Osteoporosis

Introduction
Background

Osteoporosis is a systemic skeletal disorder characterized by decreased bone mass and deterioration of bony microarchitecture. The result is fragile bones and an increased risk of fractures, even after minimal trauma. Osteoporosis is a chronic condition of multifactorial etiology and is usually clinically silent until a fracture occurs. Osteoporosis is a significant health problem in the United States and around the world.
Pathophysiology

Osteoporosis results from hereditary (primary osteoporosis) and environmental factors (secondary osteoporosis) that affect both bone mass and bone quality. Traditionally, osteoporosis was described as type I (postmenopausal) or type II (senile). Postmenopausal osteoporosis (PMO) is primarily due to estrogen deficiency; senile osteoporosis is primarily due to an aging skeleton and calcium deficiency. However, it is increasingly recognized that multiple pathogenetic mechanisms interact in the development of the osteoporotic state, regardless of age.

Cortical and trabecular (cancellous) bone differ in architecture but are similar in molecular composition. Bone consists of cells and an extracellular matrix with mineralized and nonmineralized components. The composition and architecture of the extracellular matrix is what imparts mechanical properties to bone. Bone strength is determined by collagenous proteins (tensile strength) and mineralized osteoid (compressive strength).1 The greater the concentration of calcium, the greater the compressive strength.

Adult bone undergoes constant remodeling to maintain bone strength. Osteocytes, which are terminally differentiated osteoblasts embedded in mineralized bone, direct the timing and location of remodeling. Osteoblasts not only secrete and mineralize osteoid but also appear to control the bone resorption carried out by osteoclasts; thus, bone formation and resorption are coupled. Osteoclasts require weeks to resorb bone, whereas osteoblasts need months to produce new bone. Therefore, any process that increases the rate of bone remodeling results in net bone loss over time.2 Furthermore, in periods of rapid remodeling (eg, after menopause), bone is at an increased risk for fracture because the newly produced bone is less densely mineralized, the resorption sites are temporarily unfilled, and the isomerization and maturation of collagen is impaired.3

Molecular biologists have begun to elucidate the mechanisms of bone remodeling. For example, it is now understood that the receptor activator of nuclear factor-kappa B ligand (RANKL)/receptor activator of nuclear factor-kappa B (RANK)/osteoprotegerin (OPG) system is the final common pathway for bone resorption. Osteoblasts and activated T cells in the bone marrow produce the RANKL cytokine. RANKL binds to the RANK receptor expressed by osteoclasts and osteoclast precursors to promote osteoclast differentiation. Osteoprotegerin is a soluble decoy receptor that inhibits RANK-RANKL by binding and sequestering RANKL.

Bone mass peaks by the third decade of life and slowly decreases afterward. The failure to attain optimal bone strength by this point is one factor that contributes to osteoporosis. Therefore, nutrition and physical activity are important during growth and development. Nevertheless, hereditary factors play the principal role in determining an individual’s peak bone strength. In fact, genetics account for up to 80% of the variance in peak bone mass between individuals.4
Estrogen deficiency not only accelerates bone loss in postmenopausal women but also plays a role in bone loss in men. Estrogen deficiency can lead to excessive bone resorption accompanied by inadequate bone formation. Osteoblasts, osteocytes, and osteoclasts all express estrogen receptors. In addition, estrogen affects bones indirectly through cytokines and local growth factors. The estrogen-replete state may enhance osteoclast apoptosis via increased production of transforming growth factor (TGF)–beta. In the absence of estrogen, T cells promote osteoclast recruitment, differentiation, and prolonged survival via interleukin [IL]–1, IL-6, and tumor necrosis factor (TNF)–alpha. T cells also inhibit osteoblast differentiation and activity and cause premature apoptosis of osteoblasts through cytokines such as IL-7. Finally, estrogen deficiency sensitizes bone to the effects of parathyroid hormone (PTH).

