Osteoporosis (osteoporosis) is a systemic bone disease characterized by a decrease in bone mass and destruction of the microstructure of bone, manifested by an increased brittleness of the bone and therefore a much higher risk of fracture, even with minor trauma or in the absence of trauma. Osteoporosis is a multifactorial chronic disease that affects more women than men and is common in postmenopausal women and the elderly. With the increase of the elderly population in China, the incidence of osteoporosis is on the rise and is a health concern in China and worldwide.
Primary osteoporosis is a systemic bone disease characterized by reduced bone mass and microstructural degeneration of bone, resulting in increased brittleness of bone and easy fracture. International Osteoporosis Day is celebrated every year on October 20.
Causes The specific causes of osteoporosis are not fully understood, but are generally considered to be related to the following factors.
Endocrine factors
In women, osteoporosis is caused by estrogen deficiency, while in men it is caused by a decrease in testosterone levels due to hypogonadism. Osteoporosis is particularly common in postmenopausal women, and premature ovarian failure causes osteoporosis to appear earlier, suggesting that a decrease in estrogen is an important factor in the development of osteoporosis. There is a sudden and significant acceleration of bone loss within 5 years after menopause, with an annual bone loss of 2% to 5% being common. About 20% to 30% of early menopausal women have a bone loss of >3%/year, called rapid bone loss, while 70% to 80% of women have a bone loss of <3%/year, called normal bone loss. Lean women are more prone to osteoporosis and fractures than fat women, as a result of the conversion of androgens to estrogens in the latter's adipose tissue. Compared to normal women of similar age, no significant differences in blood estrogen levels were seen in patients with osteoporosis, suggesting that decreased estrogen is not the only factor causing osteoporosis.
In general, the presence of physiological decompensation of renal function in the elderly is manifested by reduced production of 1,25-(OH2)D3 and lower blood calcium, which in turn stimulates the secretion of parathyroid hormone, so most scholars report that blood parathyroid hormone concentrations often increase with age, with increases of up to 30% or more. Studies of parathyroid function in postmenopausal women with osteoporosis have shown hypo-, normal-, and hyper-function. It is generally believed that osteoporosis in the elderly is associated with hyperparathyroidism.
Some studies have shown lower calcitonin levels in women than in men in all age groups, and lower calcitonin levels in women in the menopausal group than in menopausal women, so it is thought that lower calcitonin levels may be one of the reasons for women’s susceptibility to osteoporosis. The increased value of blood calcitonin in women after intravenous calcium drip was significantly lower than that in men, and both the basal and increased values of blood calcitonin were negatively correlated with age. The Department of Endocrinology at Peking Union Medical College Hospital reported that no significant difference in calcitonin reserve function was seen in premenopausal and postmenopausal healthy volunteers who underwent intravenous calcitonin excitation tests. In contrast, calcitonin reserve function was reduced in both patients with reduced bone mass and osteoporosis, with the latter being more pronounced, suggesting that reduced calcitonin reserve function may be involved in the development of osteoporosis. Blood calcitonin levels in postmenopausal women with osteoporosis have mostly been reported to be reduced, but normal and mildly elevated levels have also been reported.
Osteoblast function, 1-alpha-hydroxylase activity of the kidney, which is impaired with aging, and the associated decrease in 1,25-(OH2)D3 concentration, are also involved in the formation of osteoporosis. Other endocrine disorders, such as Cushing’s syndrome, which produces excessive endogenous corticosteroids or chronic thyrotoxicosis, lead to increased bone resorption or excretion, all of which are associated with osteoporosis formation.
Genetic factors
Osteoporosis is more common in whites, especially in northern European races, followed by Asians, and less common in blacks. BMD is an important indicator for the diagnosis of osteoporosis, and BMD values are mainly determined by genetic factors and, to a lesser extent, by environmental factors. In 1994, Morrison et al. reported that the vitamin D receptor genotype could predict the difference in BMD, which could account for 75% of the overall genetic influence, and after adjusting for various environmental factors, the BMD of bb genotypes was about 15% higher than that of BB genotypes; in terms of the incidence of vertebral fractures, bb Preliminary results of this study show that there are significant differences among races and countries, and the final results need to be further investigated. Other studies on the relationship between collagen and estrogen receptor genes and osteoporosis have also been reported, but no definite conclusions have been drawn yet.
