An In-Depth Overview of Osteoporosis

1. Definition
2. Pathogenesis
3. Clinical Presentation
4. Laboratory Findings
5. Differential Diagnosis
6. Initial Treatment
7. Long-Term Management Issues
8. Prognosis
9. When to Seek Referral to a Rheumatologist
10. References

I. Definition

Although bone seems hard as a rock, cells in bone are constantly being broken down (resorbed) while others are being made. Osteoporosis is a disorder in which bones lose their density. Their internal micro-architecture deteriorates. Bones become fragile and are at greater risk of breaking (fracture). Bone breakage in the back often leads to a bump - sometimes called a dowager's hump - at the top of the back. Medically, it's called a thoracic kyphosis.

There is a clear difference between normal bone and osteoporotic bone.

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Normal Bone

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Osteoporotic Bone

Low bone mass is the most accurate predictor of increased fracture risk. It is estimated that one of every two Caucasian women will have an osteoporotic fracture at some point in her life. The risk for men is lower but increases with age in both sexes. All ethnicities are affected. World Health Organization (WHO) criteria estimate that 15% of all Caucasian women in the U.S., and 35% of women over age 65, have osteoporosis. The lifetime risk of hip fracture in white women is similar to the combined risk of breast, endometrial and ovarian cancer.

The impact on public health is enormous.

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Impact of Osteoporosis

In the United States, an estimated 1.5 million fractures each year are attributed to low bone mass. The majority of fractures are in the vertebrae of the spine. One-third provoke symptoms, such as pain. The remainder are accidentally discovered on x-rays. Annually, there are about 700,000 vertebral fractures, 250,000 to 275,000 hip fractures and 250,000 wrist fractures.

Despite advances in the treatment of hip fractures, death within the first year of fracture remains in excess of 15% to 20%. Less than one-third of patients are restored to their functional status prior to the fracture. Hip fractures can be devastating. Some estimates indicate a new hip fracture costs greater than $40,000.

II. Pathogenesis

Pathogenesis refers to the origin and development of a disease. Humans reach their peak bone mass in their 30s or 40s. A healthy diet with adequae calcium and vitamin D in these early years is essential to build peak bone mass.

Thereafter, men lose density at a slow, steady pace (0.3% to 0.5% per year) throughout their lives. Women lose density at the same pace until menopause, when they begin to lose 2% to 3% per year for approximately 10 years; women resume a rate of loss comparable to men.

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Changes in Bone Mass with Growth

Osteoclasts are a type of bone cell that resorbs old bone. Osteoblasts are a type of bone cell that forms new bone. Loss of bone density results when bone resorption outstrips bone formation. Pits are created by osteoclasts and, after the age of 40, osteoblasts are unsuccessful in completely filling the pits. Some types of bone are more affected than others. Trabecular bone (i.e. vertebral, body, and hip) is affected more than cortical bone, due to its greater surface area.

It is important to maintain an adequate supply of calcium and vitamin D throughout life in order to maintain peak bone mass. Hyperparathyroidism, at times due to inadequate absorption or increased excretion of calcium, has a negative effect on calcium balance and promotes bone resorption. Hyperthyroidism also promotes bone resorption. So these diseases should be diagnosed and treated promptly and properly to help preserve bone.

Both estrogen and testosterone help achieve and maintain peak bone mass. A deficiency of either hormone will contribute to reduced bone mass.

Exercise - even just standing up and walking down the block -- places a mechanical load on bones that stimulates bone formation. Lack of mechanical load - such as too much bed rest - results in a reduced bone mass. So get up off the couch and get moving!

However, women who exercise so strenuously and for such long periods - like marathon runners - often stop having their monthly menses. This too can have a negative impact on bone density. Adequate nutrition is important to help restore bone density.

Many drugs contribute to bone loss. The most common culprit is corticosteroids, such as prednisone, which hinder the bone-forming action of osteoblasts. In addition, corticosteroids cause hypercalciuria and decreased absorption of calcium in the gut. This results in hyperparathyroidism and increased bone resorption. Other drugs implicated in bone loss include heparin, excess thyroid replacement, and anticonvulsants.

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Causes of Decreased Bone Mass

III. Clinical Presentation

The types of symptoms you have, your medical history, your age, and family history define the clinical presentation that your doctor observes.