Calcium, vitamin D, and parathyroid hormone help maintain bone homeostasis. Insufficient dietary calcium or impaired intestinal absorption of calcium due to aging or disease can lead to secondary hyperparathyroidism. Parathyroid hormone is secreted in response to low serum calcium levels. Parathyroid hormone increases calcium resorption from bone, decreases renal calcium excretion, and increases renal production of 1,25-dihydroxyvitamin D (1,25[OH]2 D). It is this active hormonal form of vitamin D that optimizes calcium and phosphorous absorption from the gut, inhibits parathyroid hormone synthesis, and plays a minor role in bone resorption.

Vitamin D deficiency can result in secondary hyperparathyroidism via decreased intestinal calcium absorption. Interestingly, the effects of parathyroid hormone and 1,25[OH]2 D on bone are mediated via binding to osteoblasts and stimulating the RANKL/RANK pathway. Osteoclasts do not have receptors for parathyroid hormone or 1,25[OH]2 D.1

Endocrinologic conditions or medications that lead to bone loss (eg, glucocorticoids) can cause osteoporosis. Corticosteroids inhibit osteoblast function and enhance osteoblast apoptosis.5 Polymorphisms of IL-1, IL-6 and TNF-alpha, as well as their receptors, have been found to influence bone mass. Other factors implicated in the pathogenesis of osteoporosis include polymorphisms in the vitamin D receptor; alterations in insulin-like growth factor-1, bone morphogenic protein, prostaglandin E2, nitrous oxide, and leukotrienes; collagen abnormalities; and leptin-related adrenergic signaling.2

Osteoporotic fractures represent the clinical significance of these derangements in bone. Fractures occur when bones fall under excess stress. Nearly all hip fractures are related to falls.6 The frequency and direction of falls can influence the likelihood and severity of fractures. The risk of falling may be amplified by neuromuscular impairment due to vitamin D deficiency with secondary hyperparathyroidism or corticosteroids. Vertebral bodies are composed primarily of cancellous bone with interconnected horizontal and vertical trabeculae. Osteoporosis not only reduces bone mass in vertebrae but also decreases interconnectivity in their internal scaffolding.1 Therefore, minor loads can lead to vertebral compression fractures.
Frequency
United States

Approximately 10 million people in the United States have osteoporosis. An additional 33.6 million people have low bone density of the hip and are at risk for osteoporosis.7
International

Osteoporosis is estimated to affect over 200 million people worldwide.8 An estimated 75 million people in Europe, the United States, and Japan have osteoporosis.9

One in 3 women older than 50 years will eventually experience osteoporotic fractures, as will 1 in 5 men.10 By 2050, the worldwide incidence of hip fracture is projected to increase by 240% in women and 310% in men.11
Mortality/Morbidity

Osteoporosis is the most common human bone disease. In 2005, over 2 million osteoporosis-related fractures occurred in the United States.12 Hip and vertebral fractures, in particular, are associated with increased morbidity and mortality.

Hip fractures

* Hip fractures increase the one-year risk of death by 10-20%.13,14
* Patients with hip fractures incur decreased independence and a diminished quality of life. Only one third of patients return to their prefracture level of function.15
* Among women who sustain a hip fracture, 50% spend time in a nursing home while recovering. In addition, 1 in 5 patients with hip fractures requires long-term nursing home care.7
* Persons with a hip fracture are twice as likely to experience another fracture as persons without fractures.16

Vertebral fractures

* Vertebral fractures increase the 5-year risk of mortality by 15%.17
* Only one third of people with radiographic vertebral fractures are diagnosed clinically.18
* Symptoms of vertebral fracture may include back pain, height loss, and disabling kyphosis.
* Compression deformities can lead to restrictive lung disease, abdominal pain, and early satiety.
* One in 5 postmenopausal women with a new vertebral fracture incurs another vertebral fracture within one year.19

Race

Whites (especially of northern European descent) and Asian persons are at an increased risk for osteoporosis.
Sex

