osteoporosis(redirected from Glucocorticoid Induced Osteoporosis)
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Causes and symptoms
- Age. Osteoporosis is more likely as people grow older and their bones lose tissue.
- Gender. Women are smaller and start out with less bone. They also lose bone tissue more rapidly as they age. While women commonly lose 30-50% of their bone mass over their lifetimes, men lose only 20-33%.
- Race. Caucasian and Asian women are most at risk for the disease, but African American and Hispanic women can get it too.
- Figure type. Women with small bones and those who are thin are more liable to have osteoporosis.
- Early menopause. Women who stop menstruating early because of heredity, surgery or lots of physical exercise may lose large amounts of bone tissue early in life. Conditions such as anorexia and bulimia also may lead to early menopause and osteoporosis.
- Lifestyle. People who smoke or drink too much, or do not get enough exercise have an increased chance of osteoporosis.
- Diet. Those who do not get enough calcium or protein may be more likely to have osteoporosis. That is why people who constantly diet are more prone to the disease.
- Genetics. Research in Europe reported in 2003 that variations of a gene on chromosome 20 might make some postmenopausal women more likely to have osteoporosis. Studies were continuing on how to identify the gene and use information from the research to prevent osteoporosis in carriers.
Getting calcium from foods
Taking calcium supplements
Getting vitamin d
Avoiding smoking and alcohol
Postmenopausal, estrogen-deficient osteoporosis is the most common type; more than half the women in the United States 50 years of age or older are likely to have radiologically detectable evidence of abnormally decreased bone mass (osteopenia) in the spine, and in more than a third, major orthopedic problems related to osteoporosis will eventually occur. Most fractures sustained by women over the age of 50 are secondary to osteoporosis. Women at risk for this disorder can reduce that risk by maintaining adequate calcium levels with dietary calcium or calcium supplements (see diet-related bone loss below), and taking estrogen in the perimenopausal period when indicated. Estrogen replacement therapy is especially recommended for women whose ovaries were removed before age 50.
Age-related osteoporosis is a type that occurs in both men and women and is caused by bone loss that normally accompanies aging.
Diet-related bone loss is caused by chronic dietary deficiencies in calcium and protein, as well as deficiency in vitamin C, which is an essential cofactor in collagen metabolism. Intestinal absorption of calcium becomes less efficient with age; hence older persons need more rather than less dietary calcium to maintain a positive calcium balance. Although dairy products are the primary source of dietary calcium, supplementary calcium is needed by some women. Healthy premenopausal women over the age of 30 may need as much as 1000 mg of calcium a day, which is the amount supplied by a quart of milk. However, for pregnant women and those over the age of 50, the recommended daily intake increases to more than 1500 mg. Lactating women need 2000 mg of calcium daily to prevent untimely catabolism of bone. The vitamin D metabolite 1,25-dihydroxycholecalciferol is the active hormone that helps maintain normal serum calcium and phosphate levels. Because of inadequate exposure to sunlight, decreased intestinal absorption of vitamin D, and limited intake of milk, elderly persons often are vitamin D–deficient. Vitamin D is a component of multivitamins, and health care providers often recommend supplemental multivitamins for the elderly.
Disuse osteoporosis is related to the response of bone mass change to mechanical stress. Net bone mass does not change throughout much of adult life; however, living bone is never metabolically at rest and constantly remodels and reappropriates its mineral stores along lines of mechanical stress. Without weight-bearing stress, bone mass diminishes. As much as 30 to 40 per cent of initial bone mass may be lost after six months of total immobilization, as in paraplegia and quadriplegia due to spinal cord injury. Movement alone is not sufficient to prevent osteoporosis. There must be weight-bearing activity and the use of antigravity muscles to maintain healthy bones.
Heritable osteoporosis includes at least four types of congenital diseases grouped under the term osteogenesis imperfecta. Symptoms of varying severity that are characteristic of these disorders include skeletal fragility, multiple pathologic fractures, generalized osteoporosis, and scoliosis. All of the diseases included under osteogenesis imperfecta are thought to be associated with defective bone matrix formation.
Endocrine-mediated bone loss can produce osteoporosis because numerous endocrine hormones affect skeletal remodeling and hence skeletal mass. Examples of endocrine disorders that can produce associated osteopenia include hypogonadism, hyperthyroidism, hyperparathyroidism, and hyperadrenalism or chronic glucocorticoid hormone excess.
Disease-related bone loss can occur with almost any kind of chronic disease that is associated with malnutrition and disuse. Osteopenia is also a common complication of most tumors of the bone marrow. Leukemia, lymphoma, and the extremely rare mast cell tumor also may be associated with osteoporosis.
Idiopathic osteoporosis, in both the adult and juvenile form, is extremely uncommon. Drug-induced bone loss may be associated with long-term use of heparin for anticoagulation therapy or with the administration of methotrexate, which has both cytotoxic and calciuric effects.