All too often, your first sign of osteoporosis is a fragility fracture. At times, this may be obvious, but more than 65% of individuals with a compression fracture have no symptoms. . Because low bone mass is asymptomatic until a fracture occurs, it is the job of health care providers to implement measures to help prevent osteoporosis, to suspect the disease, and to evaluate patients with bone density testing.

Bone mass can be determined by a number of methods. The most commonly used technique is dual energy x-ray absorptiometry (DEXA). The amount of mineralized tissue within a section of spine or hip is measured and expressed as grams per cm2. Values are compared:

• to sex- and aged-matched controls, yielding your Z Score, or
• to healthy, same sex individuals aged 35 years who are felt to have attained peak bone mass, yielding your T Score.

The World Health Organization (WHO) has established criteria for the diagnosis of osteoporosis.

• Individuals within one standard deviation of peak bone mass (T score) are considered to have normal bone density.
• If bone mass is between one and 2.5 standard deviations below peak bone mass (T score), osteopenia is diagnosed.
• If bone mass is 2.5 standard deviations below peak bone mass (T score), osteoporosis is diagnosed.
• If the patient has also had a fragility fracture, severe osteoporosis is diagnosed.

Risk factors for osteoporosis have been established.

Major risk factors include:

• family history of osteoporosis or fragility fractures;
• fragility fracture under the age of 45;
• weight under 127 lbs.; and
• current tobacco use.

Minor risk factors include:

• Caucasian women over age 65;
• estrogen deficiency;
• low calcium intake;
• alcoholism;
• sedentary lifestyle; and
• certain chronic diseases, such as rheumatoid arthritis, malabsorption syndromes, Marfan's syndrome, hyperthyroidism, and hyperparathyroidism.

Osteoporosis should also be considered if more that two inches of height are lost or if there is a thoracic kyphosis. Scoliosis is associated with osteoporosis. Although osteoporosis has long been considered a disease of Caucasian women, recent studies have demonstrated that both Asian and Latino women are at risk, as well as up to 15% of African American women.

IV. Laboratory Findings

The diagnosis of osteoporosis is based on clinical signs and symptoms, but it is supported by laboratory tests -- bone evaluations and blood and urine tests..

Standard x-rays do not provide accurate information for diagnosis. When osteoporosis is suggested on standard x-rays, perhaps 40% of bone mineral has already been lost.

Bone loss usually is first detected in trabecular bone because it has a greater surface area and a faster metabolic rate. Losses in cortical bone come later. However, there are a few exceptions. In hyperparathyroidism, bone loss may be greater in cortical bone.

Bone mineral density testing is indicated for anyone at risk for osteoporosis. Axial DEXA is considered the gold standard for measuring bone mineral density. It has a precision of +/- 3% and is used for both diagnosis and to monitor the effects of treatment. Lumbar spine and hip measurements are most commonly obtained. In order to follow density results over time, it is best to use the same machine (i.e. Hologic or Lunar). So try to go back to the same place where you had your prior tests and ask to be placed on the same machine.

Alternative methods available to measure bone density include: axial and peripheral CT; peripheral dual energy absorptiometry; and peripheral quantitative ultrasound densitometry, Peripheral modalities can measure bone density in the forearm, finger, shin, and heel. The peripheral modalities are felt to have a 0.75 correlation, at best, with axial readings. However, the machines are portable and, as such, are often used for screening.

However, if osteoporosis is suspected, a DEXA should be obtained. DEXA is also used to monitor treatment. A recent review (listed in the annotated references below) examines the various modalities available for the diagnosis of osteoporosis.

The Bone Mass Measurement Act, effective July 1, 1998, lists the justifications for Medicare reimbursement for bone mass screening. It approves testing for the following people:

• estrogen-deficient women at risk for osteoporosis.
• individuals with a vertebral abnormality suggestive of fracture;
• individuals receiving glucocorticoid therapy (more than 7.5mg daily for more than three months);
• individuals with hyperparathyroidism; and
• individuals being monitored on an FDA-approved treatment for osteoporosis.

An astute clinician would be wise to obtain a bone mineral density measurement on anyone at risk for osteoporosis. The National Osteoporosis Foundation recommends obtaining a bone density measurement on anyone with a fragility fracture. Consideration should also be given to women with an early menopause and anyone with a medical condition or using a drug known to predispose to osteoporosis.

Bone density measurements provide information about the current skeletal mass but do not provide information about metabolic activity. This is extremely important because bone is in a constant state of flux.

