Introduction to postmenopausal women with osteoporosis

Introduction Postmenopausal osteoporosis (POP) is a common disease associated with aging, mainly in postmenopausal women. Due to estrogen deficiency, bone mass is reduced and bone structure changes, making bone fragility more prone to fracture. And the pain caused by fractures, bone deformation, complication, and even death, seriously affect the health and quality of life of the elderly, and even shorten the life expectancy, increase the financial and human burden of the state and family. Osteoporosis associated with menopause is an important health issue that cannot be ignored. In 1993, WHO defined osteoporosis as a systemic reduction in bone mass, accompanied by a microstructural change in the bone, resulting in an increase in bone fragility and an increased risk of fracture. In 2001, the National Institutes of Health Consensus Conference proposed that osteoporosis is a bone disease characterized by impaired bone strength, leading to an increased risk of fracture. Bone strength is concentrated to reflect bone density and bone mass. The pathological features of osteoporosis are a proportional reduction in bone mineral content and bone matrix composition, thinning of the cortical bone, reduction and thinning of the trabecular bone, and trabecular bone fracture during postmenopausal osteoporosis. The cause is divided into primary and secondary osteoporosis according to the cause. Type I osteoporosis, also known as postmenopausal osteoporosis, is mainly due to estrogen deficiency, occurring in female patients, aged 50 to 70 years, showing rapid loss of bone mass, loss of bone cancellosis, fractures occur more often In the vertebral body with osteoporosis, the upper end of the femur and the distal end of the humerus. Type II osteoporosis is also known as senile osteoporosis. Compared with type I, the number of male patients increased, but the ratio of male to female is still 1:2. The age of onset is more than 70 years old, which is characterized by slow loss of bone mass. The rate of loss of bone cancellus and bone density is almost the same. Except for type I, the incidence of hip fractures has increased. Secondary osteoporosis is caused by other causes. Such as chronic diseases: chronic renal failure, gastrectomy, intestinal diversion, calcium malabsorption syndrome, multiple myeloma, etc.; endocrine diseases: hyperprolactinemia, hyperthyroidism, excessive secretion of adrenal cortex hormones, diabetes, thyroid Paragonadergic hyperactivity. Iatrogenic factors: long-term use of anti-epileptic drugs, aluminum-containing antacids, excessive thyroxine or long-term use of glucocorticoids, gonadotropin-releasing hormone (GnRH) agonists. Postmenopausal osteoporosis is a multifactorial disease, and genetics, lifestyle, and nutrition are all related to the disease. People with high risk factors are susceptible to postmenopausal osteoporosis: white and Asian women, family history of osteoporosis, or women with specific genes affecting bone mass, inadequate calcium intake, lack of physical activity, mass smoking and alcohol consumption , early menopause or bilateral ovarian resection before menopause. Whether or not osteoporosis occurs depends on the peak of bone and the rate of bone loss, high bone peaks and/or slow bone loss, which are not easy to occur, and low bone peaks and/or bone loss are prone to occur. 1. Bone peak Bone peak refers to the highest bone mass in a person's lifetime, usually reached at 25 to 35 years old. There are many factors affecting bone peaks, among which genetic factors are the most important, and nutrition and living habits also have some effects. (1) Genetic factors: determine 70% to 80% of bone peak. For example, black BMD is higher than whites and Asians, and the incidence of osteoporotic fractures is low. Osteoporosis has a family tendency. The difference in BMD between single and twins is smaller than that of twins. The peak of bone in men is higher than that in women. In some countries, vitamin D receptor gene, estrogen receptor gene, or collagen gene polymorphism is associated with BMD, and the bone peak is affected by genetic factors. (2) Nutrition: Those with high calcium intake during adolescence have higher bone peaks and up to 6% of mature bone BMC. The World Health Organization recommends that the elemental calcium intake during adolescence should be 1000 mg per day. (3) Lifestyle: Exercise can increase BMD. If you insist on daily exercise, the amount of physical activity is higher than the average amount of 1SD, and the bone volume is 7% to 10% higher than the average amount of activity below 1SD. However, when excessive exercise causes hypogonadism and amenorrhea occurs, the bone mass decreases. A large number of cigarettes were formed before the peak of bone formation, and the bone peak of alcoholics was low. (4) Primary hypogonadism and delayed puberty development, low bone peak. 2. Bone Loss Rate Women's bone loss is associated with age and menopause. (1) Age-related bone loss: Spinal bone loss generally begins at 40 to 50 years old, and the loss rate is 0.8% to 1.2% per year. The loss of limb bones is about 10 years later, that is, from 50 to 60 years old, the loss rate is 0.3% to 0.6% per year, which is linear, and its mechanism is unclear, which may be related to the reduction of bone formation. The consequence of this bone loss is that the trabecular bone becomes thinner and does not undergo perforation changes in the trabecular bone. (2) Bone loss associated with menopause: Regardless of age, once menopause, the estrogen in the body drops sharply, the bone loss increases logarithmically, and the trabecular bone becomes thinner, thinner, and even broken (perforated). After bilateral ovariectomy, all ovarian-derived sex hormones disappear and bone loss is faster. At this time, the bone loss is twice that of the limb bones, and the loss rate is as high as 4% to 5% per year. After 5 to 10 years, bone loss occurs. The speed is slowed down. Bone loss in the limb bones is slow and the duration of