* Overall, osteoporosis has a female-to-male ratio of 4:1.7
* Eighty percent of hip fractures occur in women.20

Age

* The frequency of postmenopausal osteoporosis is highest in women aged 50-70 years.
* Senile osteoporosis is most common in persons aged 70 years or older.
* Secondary osteoporosis can occur in persons of any age.
* Ninety percent of hip fractures occur in persons aged 50 years or older.20

Clinical
History

Osteoporosis is typically asymptomatic until a fracture occurs. The history should focus on a thorough review of risk factors, which include the following:

* Age, sex, and race
* Family history of osteoporosis, particularly maternal history of fractures
* Reproductive factors, especially regarding early menopause and estrogen replacement therapy
* Lifestyle factors associated with decreased bone density
o Smoking
o Alcohol consumption
o Low levels of physical activity
o Strenuous exercise (such as occurs in marathon runners) that results in amenorrhea
* Calcium and vitamin D intake
* History of low-trauma “fragility" fracture in patients aged 40 years or older (A fragility fracture is defined as a fracture due to trauma that would not normally cause fracture [a force equal to or less than that resulting from a fall from standing height].)
* Signs of vertebral fracture: Vertebral fracture may be asymptomatic. Patients with vertebral fractures may note progressive kyphosis with loss of height. Some may report acute back pain after bending, lifting, or coughing.
o The pain is located in the midthoracic to lower thoracic or upper lumbar spine, where most vertebral fractures occur.
o The pain is described variably as sharp, nagging, or dull; movement may exacerbate pain. In some cases, pain radiates to the abdomen.
o Acute pain usually resolves after 4-6 weeks. In the setting of multiple fractures with severe kyphosis, the pain may become chronic.
* Coexisting medical conditions associated with bone loss (see Causes)
* Medications associated with bone loss (see Causes)
* Risk factors for falls in older patients
o Poor balance
o Orthostatic hypotension
o Weakness of the lower extremity muscles, deconditioning
o Use of medications with sedative effects
o Poor vision or hearing
o Cognitive impairment

Physical

Patients with suspected osteoporosis should undergo a comprehensive medical examination. Areas of concern include the following:

* Low body weight (body mass index <19 kg/m2)
* Signs that might indicate existing osteoporosis
o Kyphosis or dowager hump
o Point tenderness over a vertebrae or other suspected fracture site
* Signs that might indicate a secondary cause of osteoporosis (see Causes)
* Signs in older patients that may indicate increased fall risk
o Difficulty with balance or gait
o Orthostatic hypotension
o Lower-extremity weakness
o Poor vision or hearing
o Cognitive impairment

Causes

Primary causes

* Estrogen deficiency
* Changes associated with aging

Secondary causes - Up to one third of postmenopausal women, as well as many men and premenopausal women, have a coexisting cause of bone loss.21,22
Risk factors for secondary osteoporosis

* Endocrine disorders -Hyperparathyroidism, hypogonadism, hyperthyroidism, diabetes mellitus, Cushing disease, prolactinoma, acromegaly, adrenal insufficiency
* Gastrointestinal/nutritional conditions -Inflammatory bowel disease, celiac disease, malnutrition, history of gastric bypass surgery, chronic liver disease, anorexia nervosa, vitamin D or calcium deficiency
* Renal disease - Chronic kidney disease, idiopathic hypercalciuria
* Rheumatologic diseases -Rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus
* Hematologic disease -Multiple myeloma, thalassemia, leukemia, lymphoma, hemophilia, sickle cell disease, systemic mastocytosis
* Genetic disorders -Cystic fibrosis, osteogenesis imperfecta, homocystinuria, Ehlers-Danlos syndrome, Marfan syndrome, hemochromatosis, hypophosphatasia
* Other - Porphyria, sarcoid, immobilization, pregnancy/lactation, chronic obstructive pulmonary disease (COPD), parenteral nutrition, HIV/AIDS

