Osteoporosis
Osteoporosis, or osteopenia, is a group of bone diseases caused by a variety of causes, where there is normal calcification of bone tissue, a normal ratio of calcium salts to matrix, and a metabolic bone lesion characterized by a decrease in the amount of bone tissue per unit volume. In most osteoporosis, the decrease in bone tissue is mainly due to increased bone resorption. It is characterized by skeletal pain and ease of fracture.
English name
osteoporosis
Departments
Endocrinology, Orthopedics
Common symptoms
Pain, fracture, shortening of body length, hunchback, decreased respiratory function
Infectious
None
Etiology
1. Idiopathic (primary)
Juvenile type adult type, menopausal, geriatric.
2. Secondary
Endocrine Cortisolism, hyperthyroidism, primary hyperparathyroidism, acromegaly, hypogonadism, diabetes mellitus, etc. ②Pregnancy, lactation. ③Nutritional Protein deficiency, vitamin C and D deficiency, low calcium diet, alcoholism, etc. ④Hereditary Osteogenesis imperfecta chromosomal abnormalities. ⑤Liver disease. ⑥Nephropathy Chronic nephritis hemodialysis. ⑦Drugs Corticosteroids, anti-epileptic drugs, antineoplastic drugs (such as methotrexate), heparin, etc. (viii) Disuse systemic osteoporosis is seen in long-term bed rest, paraplegia, space flight, etc.; localized is seen after fracture, Sudecks bone atrophy, post-injury bone atrophy, etc. ⑨ Gastrointestinal Malabsorption Gastrectomy. ⑩ rheumatoid arthritis.? Neoplastic Multiple myeloma metastatic carcinoma, monocytic leukemia, Mast-Cell disease, etc.? Other causes Bone loss, transient or migratory osteoporosis.
Clinical manifestations
1. Pain
The most common symptom of primary osteoporosis is low back pain, which accounts for 70% to 80% of the patients with pain. The pain spreads along the spine to both sides, decreases when lying down or sitting, increases when posterior extension or prolonged standing or sitting, and increases when bending, coughing, and bowel movements. Bone pain generally occurs when 12% or more of bone mass is lost. In old age osteoporosis, the vertebrae are compressed and deformed, the spine is flexed forward, and the muscles are fatigued or even spasmed, producing pain. A recent compression fracture of the thoracolumbar spine can also produce acute pain, with strong pressure and percussion pain in the spinal spinous process at the corresponding site. If the corresponding spinal nerve is compressed, radiating pain in the extremities, sensory-motor disorders in both lower extremities, intercostal neuralgia, and retrosternal pain similar to angina pectoris can be produced. If the spinal cord and cauda equina nerve are compressed, the function of bladder and rectum will also be affected.
2. Shortening of body length and hunchback
Most of the time, the pain occurs after the pain. The anterior vertebrae of the spine are heavily loaded, especially the 11th and 12th thoracic vertebrae and the 3rd lumbar vertebrae, which are heavily loaded and easily compressed and deformed, causing the spine to tilt forward and forming a hunchback, and with age, osteoporosis increases and the curvature of the hunchback increases.
3. Fracture
It is the most common and serious complication of degenerative osteoporosis.
4. Decreased respiratory function
Compression fractures of thoracic and lumbar vertebrae, backward curvature of the spine and thoracic deformity can significantly reduce lung capacity and maximum air exchange, and patients can often suffer from chest tightness, shortness of breath and dyspnea.
Examination
1. Laboratory tests
(1) 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.
(2) Blood parathyroid hormone Parathyroid function should be checked to exclude secondary osteoporosis. Blood parathyroid hormone levels may be normal or elevated in primary osteoporosis.
(3) Markers of bone renewal Some serological biochemical indicators of osteoporosis can reflect the status of bone transformation (including bone formation and bone resorption), including: bone-specific alkaline phosphatase (in response to bone formation), anti-tartrate acid phosphatase (in response to bone resorption), osteocalcin (in response to bone formation), type I procollagen peptide (in response to bone formation), urinary pyridinoline and deoxypyridinoline (in response to bone resorption), type I collagen Bone resorption), N-C-terminal cross-linked peptide of type I collagen (in response to bone resorption).
