Osteoporosis Workup

  • Author: Dana Jacobs-Kosmin, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Apr 19, 2012
 

Approach Considerations

Workup consists of appropriate laboratory studies to establish baseline values and to look for potential secondary causes of osteoporosis, along with measurement of bone mineral density (BMD) to assess bone loss and estimate the risk of fracture. Bone biopsy may be indicated in specific situations.

Imaging options include densitometry, single-photon absorptiometry (SPA), dual-photon absorptiometry (DPA), dual-energy x-ray absorptiometry (DXA), quantitative computed tomography (QCT) scanning, magnetic resonance imaging (MRI), bone scanning, and single-photon emission computed tomography (SPECT) scanning. The sensitivity, examination time, cost, and radiation exposure of the different imaging techniques differ greatly (see Table 5, below).

Table 5. Comparison of Densitometry Techniques and Cost-Effectiveness (Open Table in a new window)

Single-photon absorptiometry Dual-photon absorptiometry Dual-energy x-ray absorptiometry Quantitative computed tomography
Time5-15 min20-30 min5-10 min10-30 min
Cost$50-150$150-300$100-200$150-300
Sites scannedRadius, forearm,



calcaneus



Spine, hip (anteroposterior)Spine (lateral), hip,



radius



Spine (lateral), hip,



radius



Source:  Nayak S, Roberts MS, Greenspan SL. Cost-effectiveness of different screening strategies for osteoporosis in postmenopausal women. Ann Intern Med. Dec 6 2011;155(11):751-61.[68]

DXA of the hip and lumbar spine and quantitative calcaneal ultrasonography are the 2 most common bone measurement tests used to screen for osteoporosis[66] ; DXA quantifies bone loss, and quantitative calcaneal ultrasonography evaluates bone properties.[69] Conventional radiography is used for the qualitative and semiquantitative evaluation of osteoporosis, whereas morphometry assesses the presence of fractures.[69]

In the United States, current diagnostic and treatment criteria for osteoporosis are based solely on DXA measurements, despite quantitative calcaneal ultrasonography being as effective as DXA at predicting femoral neck, hip, and spine fractures—with lower cost, more portability, and no exposure to ionizing radiation.[66] No criteria based on quantitative ultrasonography or a combination of quantitative ultrasonography and DXA have been defined.

For information on The American College of Radiology recommendations for evaluating the appropriateness of BMD measurement tests for osteoporosis in patients at risk of developing this condition, see ACR Appropriateness Criteria for osteoporosis and bone mineral density.

Children and adolescents

The official position of the International Society for Clinical Densitometry (ISCD) is that “fracture prediction should primarily identify children at risk of clinically significant fractures” (eg, fracture of lower-extremity long bones, vertebral compression fractures, or 2 or more upper-extremity long-bone fractures).[70] However, densitometric criteria alone should not be used to diagnose osteoporosis in children and adolescents. Rather, such a diagnosis in this population must be based on a low bone mineral content (BMC) or BMD in conjunction with a clinically significant fracture history. Fractures are considered clinically significant[70] if one or more of the following are present:

  • Lower-extremity long-bone fracture
  • Vertebral compression fracture
  • 2 or more upper-extremity long-bone fractures
  • Low BMC or BMD, defined as a BMC or areal BMD Z-score that is ≤ –2.0, adjusted for age, sex, and body size, as appropriate
Next

Laboratory Studies

Laboratory studies are used to establish baseline conditions or to exclude secondary causes of osteoporosis. They are summarized in Tables 6 and 7, below.

Table 6. Baseline Studies for Baseline Conditions in Osteoporosis (Open Table in a new window)

Baseline test Disorder
Complete blood count (CBC)CBC results may reveal anemia, as in sickle cell disease (patients with anemia, particularly those older than 60 years, should also be evaluated for multiple myeloma), and may raise the suspicion for alcohol abuse (in conjunction with results from serum chemistry tests and liver function tests)
Serum chemistry levelsCalcium levels can reflect underlying disease states (eg, severe hypercalcemia may reflect underlying malignancy or hyperparathyroidism; hypocalcemia can contribute to osteoporosis)



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



levels of serum calcium, phosphate, alkaline phosphatase, and 25(OH) vitamin D may be obtained to assess osteomalacia



Creatinine levels may decrease with increasing parathyroid hormone (PTH) levels or may be elevated in patients with multiple myeloma



Creatinine levels are also used to estimate creatinine clearance, which may indicate reduced renal function in elderly patients



Magnesium is very important in calcium homeostasis[71] ; decreased levels of magnesium may affect calcium absorption and metabolism



Serum iron and ferritin levelsThese tests are helpful when malabsorption or hemochromatosis are suspected
Liver function testsIncreased levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), bilirubin, and alkaline phosphatase may indicate alcohol abuse
Thyroid-stimulating hormone (TSH) levelThyroid dysfunction has been associated with osteoporosis and should therefore be ruled out[72]
25-Hydroxyvitamin D levelThis test assesses for vitamin D insufficiency; inadequate vitamin D levels can predispose persons to osteoporosis

An important study by Tannenbaum evaluated 173 healthy women (ages 46-87 years) for secondary causes of osteoporosis and found that 55 (32%) had a previously undiagnosed disorder of bone or mineral metabolism.[73] Given that occult disorders are so common in patients with osteoporosis, minimal laboratory screening is indicated in all patients who present with decreased bone mass.

Table 7. Tests for Secondary Causes of Osteoporosis (Open Table in a new window)

Tests for Secondary Causes of Osteoporosis Disorder
24-Hour urine calcium levelThis study assesses for hypercalciuria to help rule out benign familial hypocalciuric hypercalcemia (FHH), in which urinary calcium levels are low
Parathyroid hormone (PTH) levelAn intact PTH result is essential in ruling out hyperparathyroidism; an elevated PTH level may be present in benign FHH
Thyrotropin level (if on thyroid replacement)Experts are divided on whether to include thyrotropin testing, regardless of a history of thyroid disease or replacement; however, one study showed reduced femoral neck bone mineral density (BMD) in women with subclinical hypothyroidism and hyperthyroidism[72]
Testosterone and gonadotropin levels in younger men with low bone densitiesThese tests may help evaluate a sex hormone deficiency as a secondary cause of osteoporosis
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levelsSome practitioners include ESR and CRP values in the workup, although their utility in this setting has not been proven in an evidence-based manner
Urinary free cortisol level and tests for adrenal hypersecretionThese tests are used to exclude Cushing syndrome, which, although uncommon, can lead to rapidly progressive osteoporosis when the condition is present; a urine free cortisol value or overnight dexamethasone suppression test should be ordered in suspected cases
Serum protein electrophoresis (SPEP) and urine protein electrophoresis (UPEP)These are used to identify multiple myeloma
Antigliadin and antiendomysial antibodiesThese tests can help identify celiac disease
Serum tryptase and urine N-methylhistamineThese tests help identify mastocytosis and are used to exclude the presence of multiple myeloma; serum tryptase may be performed to rule out plasma cell dyscrasias
Bone marrow biopsyThis study is obtained when a hematologic disorder is suspected
Previous
Next

Biochemical Markers of Bone Turnover

Biochemical markers of bone turnover reflect bone formation or bone resorption. These markers (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.

Currently available serum markers of bone formation (osteoblast products) include the following:

  • Bone-specific alkaline phosphatase (BSAP)
  • Osteocalcin (OC)
  • Carboxyterminal propeptide of type I collagen (PICP)
  • Aminoterminal propeptide of type I collagen (PINP)

Currently available urinary markers of bone resorption (osteoclast products) include the following:

  • Hydroxyproline
  • Free and total pyridinolines (Pyd)
  • Free and total deoxypyridinolines (Dpd)
  • N-telopeptide of collagen cross-links (NTx) (also available as a serum marker)
  • C-telopeptide of collagen cross-links (CTx) (also available as a serum marker)

Currently available serum markers of bone resorption include cross-linked C-telopeptide of type I collagen (ICTP) and tartrate-resistant acid phosphatase, as well as NTx and CTx. Of all the biochemical markers of bone turnover mentioned above, the ones most commonly used in clinical practice are BSAP, OC, urinary NTx, and serum CTx.

BSAP can be mildly elevated in patients with fractures. In addition, patients with hyperparathyroidism, Paget disease, or osteomalacia can have elevations of BSAP. Serum OC levels, if high, indicate a high-turnover type of osteoporosis.[74] Elevation of urinary NTx (>40 nmol bone collagen equivalent per mmol urinary creatine) indicates a high turnover state. NTx levels may also be used to monitor responses to anti-osteoporotic treatments.

Significant controversy exists regarding the use of these biochemical markers, and concerns have been raised about intra-assay and interassay variability. At the primary author's institution, a urine NTx value normalized to creatinine excretion from the second urination of the day is used primarily to identify osteopenic patients in a high-turnover state who would benefit from therapy and to monitor the response to therapy in all patients. However, further study is needed to determine the clinical utility of these markers in osteoporosis management.

For more information, see the Medscape Reference article Bone Markers in Osteoporosis.

Previous
Next

Plain Radiography

Plain radiography is recommended to assess overall skeletal integrity. In particular, in the workup for osteoporosis, plain radiography may be indicated if a fracture is already suspected or if patients have lost more than 1.5 inches of height (see the following image).

Asymmetric loss in vertebral body height, without Asymmetric loss in vertebral body height, without evidence of an acute fracture, can develop in patients with osteoporosis. These patients become progressively kyphotic (as shown) over time, and the characteristic hunched-over posture of severe osteoporosis develops eventually.

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 (see the following images). A scoliosis series is useful for detecting occult vertebral fractures.