During the intervals between compression fractures, the patient may be symptom-free, but kyphosis, decrease in height, and appearance of a “dowager's hump” are reliable indicators of the early progress of the disease. Two other associated effects of vertebral compression are the result of a decrease in the size of the thoracic and abdominal cavities. The patient experiences diminished activity tolerance as a result of disease-related postural changes and often reports early satiety and a bloated feeling after eating only a small amount of food.
Radiographs of the thoracic and lumbar spine show a visible loss of bone density. In general, as much as 30 to 50 per cent of the bone mass must be lost before the decrease can be seen on x-ray. Bone density measurement can help in evaluation of this disease and prediction of the likelihood of fracture.
Estrogen replacement therapy is often prescribed for women at menopause. Because it increases the risk for breast and gynecologic malignancies, careful assessment of these patients is necessary. Pharmacologic agents approved by the Food and Drug Association for osteoporosis treatment or treatment include the bisphosphonatesalendronate and risedronate; calcitonin, estrogen replacement therapy, and selective estrogen receptor modulators such as raloxifene.
Information on osteoporosis can be obtained by writing the National Osteoporosis Foundation, 1232 22nd St. NW, Washington, DC 20037-1292 or consulting their web site at http://www.nof.org. They have also published clinical guidelines for the prevention and treatment of osteoporosis on their web site.
Osteoporosis affects 20 million U.S. residents, about 80% of them women, and costs U.S. society as much as $13.8 billion annually. About 1.3 million fractures attributable to osteoporosis occur each year in people aged 45 and older, and this condition is responsible for 50% of fractures occurring in women older than age 50. Although all bones are affected, compression fractures of the vertebrae and traumatic fractures of the wrist and femoral neck are most common. Loss of body height and development of kyphosis may be the only signs of vertebral collapse. Fractures in the elderly often lead to loss of mobility and independence, social alienation, fear of further falls and fractures, and depression. After hip fracture, most elderly patients fail to recover normal activity, and mortality within 1 year approaches 20%. Osteoporosis occurs when bone resorption outpaces bone formation. Underlying mechanisms are complex and probably diverse. Bone constantly undergoes cycles of resorption and remodeling to maintain the concentration of calcium and phosphate in the extracellular fluid. When serum calcium concentration drops, increased secretion of parathyroid hormone stimulates bone resorption by osteoclasts to restore serum calcium levels to normal. Bone mass declines with age and is influenced by sex, race, menopause, and weight-for-height. Dietary intake of calcium and vitamin D as well as intestinal and renal function affect calcium and phosphate homeostasis. The risk of osteoporosis is highest in postmenopausal women. Asian or white race, underweight, dietary calcium deficiency, sedentary lifestyle, alcohol use, and cigarette smoking appear to be independent risk factors. The decline of vitamin D3 level with aging results in calcium malabsorption, which, in turn, stimulates bone resorption. Estrogen deficiency exacerbates this problem by increasing the sensitivity of bone to resorbing agents. Female athletes who become amenorrheic because of rigorous exercise and dietary restriction or eating disorders are at risk of osteoporosis. The formation and resorption of bone are also influenced by external physical factors such as body weight and exercise. Immobilization and prolonged bed rest produce rapid bone loss, whereas exercise involving weight-bearing, resistance, and high impact has been shown both to reduce bone loss and to increase bone mass. Risk factors for osteoporosis in men include alcoholism, chronic lung disease, hypogonadism, and rheumatoid arthritis, and other disorders that restrict mobility. Osteoporosis is common in young adults with cystic fibrosis and in people receiving long-term thyroid hormone or glucocorticoid therapy. The diagnosis of primary osteoporosis is established by documentation of reduced bone density after exclusion of known causes of excessive bone loss. Assessment of bone density is currently recommended for all women 65 and older and for younger women who are at increased risk of osteoporosis. Roentgenograms are insensitive indicators of bone loss, because bone density must have decreased by at least 20-30% before the reduction can be appreciated. Standard diagnostic procedures are determination of bone mineral density (BMD) at the ultradistal radius and midshaft radius by single-photon absorptiometry (SPA) and at the hip and lumbar spine by dual-energy x-ray absorptiometry (DEXA). The World Health Organization defines osteoporosis as a BMD more than 2.5 standard deviations (SD) below the mean for healthy premenopausal women and osteopenia