(4) Morning urine calcium/creatinine ratio The normal ratio is 0.13±0.01. If the urinary calcium excretion is excessive, the ratio increases, suggesting the possibility of increased bone resorption.
2. Ancillary tests
(1) Bone imaging and bone density ① X-ray of the lesion site X-ray can detect fractures and other lesions such as osteoarthritis, intervertebral disc disease and anterior displacement of the spine. Bone loss (low bone density) is seen on radiographs with increased bone translucency, reduced bone trabeculae and widening of their gaps, loss of transverse bone trabeculae, and blurring of bone structure, but this is usually observed only when there is a 30% or greater decrease in bone volume. The biconcave deformation of the vertebral body 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. ② Bone density testing Bone density testing is a predictor of fracture. Measuring bone density at any site can be used to assess the overall risk of fracture occurrence; measuring bone density at a specific site can predict the risk of local fracture occurrence.
According to the latest treatment guidelines from the National Osteoporosis Foundation, BMD testing is required for: postmenopausal women over 65 years of age, who are at risk for osteoporosis despite preventive measures and should be treated accordingly if osteoporosis is present; postmenopausal women younger than 65 years of age with one or more risk factors; postmenopausal women with fragility fractures; postmenopausal women with brittle fractures; women who require treatment based on BMD measurements; women on long-term hormone replacement therapy; men with fractures following minor trauma; and people with X-rays showing bone loss and other conditions that can lead to osteoporosis.
The WHO recommends grading osteoporosis based on BMD values, specifying that BMD values plus or minus one standard deviation (SD) in normal healthy adults are considered normal; a decrease (1 to 2.5) SD from normal is considered bone loss; a decrease of 2.5 SD or more is considered osteoporosis; and a decrease of 2.5 SD or more with a fragility fracture is considered severe osteoporosis.
Diagnosis
The diagnosis of postmenopausal and senile osteoporosis first requires the exclusion of various other causes of secondary osteoporosis, such as hyperparathyroidism and multiple myeloma, osteochondrosis, renal osteodystrophy, osteogenesis imperfecta in children, metastases, leukemia, and lymphoma.
In 1994, the WHO recommended a graded diagnosis of osteoporosis based on BMD or BMC (bone mineral content) values: normal as BMD or BMC within 1 standard deviation (SD) of the mean of normal adult BMD; reduced bone mass as BMD or BMC reduced by 1 to 2.5 standard deviations from the mean of normal adult BMD; osteoporosis as BMD or BMC reduced by 2.5 standard deviations from the mean of normal adult BMD Severe osteoporosis was defined as a decrease in BMD or BMC of more than 2.5 standard deviations from the mean of normal adult BMD and was accompanied by one or more fragility fractures. BMD or BMC in this diagnostic criterion can be measured in the mesial or peripheral bones.
Differential diagnosis
1. Osteochondrosis
There is often a clinical history of gastrointestinal malabsorption, steatorrhea, history of major gastrectomy, or history of renal disease. Early skeletal X-rays are often not easily distinguished from osteoporosis. However, if pseudo-fracture lines (Looser’s bands) or skeletal deformities are present, the disease is mostly osteochondrosis. Biochemical changes are more obvious than osteoporosis.
(1) Osteomalacia due to vitamin D deficiency is often associated with low blood calcium and phosphorus, increased blood alkaline phosphatase, and decreased urinary calcium and phosphorus.
(2) Renal bone lesions are mostly seen in tubular lesions, and if there is also glomerular lesion, blood phosphorus may be normal or high. Due to low blood calcium and high blood phosphorus, patients have secondary hyperparathyroidism.
2. Myeloma
The typical patient’s skeletal x-ray often shows well-defined decalcification, which must be distinguished from osteoporosis. Patients have normal blood alkaline phosphatase, variable blood calcium and phosphorus, but often have increased plasma globulin (immunoglobulin M) and the presence of periprotein in the urine.
3. Hereditary osteogenesis imperfecta
Osteogenesis imperfecta may be due to the low production of bone matrix by osteoblasts, resulting in osteoporosis. Calcium, phosphorus and alkaline phosphatase are normal in blood and urine. Patients often have other congenital defects such as deafness.
4. Metastatic cancerous bone lesion
There are clinical manifestations of primary cancer, blood and urine calcium are often increased with urinary stones, and there is bone invasion as seen on X-ray.