Severe osteoporosis. This radiograph shows multiplSevere osteoporosis. This radiograph shows multiple vertebral crush fractures. Source: Government of Western Australia Department of Health. http://www.imagingpathways.health.wa.gov.au/includes/dipmenu/osteo/image.html. This radiograph of the spine shows a lateral wedgeThis radiograph of the spine shows a lateral wedge fracture of L3 (yellow asterisk) and compression fracture of L5 (red asterisk) in an osteoporotic patient who suffered a recent fall. More detailed imaging, usually with computed tomography (CT) scanning, is often needed to better evaluate compression fractures and to determine the urgency of surgical interventions.

Radiographic findings can suggest the presence of osteopenia, or bone loss, although they cannot be used to diagnose osteoporosis. Using the second metacarpal or the metaphysis of a long bone, the cortical width should be at least equal to the medullary width. Osteopenia is suggested by a cortical width that is less than the medullary width. Radiographs may also show fractures or other conditions, such as osteoarthritis, disk disease, or spondylolisthesis.

Plain radiography is not as accurate as BMD testing. Because osteoporosis predominantly affects trabecular bone rather than cortical bone, radiography does not reveal osteoporotic changes until they affect the cortical bone. Cortical bone is not affected by osteoporosis until more than 30% of bone loss has occurred. Approximately 30-80% of bone mineral must be lost before radiographic lucency becomes apparent on radiographs.[75] Thus, plain radiography is an insensitive tool for diagnosing osteoporosis.

Previous
Next

Dual-Energy X-Ray Absorptiometry (DXA)

Several large prospective studies have shown that BMD measurements of the distal and proximal femur and the vertebral bodies can predict the development of the major types of osteoporotic fractures. BMD has been shown to be the best indicator of fracture risk. According to the National Osteoporosis Foundation (NOF), evaluating BMD on a periodic basis is the best way to monitor bone mass and future fracture risk.[35, 76]

DXA is currently the criterion standard for the evaluation of BMD.[76, 70] Compared with other screening tools (eg, calcaneal quantitative ultrasonography, the Simple Calculated Osteoporosis Risk Estimation [SCORE]), DXA has been found to be efficacious and cost-effective.[77] DXA is not as sensitive as quantitative computed tomography (QCT) scanning for detecting early trabecular bone loss, but it provides rapid scanning times, lower costs, and greater precision. It is done on an outpatient basis,[35] and there are no special requirements (eg, dye injection) for performing it. Also, radiation exposure is kept to a minimum.

DXA is used to calculate BMD at the lumbar spine, hip, and proximal femur (see the images below). Densitometric spine imaging can be performed at the time of DXA scanning to detect vertebral fractures. Vertebral fracture assessment (VFA) is not available with all DXA machines. When available, VFA should be considered when the results may influence clinical management of the patient.[78] Peripheral DXA is used to measure BMD at the wrist; it may be most useful in identifying patients at very low fracture risk who require no further workup.

Example of a dual energy x-ray absorption (DXA) scExample of a dual energy x-ray absorption (DXA) scan. This image is of the left hip bone. Source: Government of Western Australia Department of Health. http://www.imagingpathways.health.wa.gov.au/includes/dipmenu/osteo/image.html. Example of a dual energy x-ray absorption (DXA) scExample of a dual energy x-ray absorption (DXA) scan. This image is of the lumbar spine. Source: Government of Western Australia Department of Health. http://www.imagingpathways.health.wa.gov.au/includes/dipmenu/osteo/image.html.

Although measurement of BMD 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 BMD determination include spinal fractures, osteophytosis, and extraspinal (eg, aortic) calcification.

Bone density data from a DXA are reported as T-scores and Z-scores. The T-score is the value compared to that of control subjects who are at their peak BMD, whereas the Z-score reflects a value compared to that of patients matched for age and sex.[4, 5, 6, 7]

NOF, ISCD, and USPSTF recommendations

The NOF and the International Society for Clinical Densitometry (ISCD) recommend that BMD be measured in the following patients[35, 70] :

  • Women aged 65 years or 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 associated with low bone mass or bone loss (eg, rheumatoid arthritis)
  • Adults who take a medication associated with low bone mass or bone loss (eg, glucocorticoids, ≥5 mg of prednisone daily for ≥3 mo)
  • 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

The US Preventive Services Task Force (USPSTF) has issued updated recommendations on screening for osteoporosis.[66] The USPSTF recommends measuring BMD in the following patients:

  • Women aged 65 years and older without previous known fractures or secondary causes of osteoporosis
  • Women younger than 65 years whose 10-year fracture risk is equal to or greater than that of a 65-year-old white woman without additional risk factors

These recommendations do not contradict the NOF recommendations for screening in women. However, in contradiction to the NOF recommendation, the USPSTF makes no recommendation for screening men without risk factors. For men without previous known fractures or secondary causes of osteoporosis, current evidence is insufficient to assess the balance of benefits and harms of screening.

WHO T-score and Z-score criteria

World Health Organization (WHO) criteria define a normal T-score value as within 1 standard deviation (SD) of the mean BMD value in a healthy young adult. Values lying farther from the mean are stratified as follows[6] :

  • T-score of –1 to –2.5 SD indicates osteopenia
  • T-score of less than –2.5 SD indicates osteoporosis
  • 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. Of note, about half of osteoporotic fractures occur in women with a T-score greater than –2.5, and the other half occur in those with a T-score lower than –2.5, the WHO’s cutoff for DXA-based diagnosis of osteoporosis.

This diagnostic classification should not be applied to premenopausal women, men younger than 50 years, or children. Instead, Z-scores adjusted for ethnicity or race should be used, with values of –2.0 SD or lower defined as "below the expected range for age" and those above –2.0 SD being "within the expected range for age." The diagnosis of osteoporosis in these groups should not be based on densitometric criteria alone.

International Society of Clinical Densitometry (ISCD) positions

The following are the official positions of the ISCD on peripheral DXA (pDXA)[70] :

  • pDXA can be used in postmenopausal women for fracture risk assessment (vertebral and global fragility fracture risk), although its vertebral fracture predictive ability is weaker than central DXA and heel quantitative ultrasonography (QUS); evidence for use in men is insufficient
  • The World Health Organization (WHO) diagnostic classification can be applied only to the one-third (33%) radius region of interest measured by pDXA devices utilizing a validated young-adult reference database
  • pDXA devices should be independently validated for fracture risk prediction by prospective trials or by demonstration of equivalence to a clinically validated device
  • Bone density measurements from different pDXA devices cannot be directly compared
  • If central DXA cannot be done, radius pDXA measurements can be used to identify patients in whom pharmacologic treatment should be initiated; the fracture probability, based on both devise-specific thresholds and clinical risk factors, should be high in those patients
  • Radius pDXA plus clinical risk factors can also be used to identify patients at very low fracture probability in which no further diagnostic testing is necessary
  • pDXA cannot be used to monitor the effects of osteoporosis treatments
Previous
Next

Single- and Dual-Photon Absorptiometry

Single-photon absorptiomentry (SPA) of the proximal forearm provides precision and offers low radiation exposure, but it is relatively insensitive for detecting early-stage osteoporosis because it measures cortical rather than trabecular bone. Dual-photon absorptiomentry (DPA) can measure bone mineral density (BMD) in the spine and proximal femur, but its use is limited by poor reproducibility, prolonged scanning times, and artifacts caused by vascular calcifications.

Previous
Next

Computed Tomography

Quantitative CT scanning

Quantitative computed tomography (QCT) scanning is another method employed to measure spinal bone mineral density (BMD). It measures 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. QCT scanning of the spine is the most sensitive method for diagnosing osteoporosis, because it measures trabecular bone within the vertebral body.

QCT scanning may be useful in identifying fractures. It can be used to identify not only the fracture line but also areas of callus formation and sclerosis, consistent with healing fracture. It may also be used for evaluation of metastatic bone disease.

Compared with DXA scanning, QCT is more expensive, has relatively poor reproducibility, and requires a higher radiation dose. In addition, it is subject to possible interference by osteophytes. It is not an ideal technique when repeated measurements are needed to detect small changes in BMD. Consequently, QCT scanning is seldom used now.

International Society of Clinical Densitometry positions

The following are the official positions of the International Society of Clinical Densitometry (ISCD) on QCT of the lumbar spine[70] :

  • QCT of the spine can be used to predict vertebral fractures in postmenopausal women; but there is insufficient evidence to recommend spine QCT for spinal fracture prediction in men or hip fracture prediction in both women and men
  • Because T-scores by QCT are not equivalent to T-scores based on DXA, the World Health Organization (WHO) diagnostic classification of osteoporosis cannot be used
  • If central DXA measurements cannot be obtained, QCT of the spine along with consideration of clinical risk factors can be used to identify patients appropriate for pharmacologic treatment
  • QCT of the spine can be used to monitor age-, disease- and treatment-related BMD changes via trabecular BMD of the lumbar spine

The following are the official positions of the ISCD on peripheral QCT (pQCT) of the radius[70] :

  • pQCT of the forearm at the ultra-distal radius cannot be used for fracture risk assessment of the spine, but it does predict hip fragility fractures in postmenopausal women
  • There is insufficient evidence to recommend pQCT for fracture risk prediction in men
  • As with QCT of the spine, pQCT of the radius cannot be used to diagnose osteoporosis based on the WHO diagnostic classification
  • As with QCT of the spine, pQCT of the radius along with clinical risk factors can be used to initiate pharmacologic treatment if central DXA cannot be obtained
  • pQCT measurements of the trabecular and total BMD of the ultra-distal radius can be used to monitor age-related BMD changes

Single-photon emission CT scanning

Single-photon emission computed tomography (SPECT) scanning represents a tomographic (CT-like) bone imaging technique that offers better image contrast and more accurate lesion localization than planar bone scanning. It increases the sensitivity and specificity of bone scanning for detection of lumbar spine lesions by 20-50% over planar techniques.

SPECT scanning is helpful when accurate localization of skeletal lesions within large and/or anatomically complex bony structures is required. This localization is possible because SPECT can visualize bony structures that would overlap on planar images (eg, separating vertebral body, facet and pars interarticularis lesions).

