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Guidelines for Diagnosing Osteoporosis

Gail P. Dalsky, PhD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 24 - NO. 7 - JULY 96


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In Brief: Women who are estrogen deficient have an increased risk of osteoporosis and future fractures. In recent years, improving technology and a consensus on the definition of osteoporosis have made it easier to measure bone density and assess the risk of osteoporosis. Density should be measured at two sites, the lumbar spine and the femoral neck. If only one measurement is possible, the site should be the lumbar spine in women younger than 65 and the femoral neck in women 65 and older. Treatment is recommended if a woman's bone density is more than one standard deviation below the young adult reference value.

Women who have menstrual dysfunction and low estrogen levels face a higher risk of osteoporosis and future fractures than women who have normal estrogen (1). Fortunately, bone density measurement techniques have become more precise and more widely available in recent years, and a consensus has emerged on the definition and intervention threshold for osteoporosis. Consequently, it is now possible to measure bone density at a relevant site such as the spine or proximal femur and determine the patient's corresponding fracture risk.

Although active women often know their blood pressure, cholesterol level, and percent body fat, they are far less likely to know the status of their bone health. If they are amenorrheic—which may be the case if they train rigorously—they may incur an irreversible loss of bone density and consequently an increased risk for fracture in later life (2-4). Exercise cannot fully offset the negative effects of low estrogen levels on bone density, because a low estrogen level also reduces the positive effect of activity on bone (5).

Osteoporosis Defined

At a consensus development conference on osteoporosis in 1991, the condition was defined as "a disease characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk (6)." Quantitative criteria were supplied in 1994, when osteoporosis was defined in terms of bone density at clinically relevant sites, using comparisons with young adult values (7-9). Each reduction in bone density of 1 standard deviation (SD) is associated with a twofold to threefold increased risk of fracture (7).

Four diagnostic or risk categories have been developed by the World Health Organization (8) and are shown in table 1. Thus, a diagnosis of osteoporosis can now be made on the basis of bone density, even if no fracture has occurred (8). Further, an intervention threshold has been established: bone density at a single site that is 1 SD below the young adult reference value (8).

Table 1. Bone Health Diagnostic Categories Based on Bone Density Values Relative to the Young Adult Mean*
Normal Less than or equal to 1 standard deviation (SD) below the young adult mean (BYAM)
Osteopenia (low bone density) 1 to 2.5 SD BYAM
Osteoporosis Greater than 2.5 SD BYAM
Severe or established osteoporosis Greater than 2.5 SD BYAM in the presence of one or more fragility fractures
* Adapted from a World Health Organization report (8).

Who Should be Evaluated?

The most significant risk factor for low bone density among healthy, active women is estrogen deficiency (10). A woman of any age who has prolonged estrogen deficiency (more than 6 months of amenorrhea, either past or current) should be considered for a bone density measurement for evaluation of skeletal health (10). This is true regardless of physical activity level. Reduced cumulative estrogen exposure as a result of delayed menarche, premature menopause, amenorrhea, or oligomenorrhea is also a risk factor (11,12).

Other major risk factors include a strong family history of osteoporosis or a history of low bone density, stress fractures or low-trauma fractures, low calcium intake, poor nutrition, corticosteroid use, or malabsorptive diseases. The effects of a malabsorptive (celiac) disease were exemplified in a woman who is a patient at our center; she had low bone density at both the spine (-2.0 SD) and the femoral neck (-1.6 SD).

Measurement Recommendations

Bone density can be measured with several different techniques, including dual-energy x-ray absorptiometry (DXA), single-energy x-ray absorptiometry, and quantitated computed tomography. The most widely available technique is DXA.

The preferred site for measurement depends in part on the woman's age. Ideally, bone density should be measured at multiple sites, such as the lumbar spine and the proximal femur, because a single measurement can lead to misclassification of the risk. But if only one site can be measured, it should be the lumbar spine in premenopausal women and postmenopausal women younger than 65. The radius is not recommended because low bone density at the spine or hip can be missed if only the radius is measured, as demonstrated previously in amenorrheic athletes (1,13,14). In older (65 or over) women, the proximal femur is the preferred site for assessment because the spinal bone density may be elevated as a result of degenerative changes, osteoarthritis, osteophytes, or aortic calcification. This higher value may be interpreted incorrectly to mean an absence or reduction of risk (15).