Markers of bone formation include osteocalcin, bone alkaline phosphatase, and the C- and N-terminal propeptides of type 1 collagen.

Markers of bone resorption include urine and serum N-telopeptide, urine C-telopeptide, pyridinoline, and deoxypyridinoline. The most commonly used marker to assess bone turnover is the urine N-telopeptide, although the serum N-telopeptide assay is becoming increasingly available.

Many studies have shown a relationship between the level of various bone markers and the future bone mineral density measurements. For a 1 SD (standard deviation) increase in a bone marker value above that of a premenopausal women, there is a 1.5- to 2.5-fold increase in bone loss over the next year. In a practical sense, the higher the bone marker (i.e. the urine NTX value), the greater the risk of bone loss over the next year. For most commercial laboratories, a urine NTX level above 35-50nM BCE/mM creatinine is suggestive of ongoing bone loss. The goal in a person with osteoporosis is to provide therapy that will drive the NTX below these values, to an NTX seen in premenopausal women.

Bone markers have also been shown to predict fracture risk. The risk of fracture is greater in states of high bone turnover. Interestingly, the risk of fracture is similar in patients with low vertebral bone mass and in those with high bone turnover. One study found that each 1 SD increase in C-telopeptides or free deoxypyridinoline values was associated with a 1.3- or 1.4-fold increase in hip fracture.

Bone markers can also be used in assessing the differential diagnosis of osteoporosis. Markedly elevated markers of bone resorption can be seen in conditions such as hyperthyroidism, hyperparathyroidism, Paget's disease, multiple myeloma, hypercalcemia of malignancy, and bone metastatic disease.

Lastly, bone markers can be used to monitor therapy. After you are started on therapy, your physician will monitor you with tests to assure that bone density is increasing. Within three to six months of beginning a successful treatment, the bone resorptive marker should decrease. This has been demonstrated for hormone replacement therapy, bisphosphonates, calcitonin, and the selective estrogen receptor modulators. If a reduction in bone marker is not observed, the physician should reassess patient adherence, consider other diagnoses leading to bone loss, and consider a change in therapy.

Unfortunately, current bone markers are not completely accurate. There is a circadian rhythm to bone resorption such that it is increased at night. To maximize reliability, the urine NTX specimen should be the second voided urine in the moning. Blood in the urine will interfere with testing. Although prohibitive secondary to cost, an average of several samples would be most representative of true bone turnover. Serum NTX testing, which is becoming more commonly available will eliminate inaccuracies due to the correction for creatinine in urine samples.

V. Differential Diagnosis

Many different diseases cause problems with bone density. Differential diagnosis is the process by which the physician figures out which one is causing your problems. This is important because diseases that mimic osteoporosis are often treated in a very different manner.

If a Z-score is more than 1.5 standard deviations below expected, secondary causes of osteoporosis must be investigated. Testing should be tailored to the individual. Tests help investigate various causes of osteoporosis including inflammatory conditions, hyperparathryroidism, hyperthyroidism, vitamin D deficiency, multiple myeloma, and osteomalacia. Tests to be considered include ESR, serum calcium, serum phosphate, alkaline phosphatase, 25- Vitamin D, serum and urine immunoelectrophoresis, PTH level, and TSH level.

If a secondary cause of osteoporosis is diagnosed, as treatment of that underlying condition may improve bone density and bone strength. A recent study evaluating the treatment of hyperparathyroidism revealed an 8% increase in bone density one year after parathyroidectomy and a 12% increase after 12 years. It is common to be unable to identify a cause of osteoporosis. The vast majority of these individuals may have risk factors including: family history of osteoporosis or fragility fractures; reduced calcium intake, especially prior to development of peak bone mass; and sedentary lifestyle.

VI. Initial Treatment

A. Calcium/Vitamin D

All patients with bone loss or the potential for bone loss should be educated on the appropriate intake of calcium and vitamin D. These guidelines have recently been revised. Both the NIH , and the NOF have published such guidelines. Following are the NIH guidelines:

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NIH Guidelines for Calcium Intake

The recommended daily intake of vitamin D is 400 to 800 IU in adults and 600 to 800 IU in the elderly.