Previous
Next

Ultrasonography

Quantitative ultrasonography (QUS) of the calcaneus is a low-cost portable screening tool. It has the advantage of not involving radiation, but it is not as accurate as other imaging methods. Ultrasonography cannot be used for monitoring skeletal changes over time, nor can it be used to monitor the response to treatment, because of its lack of precision.

International Society of Clinical Densitometry positions

The following are the official positions of the ISCD on QUS:

  • Bone density measurements from QUS devices should be independently validated; measurements by different devices cannot be directly compared
  • The heel is the only validated skeletal site for the clinical use of QUS in osteoporosis management
  • Validated calcaneal QUS devices can be used in postmenopausal women to predict hip, vertebral, and global fracture risk and in men older than 65 years to predict hip and all nonvertebral fractures
  • The World Health Organization (WHO) diagnostic classification cannot be applied to T-scores from QUS measurements
  • If central DXA cannot be obtained, calcaneal QUS in combination with clinical risk factors can be used to identify patients in whom pharmacologic treatment should be initiated
  • Calcaneal QUS plus clinical risk factors can also be used to identify patients at very low fracture probability in whom no further diagnostic testing is necessary
  • QUS cannot be used to monitor the skeletal effects of treatments for osteoporosis
Previous
Next

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) may be useful in identifying fractures and in the assessment of metabolic bone disease. Using fat suppression sequences, marrow edema consistent with fracture may be noted as areas of hypointensity on T1-weighted images in association with corresponding areas of hyperintensity on T2-weighted images. MRI is a very sensitive modality and is believed by some to be the diagnostic imaging method of choice in the detection of acute fractures, such as sacral fractures.

MRI can be used to discriminate between acute and chronic fractures of the vertebrae and occult stress fractures of the proximal femur. These osteoporotic fractures demonstrate characteristic changes in the bone marrow that distinguish them from other uninvolved parts of the skeleton and the adjacent vertebrae.

Previous
Next

Bone Scanning

Bone scanning assesses the function and tissue metabolism of organs by using a radionuclide (technetium-99m [99m Tc]) that emits radiation in proportion to its attachment to a target structure. This technique detects an increase in osteoblastic activity (as seen in compression fractures).

Images may be obtained in 3 phases of the bone scanning process (immediate-flow study, immediate static blood pool study, and delayed static study). Acute fractures are visible in all phases of bone scanning and may remain beyond the reference range for up to 2 years.

Previous
Next

Biopsy and Histologic Features

Bone biopsy can help to exclude underlying pathologic conditions such as multiple myeloma, which may be responsible for presumed osteoporotic fracture. Typically, iliac crest biopsy is performed either in the minor procedure suite or in the operating room.

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 2 fluorescent labels can be measured to calculate the amount of bone formed during that interval, which may potentially indicate that too little bone formation or too much bone resorption is the cause of osteoporosis in a patient. Tetracycline labeling may also help clinicians to test potential therapy (ie, did the treatment slow bone resorption, increase bone formation, or both?) and study other metabolic bone responses.

One may also perform a vertebral body bone biopsy when performing a therapeutic procedure such as kyphoplasty (see the images below) or vertebroplasty for fixation of a vertebral compression fracture.

In kyphoplasty, a KyphX inflatable bone tamp is peIn kyphoplasty, a KyphX inflatable bone tamp is percutaneously advanced into the collapsed vertebral body (A). It is then inflated, (B) elevating the depressed endplate, creating a central cavity, and compacting the remaining trabeculae to the periphery. Once the balloon tamp is deflated and withdrawn, the cavity (C) is filled under low pressure with a viscous preparation of methylmethacrylate (D). Osteoporosis. Lateral radiograph demonstrates multOsteoporosis. Lateral radiograph demonstrates multiple osteoporotic vertebral compression fractures. Kyphoplasty has been performed at one level. Osteoporosis. Lateral radiograph of the patient seOsteoporosis. Lateral radiograph of the patient seen in the previous image following kyphoplasty performed at 3 additional levels. Percutaneous vertebroplasty, transpedicular approaPercutaneous vertebroplasty, transpedicular approach.

Histologic examination of osteoporotic bone may reveal generalized thinning of trabeculae and irregular perforation of trabeculae, reflecting unbalanced osteoclast-mediated bone resorption.[41] The following are histologic specimens from patients with osteoporosis.

Osteoporosis is defined as a loss of bone mass belOsteoporosis is defined as a loss of bone mass below the threshold of fracture. This slide (methylmethacrylate embedded and stained with Masson's trichrome) demonstrates the loss of connected trabecular bone. The bone loss of osteoporosis can be severe enoughThe bone loss of osteoporosis can be severe enough to create separate bone "buttons" with no connection to the surrounding bone. This easily leads to insufficiency fractures. Inactive osteoporosis is the most common form and Inactive osteoporosis is the most common form and manifests itself without active osteoid formation. Osteoporosis that is active contains osteoid seamsOsteoporosis that is active contains osteoid seams (red here in the Masson's trichrome). Woven bone arising directly from surrounding mesenWoven bone arising directly from surrounding mesenchymal tissue. This image depicts bone remodeling with osteoclastThis image depicts bone remodeling with osteoclasts resorbing one side of a bony trabecula and osteoblasts depositing new bone on the other side. Osteoclast, with bone below it. This image shows tOsteoclast, with bone below it. This image shows typical distinguishing characteristics of an osteoclast: a large cell with multiple nuclei and a "foamy" cytosol. In this image, several osteoblasts display a promiIn this image, several osteoblasts display a prominent Golgi apparatus and are actively synthesizing osteoid. Two osteocytes can also be seen.
Previous
Proceed to Treatment & Management
 
 
Contributor Information and Disclosures
Author

Dana Jacobs-Kosmin, MD  Attending Physician, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center; Clinical Assistant Professor of Medicine, Jefferson Medical College

Dana Jacobs-Kosmin, MD is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Nothing to disclose.

Coauthor(s)

Sucharitha Shanmugam, MD  Consulting Physician, PMA Medical Specialists, Limerick, PA

Sucharitha Shanmugam, MD is a member of the following medical societies: American College of Rheumatology

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Additional Contributors

Michael T Andary, MD, MS Professor, Residency Program Director, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine

Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists

Disclosure: Allergan Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching

Harris Gellman, MD Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine

Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, and Arkansas Medical Society

Disclosure: Nothing to disclose.

Elliot Goldberg, MD Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology

Disclosure: Nothing to disclose.

Coburn Hobar, MD Clinician in Rheumatology, Hobar Health and Wellness, and Anti-Aging & Wellness Center of Sarasota

Coburn Hobar, MD is a member of the following medical societies: American Academy of Anti-Aging Medicine and American College of Rheumatology

Disclosure: Nothing to disclose.

Robert J Kaplan, MD James E Van Zandt VA Medical Center, Staff Physician, Department of Rehabilitation Medicine

Robert J Kaplan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Joseph M Lane, MD  Professor of Orthopedic Surgery, Weill Medical College of Cornell University; Chief, Metabolic Bone Disease Service, Hospital for Special Surgery

Joseph M Lane, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of University Professors, American Federation for Aging Research, American Orthopaedic Association, American Society for Bone and Mineral Research, Association of Bone and Joint Surgeons, Medical Society of the State of New York, Musculoskeletal Tumor Society, National Osteoporosis Foundation, North American Spine Society, and Orthopaedic Research Society

Disclosure: Lilly; Aventis; Novartis; Warner Chilcott; Biomimetics; Zimmer; DFine; Innovative Solutions; Honoraria Speaking and teaching; Graftys; Bone Technologies SA; CollPlant Consulting fee Consulting

David Lenrow, MD Vice Chair of Clinical Services, Medical Director, Erdman Clinic; Associate Professor, Department of Rehabilitation Medicine, University of Pennsylvania at Philadelphia

David Lenrow, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Medical Assocation

Disclosure: Nothing to disclose.

Julie Lin, MD Assistant Professor, Department of Rehabilitation Medicine, Weill Medical College of Cornell University; Assistant Attending Physiatrist, Physiatry Department, Hospital for Special Surgery

Julie Lin, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Disclosure: Nothing to disclose.

Elizabeth A Moberg-Wolff, MD Associate Professor, Department of Physical Medicine and Rehabilitation, Children's Hospital of Wisconsin, Medical College of Wisconsin

Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation

Disclosure: Medtronic Neurological Grant/research funds Speaking and teaching

Srinivas R Nalamachu, MD Clinical Assistant Professor, Department of Internal Medicine, Kansas City University of Medicine and Biosciences; President and Medical Director, Internation Clinical Research Institute, Inc; Medical Director, Pain Management Institute

Srinivas R Nalamachu, MD is a member of the following medical societies: International Association for the Study of Pain

Disclosure: Nothing to disclose.

Richard Salcido, MD Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine

Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society

Disclosure: Nothing to disclose.

Miguel A Schmitz, MD Consulting Surgeon, Department of Orthopedics, Klamath Orthopedic and Sports Medicine Clinic

Miguel A Schmitz, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, Arthroscopy Association of North America, and North American Spine Society

Disclosure: Nothing to disclose.

Alana C Serota, MD Fellow in Metabolic Bone Disease and Osteoporosis, Department of Orthopedics, Hospital for Special Surgery

Alana C Serota, MD is a member of the following medical societies: American Academy of Family Physicians

Disclosure: Nothing to disclose.

Curtis W Slipman, MD Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center

Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, and North American Spine Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Shireesha Vuppalanchi, MD Consulting Staff, Methodist Hospital, Indianapolis; Hospitalist, Respiratory and Critical Care Consultants, PC

Disclosure: Nothing to disclose.

William S Whyte II, MD Director of Interventional Spine and Pain Management, Louisiana Pain Physicians

William S Whyte II, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Medical Association, Association of Academic Physiatrists, North American Spine Society, Physiatric Association of Spine, Sports and Occupational Rehabilitation, and Southern Medical Association

Disclosure: Nothing to disclose.

