and their consequences in the form of back pain, disorders of the function and deformities of the spine determine the level of disability and the importance of this issue for health care.
The prevalence of these fractures in Russia was 11.8%. In almost 50% of cases, osteoporosis is asymptomatic or asymptomatic and can only be detected if there are bone fractures. Postmenopausal, steroidal and hypogonadal osteoporosis is characterized by preferential loss of trabecular bone tissue and, in accordance with this, fractures of the vertebral bodies, ribs and fractures of the radial bone in a typical place (osteoporosis type I).
The predominant lesion of the cortical bone tissue is inherent in senile osteoporosis, hyperparathyroidism, and thyroid – sycosis (osteoporosis type II), with fractures of the tubular bones and neck of the thigh more common; but frequent (especially in older age groups) and vertebral body fractures. Complaints to back pain, aggravated after exercise, with a long stay in one position are typical. These pains disappear after lying down. The severity of pain may be different not only in different patients, but in the same patient at different stages of the disease.
During the examination, one should pay attention to the transformation of the patient’s posture, deformation of the chest, reduction of growth, formation of skin folds on the lateral surface of the chest, disturbance of gait.
Diagnosis of osteoporosis involves the following tasks:
1) detection of osteopenia and bone fractures;
2) an assessment of the level of metabolism in bone tissue (a study of biochemical or morphological markers of bone resorption and bone formation, as well as indicators of calcium metabolism);
3) elucidation of osteopenia and differential diagnosis with other forms of metabolic osteopathy. Primary osteoporosis is primarily differentiated from osteo
malation, primary hyperparathyroidism, osteoporotic form of Paget’s disease, multiple myeloma, and bone metastases. The diagnosis of primary osteoporosis is made after the exclusion of these diseases.
The main objectives of the treatment of osteoporosis:
1) slowing down or stopping the loss of bone mass (ideally, its growth);
2) prevention of new fractures;
3) normalization of the reconstruction of the rest;
4) reduction of pain syndrome, expansion of motor activity;
5) improving the quality of life of the patient.
Normalization of bone remodeling (suppression of
bone resorption or stimulation of bone formation) is the basis of treatment. Treatment of the underlying disease in secondary osteoporosis or withdrawal of drugs that adversely affect bone tissue metabolism are often difficult to practice. Symptomatic therapy is an essential part of treatment.
Preparations for the treatment of osteoporosis are conditionally divided into 3 groups:
1) predominantly reduce bone resorption (estrogens, calcitonins, bisphosphonates);
2) predominantly enhancing osteogenesis (fluorides, anabolic steroids, androgens, synthetic parathyroid hormone fragments, growth hormone);
3) affecting the process of bone remodeling (active metabolites of vitamin D, osseine hydroxyapatite complex, ipriflavon (osteochin)).
The choice of a particular drug is defined as a form of osteo
porosis, and the prevailing clinical symptoms. In addition, indications and contraindications to a particular type of therapy are taken into account.
In postmenopausal osteoporosis, as well as in osteoporosis of another genesis, postmenopausal women in the absence of contraindications are prescribed estrogen replacement therapy (proginova, cycloproginum, clemene, klimonorm, livial, cliogest, etc.).
Treatment with calcitonin (miacalcic) is indicated for postmenopausal, steroidal, senile, and idiopathic osteoporosis, especially for severe pain syndrome. The duration of treatment with calcitonin in intermittent mode may be 2-5 years. Treatment is desirable to combine with calcium supplements, as well as vitamin D.
Bisphosphonates (xyphon, alendronate) are indicated in the treatment of postmenopausal and senile osteoporosis in persons without severe impairment of the functions of the gastrointestinal tract.
Osteoporosis with a low level of bone metabolism serves as an indication for the use of fluorides (sodium fluoride, osxi, coreberone). To prevent the development of osteomalacia (demineralization) in the treatment with fluorides, calcium and vitamin D preparations are added. When fluorides are used, the frequency of side effects (20–30%) in the form of dyspeptic phenomena, glossitis and gingivitis, arthralgia is relatively high. The slow development of the therapeutic effect of fluoride requires patience from the patient and the doctor.
Anabolic steroids do not have self-treatment in the treatment of osteoporosis, although they are often included in complex treatment regimens.
Active metabolites of vitamin D are used in a dose of 0.5-1.0 mg per day for several years. As monotherapy, they are indicated for senile, steroid and postmenopausal osteoporosis; They are the drugs of choice for osteomalacia (1–3 µg / day), renal osteodystrophy, and rehabilitation after removal by paratyroma. Active metabolites are also used in combination therapy with estrogens, calcitonin, bisphosphonates, ipriflavone, fluorides.
Side effects occur in 2–3% of cases and manifest as dyspeptic disorders, weakness, drowsiness, and dry mouth. To prevent hypercalcemia, it is desirable to carry out treatment in individually selected doses with the control of the level of calcium and creatinine in the blood 1 time in 2 months.
Iproflavone (osteochin), a derivative of flavonoids synthesized in ferns and flowering plants, enhances bone formation, reduces the incidence of new bone fractures and has a moderate analgesic effect over 12 months of use.
Calcium salts do not have an independent value in the treatment of osteoporosis, but they must be used in combination with other drugs as the basis of pathogenetic therapy, as well as for the primary prevention of osteoporosis.
Symptomatic therapy involves analgesia, the appointment of corsets, physical therapy. Back pain reduces the patient’s motor activity and quality of life.
To reduce pain, analgesics, nonsteroidal anti-inflammatory drugs, and muscle relaxants are used along with pathogenetic agents.
Corsets are absolutely shown in the presence of compression fractures of the vertebral bodies and in severe osteoporosis. Most often recommend semi-rigid corsets and semi-corsets. The possibility of muscle atrophy when wearing corsets is small and is not confirmed in the works of recent years. In severe pain, only breathing exercises are recommended, while isometric exercises are recommended for reducing pain.
Further exercises for abdominal muscles, back, lower and upper extremities are prescribed. Then attach the exercises carried out in a standing position, metered walking, swimming. Massage is prescribed not earlier than 4-6 months after the start of drug therapy.
Primary prevention of osteoporosis implies control over adequate calcium intake during childhood, during pregnancy and lactation, adequate exposure to the sun for the elderly, an active lifestyle and physical activity with moderate exercise, avoiding alcohol and smoking abuse, and passion. various unbalanced diets and starvation.