loss is also long. Animal experiments and clinical observations have confirmed that after excretion of estrogen in ovariectomized or postmenopausal women, the bone turnover rate is reduced, which can effectively prevent bone loss. It is also proved that estrogen deficiency is the main cause of postmenopausal osteoporosis. . (B) the pathogenesis of normal bone through bone reconstruction to continuously update the bone. The osteolytic effect of osteoclasts is hollowed out under the bone surface to form a bone lacunae, which is then moved by a group of osteoblasts to the bone lacuna to synthesize and secrete collagen and polypeptide proteins involved in bone formation. After the calcium ion deposition, the bone matrix is formed, and the bone lacuna is repaired by the newly formed bone matrix, and a bone reconstruction unit is completed, and the cycle is about 3 to 4 months. Bone turnover rate refers to the rate of old bone resorption and new bone formation. Postmenopausal estrogen is reduced, bone turnover is increased, bone loss is increased, and high conversion osteoporosis is present. The effect of estrogen on the pathogenesis of osteoporosis is mainly achieved through the following routes. 1. Effects on calcium-regulating hormones Estrogen can enhance liver 25-hydroxylase, renal 1α-hydroxylase activity, increase 1,25-dihydroxyvitamin D levels, promote intestinal calcium absorption, and make calcium and phosphate salts. Deposition in bone promotes bone matrix synthesis. Estrogen also antagonizes the action of parathyroid hormone, and together with parathyroid hormone maintains the balance of calcium and phosphorus in the blood. Parathyroid hormone is a hormone that stimulates osteolysis. When estrogen is reduced, the antagonism of parathyroid hormone is weakened, which can accelerate bone ablation and gradually develop into osteoporosis. Calcitonin inhibits osteoclast activity, and estrogen promotes calcitonin secretion. 2. Participation in bone formation and absorption through the action of cytokines Since Komm demonstrated the presence of estrogen receptors in osteoblasts in 1988, Ernst found that exogenous estrogen promotes IGF-I production by rat osteoblasts. Estrogen receptors are overexpressed due to increased production of IGF-I. It has also been found that estrogen promotes the production of TGF-β in osteoblasts, indicating that these growth factors promote bone formation, and estrogen promotes bone formation through the production of these growth factors. Experiments have shown that when estrogen is deficient, IL-1 secreted by bone marrow mononuclear cells and IL-6 secreted by mesenchymal cells are increased. Pacifici et al also found that TNF-α and GM-CSF were produced in cultured peripheral blood mononuclear cells; TNF-α and GM-CSF levels were elevated in patients undergoing ovariectomy, and TNF-α and GM in estrogen-treated patients - CSF returns to normal levels. The above cytokines promote the bone resorption process, and estrogen inhibits bone resorption by inhibiting the production of the above cytokines. 3. The direct effect of estrogen on bone cells Since 1988, komm has found estrogen receptor (ER) on osteoblasts. In 1990, Penlser found estrogen receptors on osteoclasts, making estrogen more clear. Direct interaction with bone cells. Estrogen binds to estrogen receptors on osteoblasts and osteoclasts, directly inhibits lysosomal enzyme activity of osteoclasts and reduces their ability to produce lacunae on bone sections. In 1996, Shevde demonstrated that estrogen can directly inhibit the recruitment and differentiation of osteoclast precursor cells (bone marrow hematopoietic stem cells) through the receptor-binding pathway, thereby inhibiting osteoclast activity and utilizing cell morphology. Learning methods have shown that this effect of estrogen is achieved by influencing cell cycle-induced apoptosis. In 1997, Kameda also reached a similar conclusion using highly purified mammalian mature osteoclasts. Ernst confirmed that estrogen enhanced the proliferation of rat primitive skull cells and the expression of intracellular collagen and IGF-I mRNA. Symptoms Osteoporosis is a occult disease that often has no symptoms before it breaks. Once a hunchback, short stature, or bone pain is found, fractures often occur. Therefore, clinical symptoms cannot be diagnosed, and the severity of pain can be used to judge the therapeutic effect. 1. Osteoporosis of bone pain, usually due to microfracture of the trabecular bone, caused by muscle and ligament traction when the body position changes, so it can occur with sitting pain, flexion after flexion, walking pain, turning pain And lying pain and so on. The degree of pain is usually measured by a four-level scale. 0 is painless, 1 is sometimes painful, 2 is often painful, but can be tolerated, 3 is painful, and affects work and life. 2. The hunchback or the body becomes shorter when the spine undergoes a compression fracture. 3. Local tenderness or snoring is characterized by no local redness and fever. According to the above clinical manifestations, laboratory tests and auxiliary tests can make a diagnosis in the early stage of osteoporosis. Bone mineral content is the standard for the diagnosis of osteoporosis. In 1994, WHO redefined the bone mineral density as the diagnostic criteria for osteoporosis: 1. Normal bone mass BMD or BMC is within 1 standard deviation of the younger adults. 2. Bone mass reduction BMD or BMC is 1 to 2.5 standard deviations lower than the average for young adults. 3. Osteoporosis BMD or BMC is on average 2.5 standard deviations or more lower than younger adults. 4. Severe osteoporosis (determined osteoporosis) meets the above diagnostic criteria for osteoporosis. At the same time accompanied by one or more fragility fractures. Chinese experts believe that the 2.5 standard deviation of the mean bone loss is not conducive to the early diagnosis and treatment of osteoporosis, and it is more suitable for China's national conditions to lose the two standard deviations as the diagnostic criteria. Read more...