Jerome D Wiedel, MD Chair, Professor, Department of Orthopedics, University of Colorado Health Sciences Center

Disclosure: Nothing to disclose.

References

  1. Ahmed SF, Elmantaser M. Secondary osteoporosis. Endocr Dev. 2009;16:170-90. [Medline].

  2. [Best Evidence] Majumdar SR, Lier DA, Beaupre LA, Hanley DA, Maksymowych WP, Juby AG, et al. Osteoporosis case manager for patients with hip fractures: results of a cost-effectiveness analysis conducted alongside a randomized trial. Arch Intern Med. Jan 12 2009;169(1):25-31. [Medline].

  3. National Osteoporosis Foundation. Gallup survey: women's knowledge of osteoporosis. Am Fam Physician. 1991;44:1052.

  4. Kanis JA, McCloskey EV, Johansson H, Oden A, Melton LJ 3rd, Khaltaev N. A reference standard for the description of osteoporosis. Bone. Mar 2008;42(3):467-75. [Medline].

  5. Silverman SL. Selecting patients for osteoporosis therapy. Ann N Y Acad Sci. Nov 2007;1117:264-72. [Medline].

  6. Czerwinski E, Badurski JE, Marcinowska-Suchowierska E, Osieleniec J. Current understanding of osteoporosis according to the position of the World Health Organization (WHO) and International Osteoporosis Foundation. Ortop Traumatol Rehabil. Jul-Aug 2007;9(4):337-56. [Medline].

  7. Kanis JA. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis: synopsis of a WHO report. WHO Study Group. Osteoporos Int. Nov 1994;4(6):368-81. [Medline].

  8. World Health Organization. WHO scientific group on the assessment of osteoporosis at primary health care level: summary meeting report. Available at http://www.who.int/chp/topics/Osteoporosis.pdf. Accessed February 6, 2012.

  9. WebMD. Medical dictionary: T-score. Available at http://dictionary.webmd.com/terms/t-score. Accessed February 6, 2012.

  10. Bono CM, Einhorn TA. Overview of osteoporosis: pathophysiology and determinants of bone strength. Eur Spine J. Oct 2003;12 Suppl 2:S90-6. [Medline].

  11. Raisz LG. Pathogenesis of osteoporosis: concepts, conflicts, and prospects. J Clin Invest. Dec 2005;115(12):3318-25. [Medline].

  12. Seeman E, Delmas PD. Bone quality--the material and structural basis of bone strength and fragility. N Engl J Med. May 25 2006;354(21):2250-61. [Medline].

  13. Mora S, Gilsanz V. Establishment of peak bone mass. Endocrinol Metab Clin North Am. Mar 2003;32(1):39-63. [Medline].

  14. Sandhu SK, Hampson G. The pathogenesis, diagnosis, investigation and management of osteoporosis. J Clin Pathol. Dec 2011;64(12):1042-50. [Medline].

  15. Jilka RL, Hangoc G, Girasole G, Passeri G, Williams DC, Abrams JS, et al. Increased osteoclast development after estrogen loss: mediation by interleukin-6. Science. Jul 3 1992;257(5066):88-91. [Medline].

  16. Cummings SR, Melton LJ. Epidemiology and outcomes of osteoporotic fractures. Lancet. May 18 2002;359(9319):1761-7. [Medline].

  17. Rosen CJ, Tenenhouse A. Biochemical markers of bone turnover. A look at laboratory tests that reflect bone status. Postgrad Med. Oct 1998;104(4):101-2, 107-10.

  18. Ringe JD, Farahmand P. Advances in the management of corticosteroid-induced osteoporosis with bisphosphonates. Clin Rheumatol. Apr 2007;26(4):474-84. [Medline].

  19. Dennison EM, Syddall HE, Sayer AA, Gilbody HJ, Cooper C. Birth weight and weight at 1 year are independent determinants of bone mass in the seventh decade: the Hertfordshire cohort study. Pediatr Res. Apr 2005;57(4):582-6. [Medline].

  20. Fall C, Hindmarsh P, Dennison E, Kellingray S, Barker D, Cooper C. Programming of growth hormone secretion and bone mineral density in elderly men: a hypothesis. J Clin Endocrinol Metab. Jan 1998;83(1):135-9. [Medline].

  21. [Guideline] American Association of Clinical Endocrinologists medical guidelines for clinical practice for the prevention and treatment of postmenopausal osteoporosis: 2001 edition, with selected updates for 2003. Endocr Pract. Nov-Dec 2003;9(6):544-64. [Medline].

  22. Kelman A, Lane NE. The management of secondary osteoporosis. Best Pract Res Clin Rheumatol. Dec 2005;19(6):1021-37. [Medline].

  23. Adams JS, Song CF, Kantorovich V. Rapid recovery of bone mass in hypercalciuric, osteoporotic men treated with hydrochlorothiazide. Ann Intern Med. Apr 20 1999;130(8):658-60. [Medline].

  24. Mann GB, Kang YC, Brand C, Ebeling PR, Miller JA. Secondary causes of low bone mass in patients with breast cancer: a need for greater vigilance. J Clin Oncol. Aug 1 2009;27(22):3605-10. [Medline].

  25. Holick MF. Vitamin D deficiency. N Engl J Med. Jul 19 2007;357(3):266-81. [Medline].

  26. di Munno O, Mazzantini M, Sinigaglia L, Bianchi G, Minisola G, Muratore M, et al. Effect of low dose methotrexate on bone density in women with rheumatoid arthritis: results from a multicenter cross-sectional study. J Rheumatol. Jul 2004;31(7):1305-9. [Medline].

  27. Migliaccio S, Brama M, Malavolta N. Management of glucocorticoids-induced osteoporosis: role of teriparatide. Ther Clin Risk Manag. Apr 2009;5(2):305-10. [Medline]. [Full Text].

  28. van Staa TP, Leufkens HG, Cooper C. The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis. Osteoporos Int. Oct 2002;13(10):777-87. [Medline].

  29. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. Report of a WHO Study Group. World Health Organ Tech Rep Ser. 1994;843:1-129. [Medline].

  30. Lyles KW, Schenck AP, Colón-Emeric CS. Hip and other osteoporotic fractures increase the risk of subsequent fractures in nursing home residents. Osteoporos Int. Aug 2008;19(8):1225-33. [Medline]. [Full Text].

  31. Fink HA, Kuskowski MA, Taylor BC, Schousboe JT, Orwoll ES, Ensrud KE. Association of Parkinson's disease with accelerated bone loss, fractures and mortality in older men: the Osteoporotic Fractures in Men (MrOS) study. Osteoporos Int. Sep 2008;19(9):1277-82. [Medline].

  32. Sinaki M. Exercise and osteoporosis. Arch Phys Med Rehabil. Mar 1989;70(3):220-9. [Medline].

  33. Yaturu S, DjeDjos S, Alferos G, Deprisco C. Bone mineral density changes on androgen deprivation therapy for prostate cancer and response to antiresorptive therapy. Prostate Cancer Prostatic Dis. 2006;9(1):35-8. [Medline].

  34. Cummings SR, Nevitt MC, Browner WS, Stone K, Fox KM, Ensrud KE, et al. Risk factors for hip fracture in white women. Study of Osteoporotic Fractures Research Group. N Engl J Med. Mar 23 1995;332(12):767-73. [Medline].

  35. National Osteoporosis Foundation. Clinician's Guide to Prevention and Treatment of Osteoporosis. Available at http://www.nof.org/professionals/clinical-guidelines. Accessed January 13, 2011.

  36. Cooper C, Campion G, Melton LJ 3rd. Hip fractures in the elderly: a world-wide projection. Osteoporos Int. Nov 1992;2(6):285-9. [Medline].

  37. Who are candidates for prevention and treatment for osteoporosis?. Osteoporos Int. 1997;7(1):1-6. [Medline].

  38. Gullberg B, Johnell O, Kanis JA. World-wide projections for hip fracture. Osteoporos Int. 1997;7(5):407-13. [Medline].

  39. Jensen GF, Christiansen C, Boesen J, Hegedüs V, Transbøl I. Epidemiology of postmenopausal spinal and long bone fractures. A unifying approach to postmenopausal osteoporosis. Clin Orthop Relat Res. Jun 1982;75-81. [Medline].

  40. Melton LJ 3rd, Kan SH, Frye MA, Wahner HW, O'Fallon WM, Riggs BL. Epidemiology of vertebral fractures in women. Am J Epidemiol. May 1989;129(5):1000-11. [Medline].

  41. Smith R, Wordsworth P. Osteoporosis. In: Clinical and Biochemical Disorders of the Skeleton. 2005:123.

  42. National Osteoporosis Foundation. Fast facts. Available at http://www.nof.org/node/40. Accessed February 16, 2012.

  43. Balfour F. China's "Demographic Tsunami." Bloomberg Businessweek. January 5, 2012. Available at http://www.businessweek.com/magazine/chinas-demographic-tsunami-01052012.html. Accessed February 16, 2012.

  44. Melton LJ 3rd, Sampson JM, Morrey BF, Ilstrup DM. Epidemiologic features of pelvic fractures. Clin Orthop Relat Res. Mar-Apr 1981;43-7. [Medline].

  45. Cauley JA, Lui LY, Ensrud KE, Zmuda JM, Stone KL, Hochberg MC, et al. Bone mineral density and the risk of incident nonspinal fractures in black and white women. JAMA. May 4 2005;293(17):2102-8. [Medline].

  46. Bone Health and Osteoporosis: A Report of the Surgeon General. Washington, DC: Department of Health and Human Services; 2004. [Full Text].

  47. Burge R, Dawson-Hughes B, Solomon DH, et al. Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res. Mar 2007;22(3):465-75. [Medline].

  48. Cooper C, Atkinson EJ, Jacobsen SJ, et al. Population-based study of survival after osteoporotic fractures. Am J Epidemiol. May 1 1993;137(9):1001-5. [Medline].