Complications
The most common complication: osteoporosis fractures occur mostly during daily indoor activities such as twisting the body, holding objects, opening windows, etc. Fractures can occur even without significant large external forces. Fractures occur in the thoracic and lumbar vertebrae, the distal radius and the upper femur.
Treatment
Effective measures include the following.
1. Exercise
In adulthood, many types of exercise help maintain bone mass. Menopausal women who exercise consistently for 3 hours per week have increased overall calcium. However, bone loss is accelerated in those who exercise excessively to cause amenorrhea. Exercise also improves sensitivity and balance, and people with osteoporosis are encouraged to be as active as possible.
2. Nutrition
Good nutrition is important for the prevention of osteoporosis, including adequate amounts of calcium, vitamin D, vitamin C and protein. From childhood onwards, the daily diet should have an adequate intake of calcium, which influences the acquisition of peak bone mass. European and American scholars advocate a calcium intake of 800 to 1,000 mg for adults, 1,000 to 1,500 mg per day for postmenopausal women, and 1,500 mg per day for men after age 65 and other patients with risk factors for osteoporosis. The intake of vitamin D is 400 to 800 U/day.
3. Prevention of falls
The chances of falls in patients with osteoporosis should be minimized to reduce hip fractures and Colles fractures.
4. Medication
Effective drug therapy can stop and treat osteoporosis, including estrogen replacement therapy, calcitonin, selective estrogen receptor modulators, and diphosphonates, which can stop bone resorption but have a particularly small effect on bone formation. The drugs used to treat and stop the development of osteoporosis are divided into two major groups: the first group is the drugs that inhibit bone resorption, including calcium, vitamin D and active vitamin D, calcitonin, diphosphonates, estrogens, and isoflavones; the second group is the drugs that promote bone formation, including fluoride, anabolic steroids, parathyroid hormone, and isoflavones.
(1) Hormone replacement therapy Hormone replacement therapy is considered the best choice and the most effective treatment for postmenopausal women with osteoporosis, with the problem that hormone replacement therapy may bring about other systemic adverse effects. Hormone replacement therapy is avoided in patients with breast disease and in those who cannot tolerate its side effects. (1) Estradiol It is recommended to start taking it right after menopause and for life if tolerated. Take it in cycles, i.e. 3 weeks in a row and 1 week off. Contraindicated in allergy, breast cancer, thrombophlebitis and vaginal bleeding with unclear diagnosis. Also ethinylestradiol and norethindrone are progestins and are used to treat moderate to severe vasodilatory symptoms associated with menopause. (ii) Androgens Studies have shown that in male patients with osteoporosis due to severe sex hormone deficiency, testosterone replacement therapy can increase BMD in the spine but does not appear to be effective in the hip bone, so androgens can be considered an anti-bone resorption agent. (iii) Testosterone Intramuscular injections once every 2 to 4 weeks may be used to treat patients with decreased BMD in hypogonadism. Testosterone should be used with caution in patients with impaired renal function and in the elderly, as it may increase the risk of prostate enlargement; testosterone can increase the growth of subclinical prostate cancer, so the drug should be monitored for prostate-specific antigen (PSA); liver function, blood count, and cholesterol should also be monitored; the drug should be discontinued in case of edema and jaundice. Calcium and vitamin D supply should be ensured during administration. Topical testosterone is available as an alternative.
(2) Selective estrogen receptor modulators (SERMs) These drugs have weak estrogen-like effects in some organs and estrogen antagonistic effects in others. Raloxifene, a non-steroidal benzothiophene, is an estrogen agonist that inhibits bone resorption, increases BMD in the spine and hip, and reduces the risk of vertebral fracture by 40% to 50%, but is less effective than estrogen. It is prohibited for premenopausal women.
(3) Diphosphates Diphosphates are synthetic analogues of pyrophosphates bound to hydroxyapatite in bone, which can specifically inhibit osteoclast-mediated bone resorption and increase bone mineral density. It is contraindicated in pregnant women and women who are planning to become pregnant. The first generation named hydroxyethyl phosphonate sodium called etidronate sodium, therapeutic doses have adverse effects of inhibiting bone mineralization, therefore, intermittent and cyclic administration is advocated, with 2 weeks of continuous hydroxyethyl phosphonate sodium at the beginning of each cycle and 10 weeks of discontinuation, every 12 weeks as a cycle. The administration of sodium hydroxyethylphosphonate should be accompanied by calcium.