Some data from our laboratory illustrate the usefulness of bone density measurements in identifying asymptomatic women at risk for osteoporosis. Measurements at the lumbar spine and femoral neck were obtained in 47 women between 20 and 45 years of age who were grouped according to menstrual status. Results are shown in table 2. The women with normal menstrual function had normal to very active lifestyles (they engaged in various forms of exercise, but not regularly or year-round), while the women with menstrual dysfunction were endurance runners. Overall, 20 women were found to have bone density below the intervention threshold of -1 SD at one or both sites. Two of the women with menstrual dysfunction were classified as having osteoporosis, one at the spine and the other at the hip.

Table 2. Absolute Bone Mineral Density (BMD) and BMD Relative to Young Adult Values in 47 Women, Aged 20-45, Grouped According to Menstrual Status and Activity Level*
Normal menstrual
function (N=29)
Menstrual dysfunction (N=18)
Lumbar spine BMD (g/cm2) 1.229±0.125 1.02021±0.103
Standard deviation (SD) from young adult mean (YAM) +0.24±1.03 -0.85±0.86
Subjects exceeding intervention threshold (greater than 1 SD below the YAM) 17% (5/29) 44% (8/18)
Femoral neck BMD (g/cm2) 1.041±0.118 0.948±0.124
SD from YAM +0.51±0.2021 -0.27±1.03
Subjects exceeding intervention threshold (greater than 1 SD below the YAM) 7% (2/29) 28% (5/18)
* Eumenorrheic women exercised but not regularly; women with menstrual dysfunction were endurance runners.

As mentioned above, patients can be misclassified if bone density is measured at only one site. In our sample group, 32 of the 47 women (68%) would have been correctly classified as normal by either the spine or the femur value, and 5 women (11%) would have been correctly classified as having low bone density by either measurement. The risk category would have been misclassified in 10 women (21%) if only one site had been evaluated. Eight women (17%) had spinal bone density below the intervention threshold of -1 SD, although the femoral neck bone density was normal. Two women (4%) had normal bone density at the spine but were low at the proximal femur.

Causes and Treatment

When low bone density is identified in a healthy, active woman, a thorough evaluation to determine the cause or causes should include the following (16-19):

  • Menstrual history;
  • Family history of osteoporosis;
  • Nutrition status (calcium and vitamin D intake);
  • History of eating disorders (see "The Female Athlete Triad: Causes, Diagnosis, and Treatment" by Angela D. Smith, MD);
  • Medication use, especially thyroid hormone replacement, corticosteroids, and phenytoin sodium;
  • Low lean-body mass or muscle mass; and
  • Training intensity.

Women who have an increased risk of fracture may be advised to improve their bone health before osteoporosis develops. When a premenopausal woman has estrogen deficiency, the treatment recommendation would be to either restore endogenous estrogen levels or to consider an exogenous estrogen source such as oral contraceptives (see "Hormone Therapy and the Female Athlete Triad," in The Female Athlete Triad: Causes, Diagnosis, and Treatment by Angela D. Smith, MD). In premenopausal women whose menstrual dysfunction is related to calorie deficit, therapy may include reducing exercise levels or increasing calorie intake; improving nutrition status, particularly calcium intake; increasing body weight; and stopping smoking. In sedentary premenopausal women, the recommendation would be to increase weight-bearing exercise and calcium intake and avoid cigarette smoking.

Postmenopausal women may be advised to make the same lifestyle changes as recommended for premenopausal women (see "An Active Menopause: Using Exercise to Combat Symptoms" by Mona M. Shangold, MD) and to start hormone replacement therapy. Postmenopausal women who are well beyond the intervention threshold and/or have already had osteoporotic fractures should be advised to begin treatment with an antiresorptive therapy such as estrogen, bisphosphonates, or calcitonin.