  49. Kado DM, Browner WS, Palermo L, Nevitt MC, Genant HK, Cummings SR. Vertebral fractures and mortality in older women: a prospective study. Study of Osteoporotic Fractures Research Group. Arch Intern Med. Jun 14 1999;159(11):1215-20. [Medline].

  50. Cooper C, Atkinson EJ, O'Fallon WM, et al. Incidence of clinically diagnosed vertebral fractures: a population-based study in Rochester, Minnesota, 1985-1989. J Bone Miner Res. Feb 1992;7(2):221-7. [Medline].

  51. Vestergaard P, Rejnmark L, Mosekilde L. Increased mortality in patients with a hip fracture-effect of pre-morbid conditions and post-fracture complications. Osteoporos Int. Dec 2007;18(12):1583-93. [Medline].

  52. Trombetti A, Herrmann F, Hoffmeyer P, Schurch MA, Bonjour JP, Rizzoli R. Survival and potential years of life lost after hip fracture in men and age-matched women. Osteoporos Int. Sep 2002;13(9):731-7. [Medline].

  53. Michel JP, Hoffmeyer P, Klopfenstein C, et al. Prognosis of functional recovery 1 year after hip fracture: typical patient profiles through cluster analysis. J Gerontol A Biol Sci Med Sci. Sep 2000;55(9):M508-15. [Medline].

  54. Lindsay R, Silverman SL, Cooper C, et al. Risk of new vertebral fracture in the year following a fracture. JAMA. Jan 17 2001;285(3):320-3. [Medline].

  55. Klotzbuecher CM, Ross PD, Landsman PB, et al. Patients with prior fractures have an increased risk of future fractures: a summary of the literature and statistical synthesis. J Bone Miner Res. Apr 2000;15(4):721-39. [Medline].

  56. The World Health Organization Fracture Risk Assessment Tool. Available at http://www.shef.ac.uk/FRAX/. Accessed May 5, 2008.

  57. Leslie WD, Morin S, Lix LM. Before-and-After Study of Fracture Risk Reporting and Osteoporosis Treatment Initiation. Ann Intern Med. Nov 2 2010;153(9):580-6.

  58. Schwartz AV, Vittinghoff E, Bauer DC, et al. Association of BMD and FRAX score with risk of fracture in older adults with type 2 diabetes. JAMA. Jun 1 2011;305(21):2184-92. [Medline].

  59. Cook DJ, Guyatt GH, Adachi JD, Clifton J, Griffith LE, Epstein RS, et al. Quality of life issues in women with vertebral fractures due to osteoporosis. Arthritis Rheum. Jun 1993;36(6):750-6. [Medline].

  60. Schnatz PF, Marakovits KA, Dubois M, O'Sullivan DM. Osteoporosis screening and treatment guidelines: are they being followed?. Menopause. Oct 2011;18(10):1072-8. [Medline].

  61. Chon KS, Sartoris DJ, Brown SA, Clopton P. Alcoholism-associated spinal and femoral bone loss in abstinent male alcoholics, as measured by dual X-ray absorptiometry. Skeletal Radiol. 1992;21(7):431-6. [Medline].

  62. Geusens P, Dumitrescu B, van Geel T, van Helden S, Vanhoof J, Dinant GJ. Impact of systematic implementation of a clinical case finding strategy on diagnosis and therapy of postmenopausal osteoporosis. J Bone Miner Res. Jun 2008;23(6):812-8. [Medline].

  63. U.S. Preventive Services Task Force. Screening for Osteoporosis: U.S. Preventive Services Task Force Recommendation Statement. Ann Intern Med. Jan 17 2011;[Medline].

  64. Zhu K, Devine A, Lewis JR, Dhaliwal SS, Prince RL. "'Timed up and go' test and bone mineral density measurement for fracture prediction. Arch Intern Med. Oct 10 2011;171(18):1655-61. [Medline].

  65. Lynn SG, Sinaki M, Westerlind KC. Balance characteristics of persons with osteoporosis. Arch Phys Med Rehabil. Mar 1997;78(3):273-7. [Medline].

  66. Nayak S, Roberts MS, Greenspan SL. Cost-effectiveness of different screening strategies for osteoporosis in postmenopausal women. Ann Intern Med. Dec 6 2011;155(11):751-61. [Medline].

  67. [Guideline] Qaseem A, Snow V, Shekelle P, Hopkins R Jr, Forciea MA, Owens DK. Pharmacologic treatment of low bone density or osteoporosis to prevent fractures: a clinical practice guideline from the American College of Physicians. Ann Intern Med. Sep 16 2008;149(6):404-15. [Medline].

  68. Keen R. Osteoporosis: strategies for prevention and management. Best Pract Res Clin Rheumatol. Feb 2007;21(1):109-22. [Medline].

  69. Guglielmi G, Muscarella S, Bazzocchi A. Integrated imaging approach to osteoporosis: state-of-the-art review and update. Radiographics. Sep-Oct 2011;31(5):1343-64. [Medline].

  70. The International Society for Clinical Densitometry. 2007 ISCD Official Positions Brochure. Available at http://www.iscd.org/Visitors/positions/OfficialPositionsText.cfm. Accessed May 5, 2008.

  71. Paunier L. Effect of magnesium on phosphorus and calcium metabolism. Monatsschr Kinderheilkd. Sep 1992;140(9 Suppl 1):S17-20. [Medline].

  72. Lee WY, Oh KW, Rhee EJ, Jung CH, Kim SW, Yun EJ, et al. Relationship between subclinical thyroid dysfunction and femoral neck bone mineral density in women. Arch Med Res. May 2006;37(4):511-6. [Medline].

  73. Tannenbaum C, Clark J, Schwartzman K, Wallenstein S, Lapinski R, Meier D. Yield of laboratory testing to identify secondary contributors to osteoporosis in otherwise healthy women. J Clin Endocrinol Metab. Oct 2002;87(10):4431-7. [Medline].

  74. Liu JM, Zhao HY, Ning G, Chen Y, Zhang LZ, Sun LH, et al. IGF-1 as an early marker for low bone mass or osteoporosis in premenopausal and postmenopausal women. J Bone Miner Metab. 2008;26(2):159-64. [Medline].

  75. Resnick D, Kransdorf M. Osteoporosis. In: Bone and Joint Imaging. Third Edition. 2005:551.

  76. Gosfield E 3rd, Bonner FJ Jr. Evaluating bone mineral density in osteoporosis. Am J Phys Med Rehabil. May-Jun 2000;79(3):283-91. [Medline].

  77. Nayak S, Roberts MS, Greenspan SL. Cost-effectiveness of different screening strategies for osteoporosis in postmenopausal women. Ann Intern Med. Dec 6 2011;155(11):751-61. [Medline]. [Full Text].

  78. Lin JT, Lane JM. Bisphosphonates. J Am Acad Orthop Surg. Jan-Feb 2003;11(1):1-4. [Medline].

  79. Kastner M, Straus SE. Clinical decision support tools for osteoporosis disease management: a systematic review of randomized controlled trials. J Gen Intern Med. Dec 2008;23(12):2095-105. [Medline]. [Full Text].

  80. Lecart MP, Reginster JY. Current options for the management of postmenopausal osteoporosis. Expert Opin Pharmacother. Nov 2011;12(16):2533-52. [Medline].

  81. Chaiamnuay S, Saag KG. Postmenopausal osteoporosis. What have we learned since the introduction of bisphosphonates?. Rev Endocr Metab Disord. Jun 2006;7(1-2):101-12. [Medline].

  82. Mulder JE, Kolatkar NS, LeBoff MS. Drug insight: Existing and emerging therapies for osteoporosis. Nat Clin Pract Endocrinol Metab. Dec 2006;2(12):670-80. [Medline].

  83. Watts NB, Bilezikian JP, Camacho PM, Greenspan SL, Harris ST, Hodgson SF, et al. American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the diagnosis and treatment of postmenopausal osteoporosis. Endocr Pract. Nov-Dec 2010;16 Suppl 3:1-37. [Medline]. [Full Text].

  84. Abrahamsen B, Eiken P, Eastell R. Proton pump inhibitor use and the antifracture efficacy of alendronate. Arch Intern Med. Jun 13 2011;171(11):998-1004. [Medline].

  85. [Best Evidence] Black DM, Delmas PD, Eastell R, et al. Once-yearly zoledronic acid for treatment of postmenopausal osteoporosis. N Engl J Med. May 3 2007;356(18):1809-22. [Medline].

  86. Boonen S, Orwoll E, Magaziner J, Colón-Emeric CS, Adachi JD, Bucci-Rechtweg C, et al. Once-yearly zoledronic acid in older men compared with women with recent hip fracture. J Am Geriatr Soc. Nov 2011;59(11):2084-90. [Medline].

  87. US Food and Drug Administration. FDA drug safety communication: New contraindication and updated warning on kidney impairment for Reclast (zoledronic acid). Available at http://www.fda.gov/Drugs/DrugSafety/ucm270199.htm. Accessed September 1, 2011.

  88. Odvina CV, Zerwekh JE, Rao DS, Maalouf N, Gottschalk FA, Pak CY. Severely suppressed bone turnover: a potential complication of alendronate therapy. J Clin Endocrinol Metab. Mar 2005;90(3):1294-301. [Medline].

  89. Strampel W, Emkey R, Civitelli R. Safety considerations with bisphosphonates for the treatment of osteoporosis. Drug Saf. 2007;30(9):755-63. [Medline].

  90. Park-Wyllie LY, Mamdani MM, Juurlink DN, Hawker GA, Gunraj N, Austin PC, et al. Bisphosphonate use and the risk of subtrochanteric or femoral shaft fractures in older women. JAMA. Feb 23 2011;305(8):783-9. [Medline].

  91. Geusens P. Bisphosphonates for postmenopausal osteoporosis: determining duration of treatment. Curr Osteoporos Rep. Mar 2009;7(1):12-7. [Medline].