Nutritional factors
Calcium intake in adolescence has been found to be directly related to peak bone mass in adulthood. Calcium deficiency leads to increased PTH secretion and bone resorption, and those on a low-calcium diet are prone to osteoporosis. Vitamin D deficiency leads to impaired mineralization of the bone matrix and can lead to osteochondrosis. Long-term protein deficiency causes insufficient synthesis of bone mechanism protein, resulting in backward new bone production, and if there is also calcium deficiency, osteoporosis will appear faster. Vitamin C is indispensable for the synthesis of hydroxyproline in bone matrix, which can maintain the normal growth of bone matrix and maintain bone cells to produce sufficient amount of alkaline phosphatase, and the lack of vitamin C can reduce the synthesis of bone matrix.
Abuse factors
Muscle produces mechanical force on bone tissue, with strong muscles and strong bones, the bone density value is high. Due to the reduced activity of the elderly, muscle strength is weakened, mechanical stimulation is less, and bone mass is reduced. At the same time, the weakened muscle strength and coordination disorders make the elderly more prone to falls and fractures when accompanied by reduced bone mass. In addition, the elderly are prone to osteoporosis because of the loss of bone mass due to disuse factors after prolonged bed rest and inactivity after stroke and other diseases.
Drugs and diseases
Anticonvulsants, such as sodium phenytoin, phenobarbital, and carbamazepine, cause treatment-related vitamin D deficiency, as well as impaired intestinal calcium absorption, and secondary hyperparathyroidism. Excessive use of acid-forming agents, including aluminum preparations, can inhibit phosphate absorption and lead to the breakdown of bone minerals. Glucocorticoids directly inhibit bone formation, decrease intestinal absorption of calcium, increase renal excretion of calcium, secondary parathyroid dysfunction, and production of sex hormones. Long-term use of heparin is associated with osteoporosis, and the exact mechanism is not known. Chemotherapeutic agents, such as cyclosporine A, have been shown to increase bone renewal in rodents.
Cytokines produced by tumor cells in tumors, especially multiple myeloma, activate osteoclasts, as well as leukemia and lymphoma in children or adolescents, in which osteoporosis is often limited. Gastrointestinal disorders, such as inflammatory bowel disease leading to malabsorption and eating disorders; anorexia nervosa leading to rapid weight loss as well as malnutrition, and associated with absence of menstruation. Dysgerminogenic anemia, resulting from excessive bone marrow hyperplasia and thinning of the trabecular junction, and secondary hypogonadism are also seen in this group of patients.
Other factors
Alcohol abuse has a direct toxic effect on bone. Smoking increases the metabolism of estrogen by the liver and has a direct effect on bone, as well as causing weight loss and early menopause. Prolonged heavy exercise can lead to idiopathic osteoporosis.
Osteoporosis is a combination of genetic and environmental factors that affect peak bone mass and the loss of bone mass and eventual progression to osteoporosis. These factors include medications, diet, race, gender, and lifestyle. Osteoporosis can be primary or secondary. Primary osteoporosis can be classified as type I and type II, and secondary osteoporosis is also known as type III osteoporosis.
Postmenopausal osteoporosis
The main cause is thought to be a defect in gonadal (estrogen and testosterone) function, and estrogen and testosterone deficiency occurring at any age will accelerate bone loss. The exact mechanism of bone loss is not fully understood and the causes are multifaceted, the most important of which are the increased recruitment and sensitivity of preosteoclastic cells and the rate of bone resorption that exceeds bone formation. In postmenopausal women, bone loss increases at a rate of 1% to 5% per year during the first 5-7 years, resulting in a reduction in bone trabeculae and a predisposition to Colles’ fracture and vertebral fractures.