Calcium and vitamin D supplementation are necessary if diet is inadequate. Calcium and vitamin D will decrease bone resorption and mineralize osteoid. Many studies have addressed the intake of calcium and vitamin D and the effect on both bone density and fracture. The use of calcium and vitamin D decreases hip fractures by 25%. Several studies have demonstrated that patients taking adequate calcium and vitamin D have higher bone mass. Calcium and vitamin D will not prevent spinal bone loss in women who are perimenopausal. Conversely, the appendicular skeleton - your arms and legs - might be maintained in all age groups in woman who are premenopausal and in elderly women who obtain physiologic levels of calcium and vitamin D coupled with adequate exercise. In patients taking glucocorticoids, adequate calcium and vitamin D preserves bone density. The use of calcium and vitamin D without antiresorptive therapy limits the ability to increase bone density in either postmenopausal women or in patients on glucocorticoids.

The two most available forms of calcium are calcium carbonate and calcium citrate. Either type is an acceptable replacement. Some evidence supports better absorption of calcium citrate. This preparation may be a more judicious choice in patients with achlorhydria or nephrolithiasis. It can be taken with or without meals. Calcium carbonate is better absorbed with meals because it requires an acid stomach for maximal absorption.

There are many sources of supplemental vitamin D. Multivitamin tablets and vitamin D supplements usually contain 400 IU of vitamin D. Many calcium supplements contain vitamin D.

Most authorities, including the National Osteoporosis Foundation, recommend adding antiresorptive therapy if the T score is -1.5 SD or greater with major risk factors for fracture, or - 2.0 SD or greater without risk factors. Of course, decisions about treatment must be made based on each individual's bone density and associated medical conditions. Factors to consider include: menopausal status; the degree of bone turnover (i.e. an elevated NTX value); concomitant medical illnesses; the use of medications contributing to bone loss; and the patient's level of activity. If there is reason to believe that you are at risk for imminent bone loss, the use of antiresorptive therapy should be strongly considered.

It is well established that the use of glucocorticoids, such as prednisone, is associated with rapid bone loss during the first three months of therapy; thereafter, the rate of loss slows somewhat. As soon as a decision is made to use glucocorticoid for more that two weeks, a plan to combat osteoporosis should be initiated.

B. Bone-formation Agents

To date, we have not had clinically useful agents that promote bone formation. The use of sodium fluoride was generally disappointing, as it was associated with an increase in fracture rate and osteomalacia( a disease that leads to brittle bones). Studies to date with anabolic steroids have demonstrated too many masculinizing effects.

However, parathyroid hormone (PTH) is expected to gain FDA approval for the treatment of osteoporosis. It has been shown to increase bone density and prevent fractures in both postmenopausal women and patients on corticosteroids. It will most likely be used in combination with an antiresorptive agent.

Data presented at Osteoporosis: World Congress 2000 demonstrated that PTH (1-34) used in combination with hormone replacement therapy ( HRT) yielded a 12.8% increase in spine density and a 4.4% increase in hip density. There was a statistically significant reduction in fracture rate. Studies done for the treatment of glucocorticoid-induced osteoporosis have demonstrated an 11% increase in lumbar bone density after one year. Parathyroid hormone increases both bone formation and bone resorption. But the net effect is an increase in bone density. It is given as a daily subcutaneous injection. To date, side effects have been minimal.

C. Antiresorptive Agents

1. Bisphosphonates

Given the absence of agents resulting in bone formation, treatment has focused on agents decreasing bone resorption. Bisphosphonates have been the agents most studied. Etidronate, a first generation bisphosphonate, was been shown to increase bone mineral density (BMD) and reduce vertebral fracture rate but has been associated with osteomalacia. This is less of a concern for the newer bisphosphonates. Alendronate and risedronate are oral bisphosphonates approved for the treatment of osteoporosis.

Alendronate has been shown to increase spine BMD by 8% and hip BMD by 5% after three years). It decreases hip fracture by 51% and vertebral fractures by 47%. Studies with risedronate reveal fairly similar fracture and BMD data. Direct head-to-head studies between these two agents have not been done, and the available studies are not precisely comparable. Over a three-year period, risedronate-treated patients had a BMD increase of 5.4% in the lumbar spine and 1.6% in the hip. The rate of new vertebral fractures was reduced by 41%, and the rate of new nonvertebral fractures was reduced by 39%. Studies indicate there is no increase in gastrointestinal irritation compared with placebo for either risedronate or alendronate. Both agents prevent corticosteroid-induced bone loss. In general, bisphosphonates are safe and well tolerated.