  92. [Best Evidence] Grady D, Cauley JA, Stock JL, Cox DA, Mitlak BH, Song J, et al. Effect of Raloxifene on all-cause mortality. Am J Med. May 2010;123(5):469.e1-7. [Medline].

  93. Body JJ, Gaich GA, Scheele WH, Kulkarni PM, Miller PD, Peretz A. A randomized double-blind trial to compare the efficacy of teriparatide [recombinant human parathyroid hormone (1-34)] with alendronate in postmenopausal women with osteoporosis. J Clin Endocrinol Metab. Oct 2002;87(10):4528-35. [Medline].

  94. Dempster DW, Cosman F, Kurland ES, Zhou H, Nieves J, Woelfert L, et al. Effects of daily treatment with parathyroid hormone on bone microarchitecture and turnover in patients with osteoporosis: a paired biopsy study. J Bone Miner Res. Oct 2001;16(10):1846-53. [Medline].

  95. Neer RM, Arnaud CD, Zanchetta JR, Prince R, Gaich GA, Reginster JY, et al. Effect of parathyroid hormone (1-34) on fractures and bone mineral density in postmenopausal women with osteoporosis. N Engl J Med. May 10 2001;344(19):1434-41. [Medline].

  96. Kurland ES, Heller SL, Diamond B, McMahon DJ, Cosman F, Bilezikian JP. The importance of bisphosphonate therapy in maintaining bone mass in men after therapy with teriparatide [human parathyroid hormone(1-34)]. Osteoporos Int. Dec 2004;15(12):992-7. [Medline].

  97. Finkelstein JS, Hayes A, Hunzelman JL, Wyland JJ, Lee H, Neer RM. The effects of parathyroid hormone, alendronate, or both in men with osteoporosis. N Engl J Med. Sep 25 2003;349(13):1216-26. [Medline].

  98. Ste-Marie LG, Schwartz SL, Hossain A, Desaiah D, Gaich GA. Effect of teriparatide [rhPTH(1-34)] on BMD when given to postmenopausal women receiving hormone replacement therapy. J Bone Miner Res. Feb 2006;21(2):283-91. [Medline].

  99. Deal C, Omizo M, Schwartz EN, Eriksen EF, Cantor P, Wang J, et al. Combination teriparatide and raloxifene therapy for postmenopausal osteoporosis: results from a 6-month double-blind placebo-controlled trial. J Bone Miner Res. Nov 2005;20(11):1905-11. [Medline].

  100. [Best Evidence] Bouxsein ML, Chen P, Glass EV, Kallmes DF, Delmas PD, Mitlak BH. Teriparatide and raloxifene reduce the risk of new adjacent vertebral fractures in postmenopausal women with osteoporosis. Results from two randomized controlled trials. J Bone Joint Surg Am. Jun 2009;91(6):1329-38. [Medline].

  101. Peichl P, Holzer LA, Maier R, Holzer G. Parathyroid hormone 1-84 accelerates fracture-healing in pubic bones of elderly osteoporotic women. J Bone Joint Surg Am. Sep 7 2011;93(17):1583-7. [Medline].

  102. Body JJ, Facon T, Coleman RE, Lipton A, Geurs F, Fan M, et al. A study of the biological receptor activator of nuclear factor-kappaB ligand inhibitor, denosumab, in patients with multiple myeloma or bone metastases from breast cancer. Clin Cancer Res. Feb 15 2006;12(4):1221-8. [Medline].

  103. McClung MR, Lewiecki EM, Cohen SB, Bolognese MA, Woodson GC, Moffett AH, et al. Denosumab in postmenopausal women with low bone mineral density. N Engl J Med. Feb 23 2006;354(8):821-31. [Medline].

  104. [Best Evidence] Cummings SR, San Martin J, McClung MR, Siris ES, Eastell R, Reid IR, et al. Denosumab for prevention of fractures in postmenopausal women with osteoporosis. N Engl J Med. Aug 20 2009;361(8):756-65. [Medline].

  105. [Best Evidence] Smith MR, Egerdie B, Hernández Toriz N, Feldman R, Tammela TL, Saad F, et al. Denosumab in men receiving androgen-deprivation therapy for prostate cancer. N Engl J Med. Aug 20 2009;361(8):745-55. [Medline].

  106. Schwarz EM, Ritchlin CT. Clinical development of anti-RANKL therapy. Arthritis Res Ther. 2007;9 Suppl 1:S7. [Medline]. [Full Text].

  107. Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women's Health Initiative randomized controlled trial. JAMA. Jul 17 2002;288(3):321-33. [Medline].

  108. Blake GM, Fogelman I. Long-term effect of strontium ranelate treatment on BMD. J Bone Miner Res. Nov 2005;20(11):1901-4. [Medline].

  109. Burlet N, Reginster JY. Strontium ranelate: the first dual acting treatment for postmenopausal osteoporosis. Clin Orthop Relat Res. Feb 2006;443:55-60. [Medline].

  110. Jamal SA, Hamilton CJ, Eastell R, Cummings SR. Effect of nitroglycerin ointment on bone density and strength in postmenopausal women: a randomized trial. JAMA. Feb 23 2011;305(8):800-7. [Medline].

  111. [Best Evidence] Bischoff-Ferrari HA, Willett WC, Wong JB, Stuck AE, Staehelin HB, Orav EJ, et al. Prevention of nonvertebral fractures with oral vitamin D and dose dependency: a meta-analysis of randomized controlled trials. Arch Intern Med. Mar 23 2009;169(6):551-61. [Medline].

  112. Warensjö E, Byberg L, Melhus H, et al. Dietary calcium intake and risk of fracture and osteoporosis: prospective longitudinal cohort study. BMJ. May 24 2011;342:d1473. [Medline]. [Full Text].

  113. Bruni V, Dei M, Filicetti MF, Balzi D, Pasqua A. Predictors of bone loss in young women with restrictive eating disorders. Pediatr Endocrinol Rev. Jan 2006;3 Suppl 1:219-21. [Medline].

  114. Bischoff-Ferrari HA, Dawson-Hughes B, Willett WC, Staehelin HB, Bazemore MG, Zee RY, et al. Effect of Vitamin D on falls: a meta-analysis. JAMA. Apr 28 2004;291(16):1999-2006. [Medline].

  115. [Best Evidence] Tang BM, Eslick GD, Nowson C, Smith C, Bensoussan A. Use of calcium or calcium in combination with vitamin D supplementation to prevent fractures and bone loss in people aged 50 years and older: a meta-analysis. Lancet. Aug 25 2007;370(9588):657-66. [Medline].

  116. [Best Evidence] DIPART (Vitamin D Individual Patient Analysis of Randomized Trials) Group. Patient level pooled analysis of 68 500 patients from seven major vitamin D fracture trials in US and Europe. BMJ. Jan 12 2010;340:b5463. [Medline].

  117. [Best Evidence] Bolland MJ, Avenell A, Baron JA, Grey A, MacLennan GS, Gamble GD, et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. BMJ. Jul 29 2010;341:c3691. [Medline]. [Full Text].

  118. Sinaki M. Postmenopausal spinal osteoporosis: physical therapy and rehabilitation principles. Mayo Clin Proc. Nov 1982;57(11):699-703. [Medline].

  119. Tinetti ME, Speechley M. Prevention of falls among the elderly. N Engl J Med. Apr 20 1989;320(16):1055-9. [Medline].

  120. Sinaki M, Mikkelsen BA. Postmenopausal spinal osteoporosis: flexion versus extension exercises. Arch Phys Med Rehabil. Oct 1984;65(10):593-6. [Medline].

  121. Sinaki M, Itoi E, Wahner HW, Wollan P, Gelzcer R, Mullan BP, et al. Stronger back muscles reduce the incidence of vertebral fractures: a prospective 10 year follow-up of postmenopausal women. Bone. Jun 2002;30(6):836-41. [Medline].

  122. Sinaki M, Itoi E, Rogers JW, Bergstralh EJ, Wahner HW. Correlation of back extensor strength with thoracic kyphosis and lumbar lordosis in estrogen-deficient women. Am J Phys Med Rehabil. Sep-Oct 1996;75(5):370-4. [Medline].

  123. Chien MY, Wu YT, Hsu AT, Yang RS, Lai JS. Efficacy of a 24-week aerobic exercise program for osteopenic postmenopausal women. Calcif Tissue Int. Dec 2000;67(6):443-8. [Medline].

  124. Snow CM, Shaw JM, Winters KM, Witzke KA. Long-term exercise using weighted vests prevents hip bone loss in postmenopausal women. J Gerontol A Biol Sci Med Sci. Sep 2000;55(9):M489-91. [Medline].

  125. Howe TE, Shea B, Dawson LJ, et al. Exercise for preventing and treating osteoporosis in postmenopausal women. Cochrane Database Syst Rev. Jul 6 2011;CD000333. [Medline].

  126. Iwamoto J, Takeda T, Ichimura S. Effect of exercise training and detraining on bone mineral density in postmenopausal women with osteoporosis. J Orthop Sci. 2001;6(2):128-32. [Medline].

  127. Kerschan-Shindl K, Uher E, Kainberger F, Kaider A, Ghanem AH, Preisinger E. Long-term home exercise program: effect in women at high risk of fracture. Arch Phys Med Rehabil. Mar 2000;81(3):319-23. [Medline].

  128. Robertson MC, Devlin N, Gardner MM, Campbell AJ. Effectiveness and economic evaluation of a nurse delivered home exercise programme to prevent falls. 1: Randomised controlled trial. BMJ. Mar 24 2001;322(7288):697-701. [Medline]. [Full Text].

  129. Walker M, Klentrou P, Chow R, Plyley M. Longitudinal evaluation of supervised versus unsupervised exercise programs for the treatment of osteoporosis. Eur J Appl Physiol. Nov 2000;83(4 -5):349-55. [Medline].

