Postmenopausal osteoporosis is a pathological destruction of bone tissue caused by systemic metabolic disorders due to hypoestrogenism. In half of the cases, it proceeds covertly and is diagnosed after the fracture occurs. It may be manifested by pain in the sacrum, lower back, interscapular region, pelvic bones, forearm and lower leg, curvature of the spine, decreased growth. It is diagnosed using densitometry, determination of the level of calcium, phosphorus, markers of bone resorption, calcitonin, parathyroid hormone. Hormonal agents, osteoresorption inhibitors, osteosynthesis stimulators, calcium and vitamin D preparations are used for treatment.
ICD 10
M81.0 Postmenopausal osteoporosis
General information
Primary postmenopausal osteoporosis is the most common variant of osteoporetic disease, accounting for more than 85% in the structure of this metabolic disease of the musculoskeletal system. According to WHO, a densitometrically confirmed decrease in bone mineral density and a violation of their microarchitectonics is observed in 30-33% of women over 50 years of age. In the USA, the frequency of forearm fractures typical for osteoporosis is more than 560 cases per 100 thousand postmenopausal patients, osteoporetic hip fractures are over 120 per 100 thousand. The social significance of pathology is determined by its impact on disability and mortality of elderly women.
Causes
A decrease in bone mass and a violation of the microarchitectonics of bones during postmenopause is associated with involutive processes occurring in the female body and age-related lifestyle changes. Specialists in the field of gynecology have studied in detail the causes of the disorder and predisposing factors. The occurrence of osteoporosis in older women leads to:
- Reduction of estrogen levels. Female sex hormones are involved in the metabolism of calcium, an important structural component of bones that ensures their strength, renewal and restoration of bone tissue. Hypoestrogenia develops with insufficiency or extinction of ovarian function, drug suppression of estrogen secretion, surgical removal of an organ in patients with tumors, endometriosis, ectopic pregnancy.
- Irrational nutrition. Calcium deficiency occurs with limited consumption of dairy products, fish, dietary meats, legumes, greens, vegetables, fruits against the background of an excess of easily digestible carbohydrates, fats, coffee, strong tea. Such a diet is characterized by a low content of calcium, substances that contribute to the absorption of the mineral by the body, and an increased concentration of inhibitors of its absorption in the intestine.
- Low motor activity. With age, a woman’s mobility decreases. The situation is aggravated by a decrease in the time of natural insolation, the presence of excess weight, diseases and pathological conditions that limit the ability to move independently — prolonged bed rest in the treatment of chronic somatic pathology, the consequences of suffered cerebral circulatory disorders and heart attacks.
Risk factors for osteoporosis in the postmenopausal period are age over 65 years, belonging to the Caucasian race, early menopause, body weight deficiency, a history of dishormonal disorders, smoking, alcohol abuse. The influence of heredity is not excluded – the disease is more often detected in women whose close relatives suffered from osteoporosis or had frequent fractures. The probability of damage to the bone system also increases with more than three months of taking glucocorticoid drugs that affect calcium metabolism.
Pathogenesis
In postmenopausal osteoporosis, the balance between osteosynthesis and osteoresorption — the main mechanisms of bone remodeling – is disturbed. Against the background of estrogen deficiency, the secretion of calcitonin, a thyroid hormone that is a functional antagonist of the parathyroid hormone, decreases, and the sensitivity of bone tissue to the resorptive action of the parathyroid hormone increases. The main effect of parathyroid hormone is an increase in the concentration of calcium in the blood due to increased transport through the intestinal wall, reabsorption from primary urine and osteoresorption. In parallel, osteoclasts are activated — cells that destroy bone tissue, insulin-like growth factors 1 and 2, osteoprotogerin, transforming β-factor, colony stimulating factor and other cytokines that enhance bone resorption.
Additional elements of the pathogenesis contributing to the development of osteoporosis are the deterioration of mineral absorption due to intestinal epithelium subatrophy and vitamin D deficiency, for sufficient secretion of which a longer stay in the sun is required. A decrease in motor activity in the postmenopausal period leads to a decrease in dynamic loads on the musculoskeletal system, which also slows down the processes of its remodeling. The situation is aggravated by the deterioration of calcium absorption in the intestine and its increased excretion in the urine when taking glucocorticoids, often used in treatment regimens for endocrine, autoimmune, inflammatory and other diseases that elderly patients suffer from.
Symptoms of postmenopausal osteoporosis
In almost half of women, the disease is asymptomatic and is detected only after a fracture caused by a minor injury. In other cases, the symptoms progress gradually. As the bone mass is lost, the patient begins to feel pain in the lumbosacral region, which increases during lifting heavy objects, turns, walking. Subsequently, there is a feeling of heaviness in the interscapular space, soreness in the pelvic ring, long tubular bones of the lower leg. To get rid of pain and discomfort, additional rest in the prone position is required throughout the day.
The increase in the intensity of painful sensations leads to the fact that over time they disturb the patient even at rest. Usually, a violation of posture and curvature of the spine is accompanied by kyphosis. Often postmenopausal women with osteoporosis complain of weakness, fatigue during physical exertion. Extreme forms of pathology are compression fractures of the lower thoracic and upper lumbar vertebrae with a decrease in their height, spontaneous or fractures of the ankles, forearm bones, hip neck that occur with minor loads. A characteristic feature is a decrease in growth by several centimeters per year.