Medications known to cause or accelerate bone loss

* Corticosteroids - Prednisone (≥5 mg/d for ≥3 mo)23
* Anticonvulsants - Phenytoin, barbiturates, carbamazepine (These agents are associated with treatment-induced vitamin D deficiency.)
* Heparin (long-term)
* Chemotherapeutic/transplant drugs - Cyclosporine, tacrolimus, platinum compounds, cyclophosphamide, ifosfamide, methotrexate
* Hormonal/endocrine therapies - Gonadotropin-releasing hormone (GnRH) agonists, luteinizing hormone-releasing hormone (LHRH) analogs, depomedroxyprogesterone, excessive thyroid supplementation
* Lithium
* Aromatase inhibitors - Exemestane, anastrozole
Differential Diagnoses

Hyperparathyroidism
Multiple Myeloma
Osteomalacia and Renal Osteodystrophy
Paget Disease
Other Problems to Be Considered

Metastases
Leukemia
Lymphoma
Mastocytosis
Pediatric osteogenesis imperfecta
Scurvy
Sickle cell anemia
Homocystinuria
Workup
Laboratory Studies

Laboratory studies are used to establish baseline conditions or to exclude secondary causes of osteoporosis.

* CBC count
* Serum chemistries including calcium, phosphate, creatinine, liver function tests, electrolytes: levels of serum calcium, phosphate, and alkaline phosphatase are usually normal in persons with primary osteoporosis, although alkaline phosphatase levels may be elevated for several months after a fracture.
* Thyroid-stimulating hormone
* 25-hydroxyvitamin D [25(OH)D]

Other laboratory studies used to evaluate for secondary causes include the following:

* Twenty-four-hour urine calcium to assess for hypercalciuria
* Intact parathyroid hormone
* Testosterone level (in males)
* Sedimentation rate
* Urinary free cortisol and tests for adrenal hypersecretion
* Serum and urine protein electrophoresis
* Antigliadin and antiendomysial antibodies for celiac disease
* Serum tryptase, urine N-methylhistamine for mastocytosis
* Bone marrow biopsy if a hematologic disorder is suspected

Markers of bone turnover (both formation and resorption) may be elevated in high–bone-turnover states (eg, early postmenopausal osteoporosis) and may be useful in some patients for monitoring early response to therapy. However, further study is needed to determine their clinical utility in osteoporosis management. Some of these biochemical measures include the following:

* Bone formation markers - Bone-specific alkaline phosphatase, osteocalcin, type I procollagen peptides
* Bone resorption markers - Urinary deoxypyridinoline and cross-linked N- and C-telopeptide of type I collagen

Imaging Studies

Dual-energy x-ray absorptiometry

Dual-energy x-ray absorptiometry (DXA) is the standard study used to establish or confirm a diagnosis of osteoporosis, to predict future fracture risk, and to assess changes in bone mass over time. DXA is used to calculate bone mineral density (BMD) at the hip and spine. Although measurement at any site can be used to assess overall fracture risk, measurement at a particular site is the best predictor of fracture risk at that site. Whenever possible, the same technologist should perform subsequent measurements on the same patient using the same machine. This method can be used in both adults and children. Factors that may result in a falsely high bone density determination include spinal fractures, osteophytosis, and extraspinal (eg, aortic) calcification.

The National Osteoporosis Foundation and the International Society for Clinical Densitometry (ISCD) recommend that BMD be measured in the following patients:

* Women aged 65 years and older and men aged 70 years or older, regardless of clinical risk factors
* Younger postmenopausal women and men aged 50-70 years with clinical risk factors for fracture
* Women in menopausal transition with a specific risk factor associated with increased risk for fracture (ie, low body weight, prior low-trauma fracture, use of a high-risk medication)
* Adults with fragility fractures
* Adults who have a condition (eg, rheumatoid arthritis) or who take a medication (eg, glucocorticoids, ≥5 mg/d for ≥3 mo) associated with low bone mass or bone loss
* Anyone being considered for pharmacologic therapy for osteoporosis
* Anyone being treated for osteoporosis (to monitor treatment effect)
* Anyone not receiving therapy in whom evidence of bone loss would lead to treatment

Bone density data from a DXA are reported as T-scores and Z-scores. T-scores represent the number of standard deviations (SD) from the mean bone density values in healthy young adults, whereas Z-scores represent the number of SD from the normal mean value for age- and sex-matched controls.