as a BMD between 1 and 2.5 SD below that level. A quantitative ultrasound procedure is comparable with bone density measurements by dual-energy x-ray absorptiometry in predicting fractures due to osteoporosis. The goal of therapy in osteoporosis is prevention of fractures in susceptible patients. The appropriate timing and proper use of agents such as calcium, vitamin D, estrogen, bisphosphonates, calcitonin, and raloxifene and the role of exercise have generated major research efforts and considerable controversy. Intake of adequate amounts of calcium and vitamin D, and continuing moderate weight-bearing exercise, are basic preventive measures for people of all ages. Those with demonstrated reduction of bone mineral density should take 1200-1500 mg of calcium and 400-800 IU of vitamin D daily. Administration of estrogen at and after menopause does not simply halt the loss of bone, but actually increases bone mass. However, to date there is no experimental proof that hormone replacement with estrogen reduces the risk of fractures in postmenopausal women. The possible benefits of estrogen therapy must be weighed against the increased risk of endometrial hyperplasia and endometrial carcinoma (which can be offset by concomitant administration of progestogen), myocardial infarction, stroke, invasive breast cancer, venous thromboembolism, and gallbladder disease. The selective estrogen receptor modulator raloxifene has been approved for prevention of osteoporosis. It does not cause endometrial hyperplasia but is less effective than estrogen in conserving bone mass. The hormone calcitonin, administered by injection or nasal spray, inhibits bone resorption. Bisphosphonates such as alendronate and etidronate, which bind to bone crystals, rendering them resistant to enzymatic hydrolysis and inhibiting the action of osteoclasts, have been shown to increase bone mineral density. In contrast to other agents, teriparatide, a synthetic version of the biologically active segment of human parathyroid hormone, actually stimulates bone formation in osteoporosis. Strategies to prevent falls are important in elderly patients. see also estrogen replacement therapy, raloxifene.
osteoporosisBrittle bones Orthopedics A condition characterized by ↓ bone mass and density–demineralization, bone fragility; it is the most common morbid condition of elderly ♀ Statistics Age-related osteoporosis causes > 105 fractures/yr–US–vertebrae 54%, hip 23%, distal forearm or Colles fracture, 17%; 25% of ♀ > 70 have evidence of vertebral fractures, as do 50% of ♀ > 80; 90% of femoral head fractures–FHFs occur in those > 70, US Clinical Pain, loss of height, other deformities and fractures Morbidity Osteoporosis-related fractures occur in 1.5 million/yr–US Risk factors White, elderly, ♀ thin, immobilization, space travel–weightlessness, extreme exercise and/or amenorrhea, alcoholism, endocrinopathies–eg, acromegaly, Cushing's disease, hypogonadism, hyperthyroidism, hyperparathyroidism, smoking Possible risk factors Heredity, inadequate exercise, ↓ Ca2+ intake, exercise, small body frame, levels of serum and urinary Ca2+ and creatinine; Pts receiving physiologic l-thyroxine may have ↓ bone density Diagnosis Bone densitometry, N-telopeptide measurement Treatment 1. Antiresorptive agents–eg, estrogen, calcium, calcitonin, biphosphonates and others eg anabolic steroids, calcitriol; K+ bicarbonate improves Ca2+ and phosphorous balance by ↓ hydroxyproline excretion–a marker of bone resorption, and ↑ osteocalcin–a marker of bone formation 2. Bone stimulation regimens–eg, sodium fluoride, PTH, and growth factors–eg, IGF-I, IGF-II, transforming growth factor-β and 3. Ca2+ supplementation–1000 mg/day, may slow axial and appendicular bone loss in postmenopausal ♀ See Congenital cranial osteoporosis, Malignant osteoporosis.
osteoporosis(os?te-o-po-ro'sis) [ osteo- + -porosis]
Several modifiable factors contribute to bone mass and strength: increased body weight, higher levels of sex hormones, and frequent weight-bearing exercise all build up bone and prevent fractures. Bone loss and the risk of fractures increase with age, immobilization, excess of thyroid hormone, use of corticosteroids and some anticonvulsant drugs, the consumption of alcohol, tobacco, and caffeine, and after menopause. Genetics (a nonmodifiable risk factor) also contributes to osteoporosis. See: table
Bone loss progresses for many years without causing symptoms. When it results in fractures, bone pain and loss of mobility may be disabling. Signs of osteoporosis include deformities of the skeleton, e.g., kyphosis (“dowager’s hump”), and loss of height, esp. if vertebral compression fractures occur.
Supplemental calcium and regular exercise help slow or prevent the rate of bone loss and are recommended for most men and women. Bisphosphonate drugs, e.g., alendronate, calcitonin, sodium fluoride, and other agents are useful for patients of both sexes. In menopausal women, estrogen supplementation or the selective estrogen receptor modulators help prevent bone loss and fractures, but calcium supplementation has not been shown to be helpful.