In recent years, a new generation of phosphates has been used in clinical practice, such as aminodiphosphonates (alendronate), risedronate (risedronate sodium), chlordiazepoxide (chloromethyl diphosphonate) (trade name bone phosphonate) and pamidronate, which have a particularly strong effect on bone resorption and do not affect bone mineralization at therapeutic doses. Alendronate (trade name Fosamax) has been shown to reduce bone resorption and decrease the incidence of spine, hip and wrist fractures by up to 50%, and to prevent glucocorticoid-related osteoporosis when used before menopause.
(4) Calcitonin Calcitonin is a peptide hormone, which can rapidly inhibit osteoclast activity and slowly reduce the number of osteoclasts, and has the functions of pain relief, increasing activity function and improving calcium balance, and has the effect of pain relief for patients with fractures, and is suitable for patients with contraindications or intolerance to diphosphonates and estrogen. Commonly used domestic preparations include calcitonin (Miacalcin, salmon calcitonin) and etacalcitonin (Icariin). Calcitonin can be administered parenterally or intranasally, and the duration of action of parenteral administration can last up to 20 months.
(5) Vitamin D and calcium Vitamin D and its metabolites can promote calcium absorption and bone mineralization in the small intestine. Active vitamin D (e.g. rogaine, alfacalcidol) can promote bone formation and increase osteocalcin production and alkaline phosphatase activity. The incidence of vertebral and extravertebral fractures in patients with osteoporosis is better reduced with active vitamin D than with calcium alone. Combination preparations of vitamin D and calcium are also available for more reliable treatment.
(6) Fluoride Fluoride is an effective stimulant for bone formation, which can increase vertebral and hip bone density and reduce the incidence of vertebral fractures. A small daily dose of fluoride can effectively stimulate bone formation with few side effects. The active ingredients of Tridin are glutamine monofluorophosphate and calcium gluconate, which are chewed with a meal. This drug is contraindicated in children and during development.
For patients receiving treatment for osteopenia and osteoporosis, it is recommended that BMD be reviewed every 1 to 2 years. If the index of bone renewal is high on the test, the drug should be reduced. For long-term prevention of bone loss, it is recommended that women begin estrogen replacement therapy immediately after menopause and maintain it for at least 5 years, with 10 to 15 years being preferable. If the patient is diagnosed with a disease known to cause osteoporosis or is on medications that clearly cause osteoporosis, concomitant treatment with calcium, vitamin D, and diphosphonates is recommended.
5. Surgical treatment Surgical treatment is required only after a fracture has occurred due to osteoporosis.
Prognosis
Although osteoporosis cannot be completely prevented, certain preventive measures such as adequate intake of calcium, vitamin D and exercise can largely reduce osteoporosis and prevent serious complications.
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 placed on the implementation of three levels of prevention: 1.
1. Primary prevention
We should start with children and adolescents, such as paying attention to reasonable dietary nutrition and consuming more foods with high calcium and phosphorus content, such as fish, shrimp, milk, dairy products, bone broth, eggs, beans, grains, green leafy vegetables, etc. 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 childbirth, breastfeeding period should not be too long, as much as possible to preserve calcium in the body, enrich the calcium pool, increase the peak bone to the maximum is the best measure to prevent osteoporosis later in life. For the high-risk group with genetic genes, focus on follow-up and early prevention.
2. Secondary prevention
Bone loss accelerates in middle age, especially in women after menopause. Bone mineral 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, while insisting on long-term preventive calcium supplementation, in order to safely and effectively prevent osteoporosis.
3. Tertiary prevention
Patients with degenerative osteoporosis should be actively treated with drugs to inhibit bone resorption (estrogen, CT, Ca) and promote bone formation (active VitD), and measures to prevent falls and upsets should also be strengthened. Patients with middle-aged and elderly fractures should be actively operated, strong internal fixation, early activity, and given comprehensive treatment such as physical therapy, physical therapy psychology, nutrition, calcium supplementation, curbing bone loss, and improving immune function and overall quality.