Estrogen deficiency increases the sensitivity of bone to the action of parathyroid hormone (PTH), resulting in increased calcium loss from bone, decreased renal excretion of calcium, and increased production of 1,25-(OH)2D3. increased 1,25-(OH)2D3 promotes calcium absorption in the intestine and kidneys and promotes bone resorption by increasing the activity and number of osteoclasts. secretion of PTH decreases through a negative feedback mechanism, causing the opposite effect as described above. PTH secretion decreases through a negative feedback mechanism, causing the opposite effect as described above. Osteoclasts are also affected by cytokines such as TNF-α, IL-1 and IL-6, which are produced by monocytes and are increased in the presence of sex hormone deficiency.
Age-related osteoporosis
It is seen in both men and women and stems from a decrease in bone formation and a decrease in 1,25-(OH)2D3 formation by the kidneys in the elderly. These physiological changes result in loss of bone cortex as well as bone trabeculae, increasing the risk of fracture of the hip, long bones, and vertebrae.
Secondary to drugs
especially glucocorticoids, or various other lesions that increase bone loss.
In type I and type II osteoporosis, women are more common, with a male to female ratio of 6:2 (type I) and 2:1 (type II), respectively, while in type III osteoporosis, there is no difference in the incidence ratio between men and women. The peak age of onset of type I osteoporosis is 50 to 70 years old, the high incidence of type II osteoporosis is over 70 years old, and the onset of type III osteoporosis has little relationship with age and can be seen at any age.
Examination
Blood calcium, phosphorus and alkaline phosphatase
In primary osteoporosis, serum calcium, phosphorus and alkaline phosphatase levels are usually normal, and alkaline phosphatase levels may increase several months after fracture.
Blood parathyroid hormone
Parathyroid function should be checked to exclude secondary osteoporosis. Blood parathyroid hormone levels may be normal or elevated in primary osteoporosis.
Bone imaging and bone density
X-rays should be taken for patients with localized symptoms Lateral films of the area should be taken even for patients without spinal symptoms to avoid missing vertebral fractures X-rays can detect fractures and other lesions such as osteoarthritis, disc disease, and anterior spinal displacement Bone loss (low bone density) is seen on radiographs with increased bone translucency, decreased bone trabeculae and widened gaps, loss of transverse trabeculae, and blurred bone structure, but usually requires a 30% or greater decrease in bone volume to be observed. The biconcave deformation of the vertebral body due to disc bulge and the collapse of the anterior edge of the vertebral body in a wedge shape, also known as compression fracture, are commonly seen in the 11th and 12th thoracic vertebrae and the 1st and 2nd lumbar vertebrae.
Bone mineral density (BMD) is the best predictor of fracture. Measuring BMD at any site can be used to assess the overall risk of fracture; measuring BMD at a specific site can predict the risk of local fracture.
Clinical manifestations
(1) Pain. The most common symptom of primary osteoporosis is low back pain, which accounts for 70%-80% of patients with pain. The pain spreads along the spine to both sides, decreases when lying on the back or sitting, increases when posterior extension or prolonged standing or sitting, is light during the day, increases at night and when waking up in the morning, and increases when bending, muscle movement, coughing and stooling. Bone pain generally occurs when 12% or more of bone mass is lost. In old age osteoporosis, the vertebral trabeculae atrophy and decrease in number, the vertebral body compresses and deforms, the spine flexes forward, the lumbar rash muscle doubles its contraction in order to correct the forward flexion of the spine, the muscle fatigue or even spasm, producing pain. A recent compression fracture of the thoracolumbar spine can also produce acute pain, with strong pressure pain and percussion pain in the spinal spinous process at the corresponding site, which can generally be gradually reduced after 2-3 weeks, and some patients can present with chronic low back pain. If the corresponding spinal nerve is compressed, radiating pain in the extremities, sensory-motor disorders in both lower extremities, intercostal neuralgia, retrosternal pain similar to angina pectoris, or epigastric pain similar to acute abdomen may occur. If compression of the spinal cord, cauda equina also affects the bladder and rectal function.