  130. Wolf SL, Barnhart HX, Kutner NG, McNeely E, Coogler C, Xu T. Reducing frailty and falls in older persons: an investigation of Tai Chi and computerized balance training. Atlanta FICSIT Group. Frailty and Injuries: Cooperative Studies of Intervention Techniques. J Am Geriatr Soc. May 1996;44(5):489-97. [Medline].

  131. Carter ND, Khan KM, Petit MA, Heinonen A, Waterman C, Donaldson MG, et al. Results of a 10 week community based strength and balance training programme to reduce fall risk factors: a randomised controlled trial in 65-75 year old women with osteoporosis. Br J Sports Med. Oct 2001;35(5):348-51. [Medline]. [Full Text].

  132. Riggs BL, Melton LJ 3rd. The prevention and treatment of osteoporosis. N Engl J Med. Aug 27 1992;327(9):620-7. [Medline].

  133. Iwamoto J, Sato Y, Uzawa M, Takeda T, Matsumoto H. Comparison of effects of alendronate and raloxifene on lumbar bone mineral density, bone turnover, and lipid metabolism in elderly women with osteoporosis. Yonsei Med J. Feb 29 2008;49(1):119-28. [Medline]. [Full Text].

  134. Hosking D, Chilvers CE, Christiansen C, Ravn P, Wasnich R, Ross P, et al. Prevention of bone loss with alendronate in postmenopausal women under 60 years of age. Early Postmenopausal Intervention Cohort Study Group. N Engl J Med. Feb 19 1998;338(8):485-92. [Medline].

  135. Grossman JM, Gordon R, Ranganath VK, et al. American College of Rheumatology 2010 recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis. Arthritis Care Res (Hoboken). Nov 2010;62(11):1515-26.

  136. Schwab P, Klein RF. Nonpharmacological approaches to improve bone health and reduce osteoporosis. Curr Opin Rheumatol. Mar 2008;20(2):213-7. [Medline].

  137. Lin JT, Lane JM. Nonmedical management of osteoporosis. Curr Opin Rheumatol. Jul 2002;14(4):441-6. [Medline].

  138. Gourlay ML, Fine JP, Preisser JS, May RC, Li C, Lui LY, et al. Bone-density testing interval and transition to osteoporosis in older women. N Engl J Med. Jan 19 2012;366(3):225-33. [Medline]. [Full Text].

  139. Kirshblum SC. Rehabilitation Medicine: Principles and Practice. In: DeLisa JA, Gans BM. Spinal and upper extremity orthotics. 3rd. Philadelphia, Pa: Lippincott-Raven; 1998:635-50.

  140. Stillo JV. Low back orthoses. Phys Med Rehab Clin North Am. 1992;3:57-94.

  141. NIH Consensus conference. Optimal calcium intake. NIH Consensus Development Panel on Optimal Calcium Intake. JAMA. Dec 28 1994;272(24):1942-8. [Medline].

  142. Hulley SB, Grady D. The WHI estrogen-alone trial--do things look any better?. JAMA. Apr 14 2004;291(14):1769-71. [Medline].

  143. Aloia JF, Vaswani A, Yeh JK, Flaster E. Risk for osteoporosis in black women. Calcif Tissue Int. Dec 1996;59(6):415-23. [Medline].

  144. Boonen S, Orwoll E, Magaziner J, et al. Once-Yearly Zoledronic Acid in Older Men Compared with Women with Recent Hip Fracture. J Am Geriatr Soc. Nov 2011;59(11):2084-2090. [Medline].

  145. Canalis E. New treatments in osteoporosis. Bone. Sep 2001;29(3):296.

  146. Cohen A, Dempster DW, Recker RR, Stein EM, Lappe JM, Zhou H, et al. Abnormal bone microarchitecture and evidence of osteoblast dysfunction in premenopausal women with idiopathic osteoporosis. J Clin Endocrinol Metab. Oct 2011;96(10):3095-105. [Medline]. [Full Text].

  147. Cosman F, Nieves J, Zion M, Woelfert L, Luckey M, Lindsay R. Daily and cyclic parathyroid hormone in women receiving alendronate. N Engl J Med. Aug 11 2005;353(6):566-75. [Medline].

  148. Curtis JR, Carbone L, Cheng H, Hayes B, Laster A, Matthews R, et al. Longitudinal trends in use of bone mass measurement among older americans, 1999-2005. J Bone Miner Res. Jul 2008;23(7):1061-7. [Medline]. [Full Text].

  149. Jensen ME, Evans AJ, Mathis JM, Kallmes DF, Cloft HJ, Dion JE. Percutaneous polymethylmethacrylate vertebroplasty in the treatment of osteoporotic vertebral body compression fractures: technical aspects. AJNR Am J Neuroradiol. Nov-Dec 1997;18(10):1897-904. [Medline].

  150. Lau EM, Cooper C. The epidemiology of osteoporosis. The oriental perspective in a world context. Clin Orthop Relat Res. Feb 1996;65-74. [Medline].

  151. Lauderdale DS, Jacobsen SJ, Furner SE, Levy PS, Brody JA, Goldberg J. Hip fracture incidence among elderly Hispanics. Am J Public Health. Aug 1998;88(8):1245-7. [Medline]. [Full Text].

  152. Ledlie JT, Renfro M. Balloon kyphoplasty: one-year outcomes in vertebral body height restoration, chronic pain, and activity levels. J Neurosurg. Jan 2003;98(1 Suppl):36-42. [Medline].

 
Previous
Next
 
Osteoporosis. Lateral radiograph demonstrates multiple osteoporotic vertebral compression fractures. Kyphoplasty has been performed at one level.
Osteoporosis. Lateral radiograph of the patient seen in the previous image following kyphoplasty performed at 3 additional levels.
Osteoporosis of the spine. Observe the considerable reduction in overall vertebral bone density and note the lateral wedge fracture of L2.
Osteoporosis of the spine. Note the lateral wedge fracture in L3 and the central burst fracture in L5. The patient had suffered a recent fall.
Normal femoral anatomy.
Stable intertrochanteric fracture of the femur.
Percutaneous vertebroplasty, transpedicular approach.
Asymmetric loss in vertebral body height, without evidence of an acute fracture, can develop in patients with osteoporosis. These patients become progressively kyphotic (as shown) over time, and the characteristic hunched-over posture of severe osteoporosis develops eventually.
In kyphoplasty, a KyphX inflatable bone tamp is percutaneously advanced into the collapsed vertebral body (A). It is then inflated, (B) elevating the depressed endplate, creating a central cavity, and compacting the remaining trabeculae to the periphery. Once the balloon tamp is deflated and withdrawn, the cavity (C) is filled under low pressure with a viscous preparation of methylmethacrylate (D).
Reduction in kyphotic angulation after kyphoplasty.
Osteoporosis is defined as a loss of bone mass below the threshold of fracture. This slide (methylmethacrylate embedded and stained with Masson's trichrome) demonstrates the loss of connected trabecular bone.
The bone loss of osteoporosis can be severe enough to create separate bone "buttons" with no connection to the surrounding bone. This easily leads to insufficiency fractures.
Inactive osteoporosis is the most common form and manifests itself without active osteoid formation.
Osteoporosis that is active contains osteoid seams (red here in the Masson's trichrome).
Woven bone arising directly from surrounding mesenchymal tissue.
This image depicts bone remodeling with osteoclasts resorbing one side of a bony trabecula and osteoblasts depositing new bone on the other side.
Osteoclast, with bone below it. This image shows typical distinguishing characteristics of an osteoclast: a large cell with multiple nuclei and a "foamy" cytosol.
In this image, several osteoblasts display a prominent Golgi apparatus and are actively synthesizing osteoid. Two osteocytes can also be seen.
Severe osteoporosis. This radiograph shows multiple vertebral crush fractures. Source: Government of Western Australia Department of Health. http://www.imagingpathways.health.wa.gov.au/includes/dipmenu/osteo/image.html.
This radiograph of the spine shows a lateral wedge fracture of L3 (yellow asterisk) and compression fracture of L5 (red asterisk) in an osteoporotic patient who suffered a recent fall. More detailed imaging, usually with computed tomography (CT) scanning, is often needed to better evaluate compression fractures and to determine the urgency of surgical interventions.
Lateral spine radiograph depicting osteoporotic wedge fractures of L1-L2. Source: Wikimedia Commons.
Dual-energy computed tomography (CT) scan in a patient with involutional osteoporosis. Insufficiency fractures of the sacrum and the pubic rami are seen on an isotopic bone scan as a characteristic H, or Honda, sign (arrows), which appears as intense radiopharmaceutical uptake at the fracture sites.
Schematic example of an early bone densitometer: the QDR-1000 System (spine scan). (From: Third National Health and Nutrition Examination Survey Bone Densitometry Manual. Rockville, Md: Westat, Inc; 1989 [revised].)
Bone density scanner. This machine measures bone density to check for osteoporosis in the elderly and other vulnerable subjects. Source: Wikimedia Commons.
Example of a dual energy x-ray absorption (DXA) scan. This image is of the left hip bone. Source: Government of Western Australia Department of Health. http://www.imagingpathways.health.wa.gov.au/includes/dipmenu/osteo/image.html.
Example of a dual energy x-ray absorption (DXA) scan. This image is of the lumbar spine. Source: Government of Western Australia Department of Health. http://www.imagingpathways.health.wa.gov.au/includes/dipmenu/osteo/image.html.
Table 1. WHO Definition of Osteoporosis Based on BMD Measurements by DXA
Definition Bone Mass Density Measurement T-Score
NormalBMD within 1 SD of the mean bone density for young adult womenT-score ≥ –1
Low bone mass (osteopenia)BMD 1–2.5 SD below the mean for young-adult womenT-score between –1 and –2.5
OsteoporosisBMD ≥2.5 SD below the normal mean for young-adult womenT-score ≤ –2.5
Severe or “established” osteoporosisBMD ≥2.5 SD below the normal mean for young-adult women in a patient who has already experienced ≥1 fracturesT-score ≤ –2.5 (with fragility fracture[s])
Sources:



(1) World Health Organization (WHO). WHO scientific group on the assessment of osteoporosis at primary health care level: summary meeting report. Available at: http://www.who.int/chp/topics/Osteoporosis.pdf. Accessed February 6, 2012.[8]



(2) Kanis JA. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis: synopsis of a WHO report. WHO Study Group. Osteoporos Int. Nov 1994;4(6):368-81.[7]



(3) Czerwinski E, Badurski JE, Marcinowska-Suchowierska E, Osieleniec J. Current understanding of osteoporosis according to the position of the World Health Organization (WHO) and International Osteoporosis Foundation. Ortop Traumatol Rehabil. Jul-Aug 2007;9(4):337-56.[6]



BMD = bone mass density; DXA = dual x-ray absorptiometry; SD = standard deviation; T-score = a measurement expressed in SD units from a given mean that is equal to a patient's BMD measured by DXA minus the value in a young healthy person, divided by the SD measurement in the population.[9] .