Complications
The most serious consequence of postmenopausal osteoporosis is disability due to curvature of the spine and frequent fractures of the limbs, aggravated by constant pain in the bones. It is difficult for the patient to move not only over long distances, but also around the house, take care of herself, perform simple household actions. A significant deterioration in the quality of life can provoke emotional disorders — anxiety, tearfulness, hypochondriac, a tendency to depressive reaction. Some women with osteoporosis have prolonged insomnia.
Diagnostics
When detecting compression changes in the spine or typical limb fractures in a postmenopausal patient, osteoporosis should be excluded first of all. For diagnostic purposes, methods are used to assess the architectonics of bone tissue and the degree of its saturation with calcium, as well as to detect biochemical markers of bone damage. The most informative are:
- Densitometry. Modern dual-energy X-ray osteodensitometers determine with high accuracy how much the density of bone tissue is reduced. With their help, it is easy to assess the mineralization of “marker” bones (forearm, hip joint, lumbar vertebrae) and the whole body. The method is applicable for the diagnosis of the early stages of postmenopausal osteoporosis. Instead of the classical two-energy study, ultrasound screening of bone density (echodensitometry), CT-densitometry can be performed.
- Biochemical blood testing. During laboratory tests, the content of calcium, phosphorus and some specific markers indicating a violation of bone remodeling are determined. With increased age-related bone resorption, the level of alkaline phosphatase, osteocalcin in the blood, and deoxypyridonoline in the urine increases. When correlated with creatinine excretion, the determination of calcium in urine is quite specific, the content of which increases with increased resorptive processes in bone tissue.
- Analysis of hormone content. Since postmenopausal osteoporosis is pathogenetically associated with age-related hormonal imbalance, the study of thyrocalcitonin and parathyrin levels is indicative for diagnosis. With an involutive violation of bone resorption, the concentration of calcitonin in the blood decreases, while the level of parathyroid hormone remains normal or lowered. A control study of the content of sex hormones confirms the natural age-related hypoestrogenism.
Differential diagnosis is performed with senile and secondary osteoporosis, malignant bone tumors and bone metastases, myeloma, fibrotic dysplasia, Paget’s disease, common traumatic fractures, scoliosis, spinal osteochondropathy, peripheral neuropathy. If necessary, the patient is consulted by an orthopedist, traumatologist, endocrinologist.
Treatment
The main goal of therapy is to prevent possible fractures by improving the mineralization and architectonics of bones while improving the quality of life of patients. For this purpose, complex anti-osteoporetic therapy is used, aimed at various links in the pathogenesis of the disease. The standard treatment regimen for osteoporosis caused by postmenopausal changes in a woman’s body includes the following groups of drugs:
- Bone resorption inhibitors. Estrogens, their combinations with progestins or androgens prevent premature bone destruction and are recommended when menopausal manifestations persist in the first years of postmenopause. If there are contraindications or the patient refuses to take sex hormones, it is possible to replace them with phytoestrogens, selective modulators of estrogen activity or estrogen receptors. In addition to hormone replacement therapy, calcitonin, bisphosphonates, and strontium preparations have the effect of slowing resorption.
- Bone formation stimulants. The appointment of parathyroid hormone, anabolic steroids, androgens, somatotropin, fluorides contributes to the strengthening of osteogenesis. Accelerated bone remodeling with the use of these drugs is achieved by activating osteoblasts, enhancing anabolic processes, and stimulating hydroxylation. It should be borne in mind that in postmenopausal disorders, the use of such drugs is limited by a number of contraindications and possible complications.
- Means of multidimensional action. Mineralization and architectonics of bone tissue improves when taking calcium preparations, especially in combination with vitamin D, which makes it possible to classify such funds as basic. Ossein-hydroxylate complex and flavone compounds also have a versatile effect on the processes of osteogenesis and bone destruction, which, with a minimal probability of complications, effectively inhibit the function of osteoclasts responsible for resorption and demineralization, stimulating osteoblastic osteopoiesis.
Effective treatment of osteoporosis in postmenopausal women is impossible without lifestyle and diet correction. Elderly patients are recommended moderate physical activity with the exception of falls, lifting weights, sudden movements. It is necessary to add calcium—rich foods to the diet – milk, cottage cheese, hard cheese, legumes, fish, and other seafood, giving up the abuse of coffee and alcoholic beverages.
Prognosis and prevention
Although postmenopausal osteoporosis is a progressive disease, regular supportive treatment and a healthy lifestyle can significantly reduce the likelihood of fractures. For preventive purposes, postmenopausal women are recommended to take calcium supplements containing vitamin D, dosed insolation, diet correction, sufficient physical activity taking into account the age norm, smoking cessation, limited consumption of products containing caffeine (coffee, tea, chocolate, cola, energy drinks). When signs of osteoporosis are detected, corsets and hip protectors can become effective protection against loads that provoke fractures.