(2) Shortening of body length and hunchback. Mostly appear after the pain. The front part of the vertebrae of the spine is almost mostly composed of cancellous bones, and this part is the pillar of the body with a large weight, especially the 11th and 12th thoracic vertebrae and the 3rd lumbar vertebrae, which have a greater load and are easily compressed and deformed, causing the spine to tilt forward and the back curve to increase, resulting in hunchback, and as we grow older, osteoporosis increases and the curvature of the hunchback increases, resulting in significant knee contracture. Each person has 24 vertebrae, the height of each vertebra is about 2cm in normal people, when the elderly osteoporosis vertebral compression, each vertebrae shortened by about 2mm, the average length of the body shortened by 3-6cm.
(3) Fracture. This is the most common and serious complication of degenerative osteoporosis, which not only increases the patient’s pain and aggravates the economic responsibility, but also severely limits the patient’s activities and even shortens the life span. According to our statistics, the incidence of fractures in the elderly is 6.3%-24.4, especially in elderly women of advanced age (80 years or older). Fractures caused by osteoporosis are more common in the early stages of old age with distal radius fractures (Colles fractures) and later in old age with fractures of the lumbar spine and upper femur. Fractures generally occur when 20% or more of bone mass is lost, and for every 1.0 DS decrease in BMD, the incidence of vertebral fractures increases 1.5-2 times. About 20%-50% of patients with vertebral compression fractures have no obvious symptoms.
(4) Decreased respiratory function. Compression fractures of the thoracic and lumbar spine, backward curvature of the spine, and thoracic deformity can significantly reduce lung capacity and maximum ventilation, and the incidence of lobar emphysema in the anterior region of the upper lobe of the lung can be as high as 40%. Most elderly people have no degree of emphysema, lung function decreases with age, if combined with thoracic deformity due to osteoporosis, patients often have chest tightness, shortness of breath, dyspnea and other symptoms.
Classification
Osteoporosis can be divided into three main categories.
The first category is primary osteoporosis, which is a physiological degenerative lesion that inevitably occurs with age. This type is divided into 2 types, type Ι for postmenopausal osteoporosis, which is seen in women shortly after menopause. type Π for senile osteoporosis, which occurs mostly after the age of 65.
The second type is secondary osteoporosis, which is triggered by some factors such as other diseases (e.g. kidney failure, excess thyroid hormones or leukemia), or drugs (e.g. steroids).
The third category is idiopathic osteoporosis, mostly seen in adolescents or adults between the ages of 8 and 14, most of whom have a genetic family history and more women than men. Women with osteoporosis during pregnancy and lactation can also be included in idiopathic osteoporosis.
Treatment
1. Hormonal supplementation therapy: Estrogen plus luteinizing hormone can prevent and treat osteoporosis. If there is no uterus, progesterone is not needed.
2, alendronate (alendronate): inhibit the role of osteoclasts, while having the effect of prevention and treatment of osteoporosis.
3.Calcitonin: absorbed by subcutaneous, intramuscular injection or nostril, effective for women with osteoporosis who have stopped menstruating for more than five years. Side effects include loss of appetite, flushing, rash, nausea and dizziness.
However, as soon as the medication is stopped, the rate of bone loss will begin to accelerate, so long-term treatment is necessary.
4.Calcium and vitamin D: the combination is more effective.
5.Bone peptide preparation: It is a new clinical drug used to treat rheumatoid rheumatism, which is effective for osteoporosis.
6.Chinese herbal medicine.
Prevention
Osteoporosis brings great inconvenience and pain to patients’ lives, and the treatment is slow, and once the fracture is fractured, it can be life-threatening, therefore, special emphasis should be put on the implementation of three-level prevention.