Averting a Silent Disease

Osteoporosis, like hypertension, has often been called the silent disease. It would be tragic if the risk for osteoporosis were ignored in active, healthy women with reduced estrogen levels. With the judicious use of bone density measurements to evaluate patients, low bone mass can be identified early so that fractures at a later age, particularly hip fractures, can be averted.

References

  1. Myburgh KH, Bachrach LK, Lewis B, et al: Low bone mineral density at axial and appendicular sites in amenorrheic athletes. Med Sci Sports Exerc 1993;25(11):1197-1202
  2. Drinkwater BL, Nilson K, Chesnut CH III, et al: Bone mineral content of amenorrheic and eumenorrheic athletes. N Engl J Med 120214;311(5):277-281
  3. Keen AD, Drinkwater BL: No gain in vertebral bone density over 10 years in previously amenorrheic athletes (abstract). J Bone Miner Res 1995;10(suppl 1):S243
  4. Fisher EC, Nelson ME, Frontera WR, et al: Bone mineral content and levels of gonadotropins and estrogens in amenorrheic running women. J Clin Endocrinol Metab 120216;62(6):1232-1236
  5. Dalsky GP: Effect of exercise on bone: permissive influence of estrogen and calcium. Med Sci Sports Exerc 1990;22(3):281-285
  6. Consensus development conference: prophylaxis and treatment of osteoporosis. Amer J Med 1991; 90(1):107-110
  7. Kanis JA, Melton LJ III, Christiansen C, et al: The diagnosis of osteoporosis. J Bone Miner Res 1994;9(8): 1137-1141
  8. World Health Organization: Assessment of Fracture Risk and Its Application to Screening for Postmenopausal Osteoporosis. WHO Technical Report Series No. 843. Geneva, WHO, 1994
  9. Kanis JA: Assessment of fracture risk and its application to screening for postmenopausal osteoporosis: synopsis of a WHO report. Osteoporosis Int 1994; 4(6):368-381
  10. Johnston CC Jr, Melton LJ III, Lindsay R, et al: Clinical indications for bone mass measurements: a report from the Scientific Advisory Board of the National Osteoporosis Foundation. J Bone Miner Res 120219;4(suppl 2):1-28
  11. Nguyen TV, Jones G, Sambrook PN, et al: Effects of estrogen exposure and reproductive factors on bone mineral density and osteoporotic fractures. J Clin Endocrinol Metab 1995;80(9):2709-2714
  12. Drinkwater BL, Bruemmer B, Chesnut CH III: Menstrual history as a determinant of current bone density in young athletes. JAMA 1990;263(4):545-548
  13. Linnell SL, Stager JM, Blue PW, et al: Bone mineral content and menstrual regularity in female runners. Med Sci Sports Exerc 120214;16(4):343-348
  14. Schlechte J, el-Khoury G, Kathol M, et al: Forearm and vertebral bone mineral in treated and untreated hyperprolactinemic amenorrhea. J Clin Endocrinol Metab 120217;64(5):1021-1026
  15. Reid IR, Evans MC, Ames R, et al: The influence of osteophytes and aortic calcification on spinal mineral density in postmenopausal women. J Clin Endocrinol Metab 1991;72(6):1372-1374
  16. Cummings SR, Nevitt MC, Browner WS, et al: Risk factors for hip fracture in white women: study of Osteoporotic Fractures Research Group. N Engl J Med 1995;332(12):767-773
  17. Davies KM, Pearson PH, Huseman CA, et al: Reduced bone mineral in patients with eating disorders. Bone 1990;11(3):143-147
  18. Sowers MF, Kshirsagar A, Crutchfield MM, et al: Joint influence of fat and lean body composition compartments on femoral bone mineral density in premenopausal women. Am J Epidemiol 1992;136(3):257-265
  19. Snow-Harter CM: Bone health and prevention of osteoporosis in active and athletic women. Clin Sports Med 1994;13(2):389-404

Dr Dalsky is an assistant professor of medicine and director of the Exercise Research Laboratory in the Osteoporosis Center at the University of Connecticut Health Center in Farmington. Address correspondence to Gail P. Dalsky, PhD, University of Connecticut Health Center, Osteoporosis Center, 263 Farmington Rd, Farmington, CT 06030-6145.


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