Table 2. Types of Primary Osteoporosis
Type of Primary OsteoporosisCharacteristics
Juvenile osteoporosis
  • Usually occurs in children or young adults of both sexes
  • Normal gonadal function
  • Age of onset: usually 8-14 years
  • Hallmark characteristic: abrupt bone pain and/or a fracture following trauma
Idiopathic osteoporosis
  • Postmenopausal osteoporosis (type I osteoporosis)
  • Occurs in women aged 50-65 years
  • Characterized by a phase of accelerated bone loss, primarily from trabecular bone
  • Fractures of the distal forearm and vertebral bodies common
  • Age-associated or senile osteoporosis (type II osteoporosis)
  • Occurs in women and men older than 70 years
  • Represents bone loss associated with aging
  • Fractures occur in cortical and trabecular bone
  • Wrist, vertebral, and hip fractures often seen in patients with type II osteoporosis
Table 3. Causes of Secondary Osteoporosis in Adults
Cause Examples
Genetic/congenital
  • Renal hypercalciuria – one of the most important secondary causes of osteoporosis; can be treated with thiazide diuretics
  • Cystic fibrosis
  • Ehlers-Danlos syndrome
  • Glycogen storage disease
  • Gaucher disease
  • Marfan syndrome
  • Menkes steely hair syndrome
  • Riley-Day syndrome
  • Osteogenesis imperfecta
  • Hemochromatosis
  • Homocystinuria
  • Hypophosphatasia
  • Idiopathic hypercalciuria
  • Porphyria
  • Hypogonadal states
Hypogonadal states
  • Androgen insensitivity
  • Anorexia nervosa/bulimia nervosa
  • Female athlete triad
  • Hyperprolactinemia
  • Panhypopituitarism
  • Premature menopause
  • Turner syndrome
  • Klinefelter syndrome
Endocrine disorders[24]
  • Cushing syndrome
  • Diabetes mellitus
  • Acromegaly
  • Adrenal insufficiency
  • Estrogen deficiency
  • Hyperparathyroidism
  • Hyperthyroidism
  • Hypogonadism
  • Pregnancy
  • Prolactinoma
Deficiency states
  • Calcium deficiency
  • Magnesium deficiency
  • Protein deficiency
  • Vitamin D deficiency[24, 25]
  • Bariatric surgery
  • Celiac disease
  • Gastrectomy
  • Malabsorption
  • Malnutrition
  • Parenteral nutrition
  • Primary biliary cirrhosis
Inflammatory diseases
  • Inflammatory bowel disease
  • Ankylosing spondylitis
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
Hematologic and neoplastic disorders
  • Hemochromatosis
  • Hemophilia
  • Leukemia
  • Lymphoma
  • Multiple myeloma
  • Sickle cell anemia
  • Systemic mastocytosis
  • Thalassemia
  • Metastatic disease
Medications
  • Anticonvulsants: phenytoin, barbiturates, carbamazepine (these agents are associated with treatment-induced vitamin D deficiency)
  • Antipsychotic drugs
  • Antiretroviral drugs
  • Aromatase inhibitors: exemestane, anastrozole
  • Chemotherapeutic/transplant drugs: cyclosporine, tacrolimus, platinum compounds, cyclophosphamide, ifosfamide, high-dose methotrexate[26]
  • Furosemide
  • Glucocorticoids and corticotropin[27] : prednisone (≥5 mg/day for ≥3 mo)[28]
  • Heparin (long term)
  • Hormonal/endocrine therapies: gonadotropin-releasing hormone (GnRH) agonists, luteinizing hormone-releasing hormone (LHRH) analogues, depomedroxyprogesterone, excessive thyroxine
  • Lithium
  • Selective serotonin reuptake inhibitors (SSRIs)
Miscellaneous
  • Alcoholism
  • Amyloidosis
  • Chronic metabolic acidosis
  • Congestive heart failure
  • Depression
  • Emphysema
  • Chronic or end-stage renal disease
  • Chronic liver disease
  • HIV/AIDS
  • Idiopathic scoliosis
  • Immobility
  • Multiple sclerosis
  • Ochronosis
  • Organ transplantation
  • Pregnancy/lactation
  • Sarcoidosis
  • Weightlessness
Sources:



(1) American Association of Clinical Endocrinologists medical guidelines for clinical practice for the prevention and treatment of postmenopausal osteoporosis: 2001 edition, with selected updates for 2003. Endocr Pract. Nov-Dec 2003;9(6):544-64.[21]



(2) Kelman A, Lane NE. The management of secondary osteoporosis. Best Pract Res Clin Rheumatol. Dec 2005;19(6):1021-37.[22]



Table 4. Prevalence of Osteoporosis Among Racial and Ethnic Groups
Race/Ethnicity Sex (age ≥50 y) % Estimated to have osteoporosis % Estimated to have low bone mass
Non-Hispanic white; AsianWomen2052
Men735
Non-Hispanic blackWomen5*
Men419
HispanicWomen1049
Men323
Source:  National Osteoporosis Foundation. Fast facts. Available at: http://www.nof.org/node/40. Accessed: February 16, 2012.[42]



* Low bone density is present in an additional 35% of black women, increasing their risk of developing osteoporosis.



Table 5. Comparison of Densitometry Techniques and Cost-Effectiveness
Single-photon absorptiometry Dual-photon absorptiometry Dual-energy x-ray absorptiometry Quantitative computed tomography
Time5-15 min20-30 min5-10 min10-30 min
Cost$50-150$150-300$100-200$150-300
Sites scannedRadius, forearm,



calcaneus



Spine, hip (anteroposterior)Spine (lateral), hip,



radius



Spine (lateral), hip,



radius



Source:  Nayak S, Roberts MS, Greenspan SL. Cost-effectiveness of different screening strategies for osteoporosis in postmenopausal women. Ann Intern Med. Dec 6 2011;155(11):751-61.[68]
Table 6. Baseline Studies for Baseline Conditions in Osteoporosis
Baseline test Disorder
Complete blood count (CBC)CBC results may reveal anemia, as in sickle cell disease (patients with anemia, particularly those older than 60 years, should also be evaluated for multiple myeloma), and may raise the suspicion for alcohol abuse (in conjunction with results from serum chemistry tests and liver function tests)
Serum chemistry levelsCalcium levels can reflect underlying disease states (eg, severe hypercalcemia may reflect underlying malignancy or hyperparathyroidism; hypocalcemia can contribute to osteoporosis)



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



levels of serum calcium, phosphate, alkaline phosphatase, and 25(OH) vitamin D may be obtained to assess osteomalacia



Creatinine levels may decrease with increasing parathyroid hormone (PTH) levels or may be elevated in patients with multiple myeloma



Creatinine levels are also used to estimate creatinine clearance, which may indicate reduced renal function in elderly patients



Magnesium is very important in calcium homeostasis[71] ; decreased levels of magnesium may affect calcium absorption and metabolism



Serum iron and ferritin levelsThese tests are helpful when malabsorption or hemochromatosis are suspected
Liver function testsIncreased levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), bilirubin, and alkaline phosphatase may indicate alcohol abuse
Thyroid-stimulating hormone (TSH) levelThyroid dysfunction has been associated with osteoporosis and should therefore be ruled out[72]
25-Hydroxyvitamin D levelThis test assesses for vitamin D insufficiency; inadequate vitamin D levels can predispose persons to osteoporosis
Table 7. Tests for Secondary Causes of Osteoporosis
Tests for Secondary Causes of Osteoporosis Disorder
24-Hour urine calcium levelThis study assesses for hypercalciuria to help rule out benign familial hypocalciuric hypercalcemia (FHH), in which urinary calcium levels are low
Parathyroid hormone (PTH) levelAn intact PTH result is essential in ruling out hyperparathyroidism; an elevated PTH level may be present in benign FHH
Thyrotropin level (if on thyroid replacement)Experts are divided on whether to include thyrotropin testing, regardless of a history of thyroid disease or replacement; however, one study showed reduced femoral neck bone mineral density (BMD) in women with subclinical hypothyroidism and hyperthyroidism[72]
Testosterone and gonadotropin levels in younger men with low bone densitiesThese tests may help evaluate a sex hormone deficiency as a secondary cause of osteoporosis
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levelsSome practitioners include ESR and CRP values in the workup, although their utility in this setting has not been proven in an evidence-based manner
Urinary free cortisol level and tests for adrenal hypersecretionThese tests are used to exclude Cushing syndrome, which, although uncommon, can lead to rapidly progressive osteoporosis when the condition is present; a urine free cortisol value or overnight dexamethasone suppression test should be ordered in suspected cases
Serum protein electrophoresis (SPEP) and urine protein electrophoresis (UPEP)These are used to identify multiple myeloma
Antigliadin and antiendomysial antibodiesThese tests can help identify celiac disease
Serum tryptase and urine N-methylhistamineThese tests help identify mastocytosis and are used to exclude the presence of multiple myeloma; serum tryptase may be performed to rule out plasma cell dyscrasias
Bone marrow biopsyThis study is obtained when a hematologic disorder is suspected
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.