The doses of alendronate originally approved were 5 mg daily for the prevention of osteoporosis and 10 mg daily for treatment the disease. More recently, a dose of 70 mg weekly has been approved for treatment. Efficacy and toxicity seem comparable to the originally approved dose. Most patients find the weekly dose more suitable, which increases adherence.

The dose of risedronate for the treatment and prevention of osteoporosis is 5mg per day or 35mg per week. The weekly dose was recently FDA-approved.

The use of bisphosphonates in women prior to childbearing has not been well studied. So their use in younger women should be carefully discussed with your physician. However, bisphosphonates are often an excellent choice for the treatment of men with osteoporosis.

Although not FDA-approved for the treatment of osteoporosis, pamidronate has been fairly well studied for this application. It increases BMD and decreases fracture rate. Most studies have given 30 mg intravenously every three months. Occasionally, flu-like symptoms are noted after the infusion. This can often be managed by taking diphenhydramine and acetaminophen beforehand.

Over the next several years, other intravenous bisphosphonates should be approved for the treatment of osteoporosis. Zoledronic acid (Zometa) is FDA-approved for the treatment of hypercalcemia of malignancy; studies are underway for its use in osteoporosis. The proposed yearly dose will probably be 4mg IV over 45 minutes.

2. Hormone Replacement Therapy

The effect of hormone replacement therapy (HRT) on bone health has not been studied with the same methodological rigor as the newer agents. Estrogen in the form of Premarin 0.625 mg daily has been studied in the treatment and prevention of osteoporosis. It will increase bone mass by 2% per year. In non-randomized trials, it has been shown to decrease fracture rates at all sites by 50%. Conflicting data make it unclear if a dose of 0.3 mg is sufficient to prevent and treat osteoporosis. This dose may be sufficient in some women of low weight, but should be carefully discused with your physician.

The use of estrogen for the treatment of osteoporosis must be weighed against the possible risks. Use of HRT increases the risk of breast cancer, especially after 10 years of use. The increased risk seems to be 2% per year of use. HRT is also associated with an increased incidence of thrombosis and, if used without progesterone, an increased incidence of uterine cancer. HRT improves cholesterol values and the lipid profile, but recent data suggests it may increase the risk of myocardial infarction in someone with unstable coronary artery disease.

The estrogen/progesterone arm of the Women's Health Initiative study was recently halted early due to an excess number of cardiovascular and thrombotic events. However, there were fewer hip fractures in the estrogen/progesterone treated women than in those on placebo. The estrogen-only arm of the study was not halted.

3. Selective Estrogen Receptor Modulators

Selective estrogen receptor modulators (SERMs) are a new class of agents that includes tamoxifen and raloxifene. Raloxifene increases BMD in the spine by 3% over three years. It decreases vertebral fracture by 40%. No benefit has yet been demonstrated in reducing hip fractures. Therefore, the SERMs are less effective than estrogen and the newer bisphosphonates in increasing bone mass and preventing fracture. These agents can precipitate menopausal symptoms, but they do reduce the risk of breast cancer - a marked concern for many women. There is no increased risk of uterine cancer. The benefit on lipids is favorable, although not as beneficial as with HRT.

4. Calcitonin

Calcitonin is available in a nasal spray. Side effects, including nasal irritation, are rare. The dose is 200 IU intranasally each day, alternating nostrils. It is the least effective antiresorptive agent. It is indicated for patients who cannot, or prefer not to, take other agents. It increases spine BMD and reduces spine fractures by 37%. No benefit has been noted in the hip. Limited data suggests that it may reduce pain associated with an acute fracture. There is a 2% risk of epistaxis (nosebleeds), which is usually minor.

If the T-score is less than -2.5 SD, combination therapy should be considered. A combination of alendronate and estrogen produced larger increases in BMD than either agent alone and is well- tolerated. The use of bisphosphonates and raloxifene has not been well studied, but perhaps the combined effect would be advantageous to increased bone density.

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Treatment of Osteoporosis

5. Falls Prevention/Exercise

The loss of muscle mass, flexibility, and balance occurs almost universally as we age. These losses are accompanied by an increase in the frequency of falls. If falls can be prevented, a significant number of fragility fractures can be avoided.

The living environment should be carefully reviewed with this goal in mind. Lighting, especially at night should be adequate. Rugs should be secured to the floor. Grab bars should be installed in the bathroom beside the toilet and the tub. The use of sedating medications should be kept to an absolute minimum.