* Criteria by the World Health Organization (WHO) define a normal T-score value as within 1 SD of the mean bone density value in a healthy young adult.
o T-score of -1 to -2.5 SD indicates osteopenia.
o T-score of less than -2.5 SD indicates osteoporosis.
o T-score of less than -2.5 SD with fragility fracture(s) indicates severe osteoporosis.
* For each SD reduction in BMD, the relative fracture risk is increased 1.5-3 times.
* The WHO BMD diagnostic classification should not be applied to premenopausal women, men younger than 50 years, or children. Z-scores adjusted for ethnicity or race should be used, with Z-scores of -2.0 or lower defined as "below the expected range for age" and those above -2.0 being "within the expected range for age." The diagnosis of osteoporosis in these groups should not be based on densitometric criteria alone.

WHO fracture risk algorithm24

This algorithm (www.shef.ac.uk/FRAX/) was developed to calculate the 10-year probability of a hip fracture and the 10-year probability of any major osteoporotic fracture (defined as clinical spine, hip, forearm, or humerus fracture) in a given patient. These calculations account for femoral neck BMD and other clinical risk factors, as follows:

* Age
* Sex
* Personal history of fracture
* Low body mass index
* Use of oral glucocorticoid therapy
* Secondary osteoporosis (ie, coexistence of rheumatoid arthritis)
* Parental history of hip fracture
* Current smoking status
* Alcohol intake (3 or more drinks per day)

This algorithm is most useful in identifying patients with osteopenia who are most likely to benefit from treatment. The National Osteoporosis Foundation recommends osteoporosis treatment in patients with a low bone mass in whom a US-adapted WHO 10-year probability of a hip fracture is 3% or more or in whom the risk for a major osteoporosis-related fracture is 20% or more.7

Vertebral fracture assessment

Densitometric spine imaging can be performed at the time of DXA scanning to detect vertebral fractures. Vertebral fracture assessment (VFA) should be considered when the results may influence clinical management of the patient.25

Radiography

Obtain radiographs of the affected area in symptomatic patients. Lateral spine radiography can be performed in asymptomatic patients in whom a vertebral fracture is suspected, in those with height loss in the absence of other symptoms, or in those with pain in the thoracic or upper lumbar spine.

* Radiographs may show fractures or other conditions such as osteoarthritis, disk disease, or spondylolisthesis.
* Plain radiography is not as accurate as BMD testing. Approximately 30-80% of bone mineral must be lost before radiographic lucency becomes apparent on radiographs.26

Additional imaging modalities

* Quantitative CT scanning: This is used to measure BMD as a true volume density in g/cm3, which is not influenced by bone size. This technique can be used in both adults and children but assesses BMD only at the spine. Other limitations include significant radiation exposure, high cost, and possible interference by osteophytes.
* Peripheral DXA: This is used to measure BMD at the wrist. Peripheral DXA may be most useful in identifying patients at very low fracture risk who require no further workup.
* Quantitative ultrasonography of the calcaneus: This is a low-cost portable screening tool. This method does not involve radiation but is not as accurate as other methods and cannot be used to monitor the response to treatment because of its lack of precision.

Procedures

Undecalcified iliac bone biopsy with double tetracycline labeling is rarely necessary but may be considered when no cause for osteoporosis is apparent, therapy is not eliciting a response, or osteomalacia is suspected. Tetracycline double labeling is a process used to calculate data on bone turnover. In this procedure, patients are given tetracycline, which binds to newly formed bone. This appears on biopsy samples as linear fluorescence. A second dose of tetracycline is given 11-14 days after the first dose; this appears on a biopsy sample as a second line of fluorescence. The distance between the two fluorescent labels can be measured to calculate the amount of bone formed during that interval.