Protection against osteoporosis should begin in childhood and adolescence and focus on building bone mass. Children should be encouraged to eat foods rich in calcium; parents should be taught to encourage regular exercise, including school gym classes and sports programs, to build strong bones and establish healthy habits. Parents should also be informed about the effects that eating disorders, excessive dieting, excessive exercise, alcohol consumption, and smoking have on bone density. From the mid-20s through age 35, focus continues to be placed on building and maintaining bone mass through a calcium-rich diet. After age 35, bone resorption exceeds bone formation. Emphasis is placed on preventing bone loss through a healthy diet, use of calcium (plus vitamin D) supplements (an intake of at least 1000 mg of calcium per day), and weight-bearing exercises, e.g., weight-lifting, walking, jogging, dancing, and climbing stairs. High-impact aerobics may create too much stress on the bones of older adults and should be avoided.
After patients have been diagnosed with osteoporosis, time should be spent assessing their diets and activity levels. Although patients should engage in walking or other weight-bearing activity for 30 to 60 min three to four times a week, this goal may need to be approached slowly. Foods rich in calcium include dairy products, spinach, sardines, and nuts. Calcium supplements totaling 1000 to 1500 mg per day should be consumed and can prevent further bone loss. Based on bone density testing, alendronate or another drug that inhibits bone resorption may be prescribed in a daily or weekly formulation. Bisphosphonates like alendronate should be taken on an empty stomach with a full glass (8 oz) of water. The patient should remain in an upright position for 30 min after taking these medications to avoid pill-induced esophagitis.
The National Osteoporosis Foundation (NOF) and the World Health Organization (WHO) recommend tests to determine bone mineral density, e.g., dual energy x-ray absroptiometry (DEXA scanning) in patients with specific diseases or conditions. The NOF recommends that all women over 65 and all men over 70 undergo testing. The NOF also recommends bone density testing for anyone over 50 who fractures a bone and for women of menopausal age who have risk factors (see Table "Risk Factors for Osteoporosis").
osteoporosis circumscripta cranii
osteoporosis of disuse
idiopathic juvenile osteoporosisJuvenile osteoporosis.
|White or Asian|
|Thin, small-framed body|
|Positive family history|
|Low calcium intake|
|Early menopause (before age 45)|
|Excessive alcohol or caffeine intake|
|High protein intake|
|High phosphate intake|
|Certain medications, when taken for a long time (e.g., aromatase inhibitors, glucocorticoid, phenytoin, proton pump inhibitors, selective serotonin reuptake inhibitors, thiazolidinediones, thyroid medication)|
|Endocrine diseases (hyperthyroidism, Cushing's disease, acromegaly, hypogonadism, hyperparathyroidism)|
|Diseases such as anorexia nervosa, autoimmune disorders, celiac disease, HIV/AIDS, multiple myeloma, multiple sclerosis, Parkinson disease, sickle cell disease|
osteoporosisA form of bone atrophy involving both the COLLAGEN scaffolding and the mineralization. WHO has defined osteoporosis as bone mineral density that is 2.5 standard deviations or more below the normal mean value for young adults. It is thought to be due to predominance of reabsorption of bone over natural bone formation with resulting loss of architecture and structural strength. It is commonest in women after the menopause and tends to be progressive, giving rise to the high risk of fractures from minimal trauma. Osteoporosis has many causes, the most important being long-term disuse and loss of sex hormones. Other causes include overactivity of the thyroid and parathyroid glands, CUSHING'S SYNDROME, malnutrition and prolonged treatment with corticosteroid drugs. Assessment is by bone densitometry. The progress of osteoporosis can be reduced in women by HORMONE REPLACEMENT THERAPY and by BISPHOSPHONATE drugs and calcium supplements. In some cases fluoride or ANABOLIC STEROIDS are recommended.
osteoporosisa condition in which there is a loss of bony tissue, leading to bones that are brittle and prone to fracture. Osteoporosis is common in the elderly and in women after the MENOPAUSE.
Patient discussion about osteoporosis
Q. Is osteoporosis preventable? My mother had osteoporosis and I already have osteopenia which may lead to it. How can I prevent it??
There are also medications to treat osteoporosis, mainly from the bisphosphanate class. However, remember to consult your doctor before you make any change in your diet or start exercise program.
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Q. My mom have seen her bad days with osteoporosis. My mom have seen her bad days with osteoporosis. I know her pain during winter where she cannot make herself move every morning. I have been seeing her for many years on medications. Looking over my mom`s condition I started to keep myself fit. This will help to control the future chances of osteoporosis for me. I have heard that it runs in families. I do jogging but I was concerned as is this enough?
Q. I am excited to know in what way diet helps in preventing osteoporosis? my mother is suspecting to be having osteoporosis. She regularly complains of leg pain. Upon consultation with the doctor it was found with low calcium in her blood. She was given calcium tablets and was told to increase in the diet rich in calcium. She is taking milk and yoghurt especially. She is not well yet but shows some improvement. I am excited to know in what way diet helps in preventing osteoporosis?