1, primary prevention: should start from children and adolescents, such as pay attention to reasonable dietary nutrition, more food containing high Ca, P, such as fish, shrimp, shrimp, kelp, milk (250ml contains Ca300mg), dairy products, bone broth, eggs, beans, refined grains, sesame, melon seeds, green leafy vegetables, etc.. Try to get rid of “risk factors”, adhere to a scientific lifestyle, such as adhere to physical exercise, more sunbathing, do not smoke, do not drink alcohol, less coffee, strong tea and carbonated beverages, less sugar and salt, animal protein should not be too much, late marriage, less childbearing, breastfeeding period should not be too long, as far as possible to preserve the calcium in the body, enrich the calcium pool, the bone The best measure to prevent osteoporosis in the later stages of life is to increase the peak value of calcium to the maximum. Strengthen the basic research of osteoporosis, and focus on the follow-up and early prevention for the high-risk groups with genetic predisposition.
2.Secondary prevention: bone loss accelerates in middle age, especially after menopause in women. Bone density examination should be conducted annually during this period, and prevention and control measures should be taken early for people with rapid bone loss. In recent years, most scholars in Europe and the United States advocate starting long-term estrogen replacement therapy within 3 years after menopause, and at the same time insisting on long-term preventive calcium supplementation or using bone peptide oral preparation bone peptide tablets for preventive treatment, in order to safely and effectively prevent osteoporosis. In Japan, it is mostly advocated to prevent osteoporosis with active Vit D (rocalciferol) and calcium, and to pay attention to the active treatment of diseases related to osteoporosis, such as diabetes, rheumatoid arthritis, steatorrhea, chronic nephritis, hyperparathyroidism/hyperthyroidism, bone metastasis cancer, chronic hepatitis, liver cirrhosis, etc.
3.Tertiary prevention: Patients with degenerative osteoporosis should be actively treated with medication to inhibit bone resorption (estrogen, CT, Ca), promote bone formation (active Vit D), oral preparation of bone peptide (bone peptide tablets), and should also strengthen measures to prevent falling, bumping, tripping and upsetting. For middle-aged and elderly fracture patients should be actively operated, implement strong internal fixation, early activity, physical therapy, physiotherapy psychological, nutrition, calcium supplementation, pain relief, promote bone growth, curb bone loss, improve immune function and overall quality and other comprehensive treatment.
The following points should be done in life, which can also play a good preventive role
Calcium supplementation
Calcium is an important component of bones and is mainly derived from food. If you cannot take in sufficient amount of calcium from food, you can supplement calcium. It is not harmful to consume slightly more calcium than needed. One to two tablets per day can adequately replenish the daily calcium requirement, and because it contains vitamin D, it can make calcium absorption more complete.
Vitamin D supplementation Vitamin D is essential in the prevention and treatment of osteoporosis. Without vitamin D, the body cannot absorb and use calcium. Regular people need about 400 international units of vitamin D per day (equivalent to] 100 ml of milk, – tablets of multivitamin pills or 30-60 minutes of sunbathing per week), and excess vitamin D is harmful to the body. After entering the liver, vitamin D undergoes a series of hydroxylation enzymatic reactions to produce 1,25(OH2)D and other active metabolites involved in bone metabolism. Roscalciferol, also known as calcitriol, is one of the active metabolites of vitamin D. It not only promotes intestinal calcium ion absorption and increases urinary calcium reabsorption by the distal tubule, but also activates osteoclasts to enable bone resorption and activates osteoblasts to promote bone formation.
Estrogen supplementation
After menopause, estrogen level decreases, causing bone loss and making bones begin to become brittle. Estrogen replacement therapy can prevent and control osteoporosis and reduce the incidence of fractures; reduce symptoms of menopause, such as flushing, reduced vaginal secretion, irritability, insomnia and excessive sweating; reduce blood cholesterol level, thus reducing the occurrence of heart disease. Estrogen replacement methods can be given orally, by injection or by subcutaneous implantation. Estrogen replacement methods can cause breast tenderness and fluid retention. Some women may menstruate again, but not become pregnant. Some people are concerned about estrogen causing cancer, and the risk of cancer can be reduced if progestins are used in conjunction with treatment. For those who already have typical osteoporosis, the use of calcitonin, diphosphonate and sodium fluoride can rapidly reduce pain and relieve the condition, but they should be used under the guidance of physicians. In patients with existing fractures, surgical treatment is intensified to prevent complications.