Exercise programs that promote mobility, muscle strengthening, balance, and flexibility should be emphasized. Tai Chi is an exercise program that meets many of these goals. For maximum benefit, it should be practiced regularly. It is well tolerated by the population at risk. Classes are readily available.

VII. Long-Term Management Issues

A. Medication

If the bone marker remains elevated despite what appears to be an adequate regimen for the treatment of osteoporosis, consideration must be given to secondary causes of the disease. Appropriate laboratory evaluations should be performed. At times, patients appear to fracture with a relatively normal bone density. One then worries about the quality of the bone. In addition to a metabolic work-up, a bone biopsy with tetracycline labeling may be indicated.

Some patients appear to respond more to one agent or another, i.e. HRT or a bisphosphonate. In this instance, changing the regimen and following a bone marker would be helpful.

B. New Advances: Vertebroplasty/Kyphoplasty

Vertebral fractures in your back can be extremely painful. In addition, their effect on posture, overall mobility, and cardiopulmonary function can cause marked morbidity - other illnesses. Several new techniques have recently become available to treat vertebral fractures.

Vertebroplasty involves injecting cement directly into fractured vertebral bodies. This has been shown to decrease pain, increase mobility and improve spine stability. There is no effect on fracture reduction or deformity. The technique is still fairly new, and there can be a 6% complication rate per level.

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Kyphoplasty involves using an inflatable bone tamp to inject bone void filler under low pressure into the involved vertebral body. The fracture may be reduced, and pain relief is rapid. The procedure seems well-tolerated.

Click Thumbnail to Enlarge Thoracic Kyphosis	Click Thumbnail to Enlarge Kyphoplasty: Procedure to reduce kyphosis, restore stability
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Both of these new procedures are available at The Hospital for Special Surgery.

VIII. Prognosis

Can your doctor foretell how bad your osteoporosis will become? Not necessarily. Your doctor can tell you about your risk -- based on your DEXA results and how those results change with monitoring.

With regard to BMD, a loss of one standard deviation gives rise to a two-fold risk of spine fracture and a 2.5 fold risk of hip fracture. There is also data to support a higher rate of fracture in states of high bone turnover. If an intervention works to lower bone turnover, it should be associated with lower fracture risk. This may, in part, explain why a modest increase in bone density may be associated with a lower fracture rate.

Needless to say, a fragility fracture, especially of the hip is associated with significant morbidity and mortality. Vertebral fractures can be associated with severe pain and morbidity due to a postural effect on cardiopulmonary and gastrointestinal symptoms. When you have bad posture and stand or sit crouched over, your internal organs get crushed and can't function properly.

Osteoporosis and its consequences can pose a significant psychological burden on those affected. The goal of therapy is to prevent osteoporosis and the associated fragility fractures.

IX. When to Seek Referral to a Rheumatologist

All physicians should be cognizant of patients with possible bone loss. In particular, family practitioners, internists, gynecologists, and Orthopaedists will be in optimal positions to assess their patients for increased risk of fragility fractures. Any physician treating disorders that predispose to osteoporosis or any physician prescribing drugs that predispose to osteoporosis should be evaluating bone density.

However, you should seek referral to a physician who specializes in osteoporosis, such as a rheumaologist, in the following situations:

• If the physician is unfamiliar with the appropriate work-up if bone density is less than that expected for age-matched controls;
• if the physician is unfamiliar with the various treatment options available for osteoporosis;
• if your bone density and/or bone markers do not improve with seemingly appropriate therapy.

X.  References         

1. Riggs BL. Overview of osteoporosis. West J Ed. 1991 Jan;154(1):63-77.
2. Favus, Murray J (editor) et al. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 1993, Raven Press.
3. Lane JM, Riley EH, Wirganowizc PZ. Instructional Course Lectures, The American Academy of Orthopaedic Surgeons - Osteoporosis: Diagnosis and treatment. J Bone Joint Surg. 1996; 78:618-32.
4. Miller PD, Zapalowski C, Kulak CAM, Bilezikian JP. Bone Densitometry: The Best Way to Detect Osteoporosis and to Monitor Therapy. J Clin Endo Metab. 1988;84(6):1867-71.
5. DHHS 1998 Medicare Program: Medicare coverage of and payment for bone mineral measurements. Federal Register. Washington DC, U.S. Govt Printing Office.
6. O'Connor WJ, Lane JM. The benefits of Tai Chi in osteoporosis. Amer J Spor Med. 1999 Sep/Oct;1(5):255-259.

posted 10/21/2002