Histologic Findings

Histologic examination of osteoporotic bone may reveal generalized thinning of trabeculae and irregular perforation of trabeculae, reflecting unbalanced osteoclast-mediated bone resorption.
Treatment
Medical Care

Osteoporosis is typically asymptomatic until a fracture occurs. Patients identified as at risk for osteoporosis (including children and adolescents) should undergo preventive measures, including adequate calcium intake, vitamin D intake, and exercise. Counsel patients to avoid tobacco use. Identify and treat alcoholism.

Protective measures should be taken in patients who must take glucocorticoids for other medical conditions. These include using the minimum effective dose, discontinuing the drug as soon as possible, and supplementing with calcium and vitamin D.

A meta-analysis was performed to evaluate the efficacy of oral supplemental vitamin D in preventing nonvertebral and hip fractures among older individuals (³ 65 y). The meta-analysis included 12 double-blind, randomized, controlled trials of nonvertebral fractures (n = 42,279) and 8 randomized controlled trials of hip fractures (n = 40,886) and compared oral vitamin D (with or without calcium) with either calcium alone or placebo. The results showed that nonvertebral fracture prevention with vitamin D is dose-dependent, and a higher dose reduced fractures by at least 20% in individuals aged 65 years or older.27

The National Osteoporosis Foundation recommends that pharmacologic therapy should be reserved for postmenopausal women and men aged 50 years or older who present with the following:

* A hip or vertebral fracture (Vertebral fracture may clinical or morphometric [ie, identified on a radiograph alone].)
* Other prior fractures and low bone mass (T-score between -1.0 and -2.5 at the femoral neck, total hip, or spine)
* T-score less than -2.5 at the femoral neck, total hip, or spine after appropriate evaluation to exclude secondary causes
* Low bone mass (T-score between -1.0 and -2.5 at the femoral neck, total hip, or spine) and secondary causes associated with high risk of fracture (eg, glucocorticoid use or total immobilization)
* Low bone mass (T-score between -1.0 and -2.5 at the femoral neck, total hip, or spine) and (1) 10-year probability of hip fracture of 3% or more or (2) a 10-year probability of any major osteoporosis-related fracture of 20% or more based on the US-adapted WHO algorithm24

Surgical Care

The goals of surgical treatment of osteoporotic fractures include rapid mobilization and return to normal function and activities.

* Fixation and stabilization of hip or wrist fracture
* Vertebroplasty to reduce vertebral fracture–associated pain
* Kyphoplasty to restore height or to treat the deformity associated with osteoporotic vertebral fractures

Consultations

* Rheumatologist or endocrinologist to assist with management and determination of underlying etiologies in complex cases
* Orthopedist to assist with fracture management

Diet

Adequate calcium and vitamin D intake are important in persons of any age, particularly in childhood as the bones are maturing. If dietary intake is inadequate, add supplements.

Calcium

* Premenopausal women and men younger than 50 years without risk factors for osteoporosis should receive a total of 1000 mg of calcium daily.
* Postmenopausal women, men older than 50 years, and other persons at risk for osteoporosis should receive a total of 1200-1500 mg of calcium daily.
* See the National Osteoporosis Foundation Web site for further calcium recommendations.

Vitamin D

* Adults younger than 50 years should receive 400-800 IU of vitamin D 3 daily.
* All adults older than 50 years should receive 800-1000 IU of vitamin D 3 daily.
* See the National Osteoporosis Foundation Web site for further vitamin D recommendations.

Activity

* Weight-bearing exercise has been shown to positively affect BMD. Regular exercise should be encouraged in all patients, including children and adolescents (in order to strengthen the skeleton during the maturation process). Exercise also improves agility and balance, thereby reducing the risk of falls.
* Physical therapists can assist in developing exercise regimens and instructing patients in proper techniques.

Medication

Antiresorptive agents, including bisphosphonates (both oral and intravenous), the selective estrogen-receptor modulator (SERM) raloxifene, calcitonin, and the anabolic agent teriparatide, are currently used for osteoporosis treatment. The efficacy of these drugs in preventing fracture has not been directly compared in randomized controlled trials. A combination of calcium and vitamin D supplementation, which has been shown to reduce fracture risk, should also be used.28 The American College of Physicians recently reviewed the evidence and proposed guidelines for these pharmacologic treatments.29

Hormone replacement therapy (HRT) was once considered a first-line therapy for the prevention and treatment of osteoporosis in women. Data from the Women's Health Initiative confirmed that HRT can reduce fractures. However, HRT was associated with an increased risk of breast cancer, myocardial infarction, stroke, and venous thromboembolic events.30 HRT is approved for management of menopausal symptoms and prevention of osteoporosis. It is no longer recommended as a treatment of osteoporosis in postmenopausal women.

Experimental evidence indicates that strontium ranelate (available in Europe) reduces the risk of fracture. Stronitium is not approved for the treatment of osteoporosis in the United States. Denosumab, a humanized monoclonal antibody directed against RANKL, is currently being studied as a potential treatment for postmenopausal osteoporosis. Additional SERMs and other antiresorptives and anabolic agents are being studied.
Bisphosphonate Derivative

Bisphosphonates are stable analogues of inorganic pyrophosphate. Bisphosphonates have a high affinity for hydroxyapatite crystals, and by binding at sites of active bone resorption, these agents can inhibit osteoclastic resorption. All oral bisphosphonates have a poor absorption and a bioavailability of less than 5%. Bone uptake is 20-80%, with the remainder being rapidly excreted through the kidney.31 Bisphosphonates are approved in the United States for the prevention and treatment of postmenopausal osteoporosis, osteoporosis in males, and steroid-induced osteoporosis.
Follow-up
Further Outpatient Care

DXA should be repeated every 2-3 years if the baseline test results are normal. DXA should be performed every 1-2 years in patients who are undergoing osteoporosis treatment.

Deterrence/Prevention

Primary prevention of osteoporosis starts in childhood. Patients require adequate calcium intake, vitamin D intake, and weight-bearing exercise. Patients should be counseled on smoking cessation and moderated alcohol intake. Patients who have disorders or who take medications that can cause or accelerate bone loss should receive calcium and vitamin D supplementation (see Causes).

Complications

The most serious consequences of osteoporosis include fractures and, in some patients, death due to postfracture complications.

Respiratory compromise can occur in patients with multiple vertebral fractures that result in severe kyphosis.
Prognosis

If full recovery is not achieved, osteoporotic fractures may lead to chronic pain, disability, and, in some cases, death.

Patient Education

* Educate patients about osteoporosis and encourage them to follow preventive measures, including adequate calcium and vitamin D intake, exercise, cessation of smoking, and moderation of alcohol consumption.
* For excellent patient education resources, visit eMedicine's Bone Health Center; Eating Disorders Center; Esophagus, Stomach, and Intestine Center; and Women's Health Center.
* Also, see eMedicine's patient education articles Understanding Osteoporosis Medications, Anorexia Nervosa, Inflammatory Bowel Disease, Menopause, and Hormone Replacement and Osteoporosis.

Miscellaneous
Medicolegal Pitfalls

Osteoporosis is a preventable disease with potentially devastating consequences. Failure to identify at-risk patients, to educate them, and to implement preventive measures may lead to tragic consequences.
Special Concerns

* Recognize the increased mortality and morbidity associated with osteoporotic fractures.
* Many patients have a coexisting cause of bone loss. This should be investigated and treated.
* WHO criteria for T-scores should not be applied to premenopausal women, men younger than 50 years old, and children. Z-scores should be used for these individuals, and, in these cases, a diagnosis of osteoporosis should not be based on densitometric criteria alone.