Eduardo J. Balbona, M.D.
Millions of American women have osteoporosis. These women are at risk for pathologic fractures leading to pain, deformity, disability and even death. Simple, inexpensive, rapid and reliable screening tests are available, yet less than 10% of osteoporotic individuals are aware of their diagnosis. Several effective interventions are proven to reduce complications, yet less than half of the women at risk have even discussed osteoporosis with their physician. An estimated 28 million American women have osteopenia or osteoporosis and these num bers threaten to explode with current demographic trends (Figure 1). The direct medical expenses associated with osteoporotic fractures approach $14 billion dollars annually and the indirect costs are staggering. A quarter of individuals will require long term nursing home care following a hip fracture and only 1 in 3 of those affected will ever regain their level of pre-fracture independence.
The gradual decline in bone density with age means that all one requires to develop osteoporosis is simply to live long enough. The timely detection and institution of preventive measures must be the foundation of any effective osteoporosis manage ment program.
Bone mineral density (BMD) is the accepted surrogate for osteoporotic fracture risk. Bone density is a better predictor of fractures than blood pressure is of strokes or cholesterol is of heart attacks. Bone mineral density is felt to account for 80% of the variance in bone strength and resistance to fracture. Peak adult bone mass (PABM) is reached in both genders near age thirty. From that point onward, bone mineral density steadily declines. (Figure 2) The risk of fracture doubles with each standard deviation below peak adult bone mass (Table 2). The World Health Organization (WHO) bas defined osteoporosis as a bone density below 2 .5 standard deviations the mean BMD of young healthy adults.These alarming statistics demand the renewed commitment of the medical community to a program of increased public awareness, patient education, wide spread screening and regular monitoring of fracture risk
Osteoporosis quietly progresses without symptoms until late stage complications occur (Table 1). Without proactive screening , osteoporosis may go undetected and unchecked for years although it is a largely preventable.
Osteopenia or low bone density is defined as a BMD reduced between 1.0 to 2.5 standard deviations relative to this BMD. Normal bone density is defined as within 1 standard deviation of the mean young adult BMD. Bone density may now be determined via several modali ties from quantitative computed tomography (qCT) to dual energy x-ray absorptiometry (DEXA) or peripheral ultrasound measurement. Each modality has been shown to be independently predictive of fracture risk, yet each has it's own limitations and results may not be comparable between modalities.
Quantitative computed tomography may be the most accurate and sensitive means of determining bone mineral density. The qCT exam measures the density of a three dimensional area of interest. This can be used to isolate the trabecular bone that is the most metabolically sensitive. Nevertheless, the applicat1on of qCT has been somewhat limited because of the added expense and radiation exposure as compared to alternatives. One alternative,dual x-ray absorptiometry (DEXA) measures the difference in absorption of low energy and high energy photons passing through tissues. The two dimen sional result is more likely to be influenced by overlying or nearby structures such as vascular or ligamentous calcifications or bony osteophytes. This may lead to artificially elevated and inaccurate results especially in the case of spinal measurements. For this reason, when there are discrepancies between the spinal and femoral BMD measurements, the femoral value may be more accurate. Finally, peripheral ultrasound of the calcaneus measures broadband ultrasound attenuation (BUA) and the speed of sound (SOS) through this weight bearing area. There is a high level of correlation between these values and bone mineral density as well as between calcaneal and central BMD. The ease of use, non invasive and cost effective qualities of the peripheral ultrasound have made it useful as an initial screening tool. However, an abnormal peripheral BMD screen should always be followed by a central BMD exam, be it qCT or DEXA based.
All women should be evaluated for osteoporotic risk in the same manner other medical risk factors are reviewed . Modifiable and non-modifiable risk factors should be discussed and will drive the need for further testing (Table 3). Non-modifiable risk factors include: female gender, Caucasian or Asian race, family history and a personal history of fracture as an adult. Modifiable factors include: smoking, inadequate dietary calcium, estrogen deficiency, excess dietary sodium, alcoholism, low body weight (<127 lbs), inactivity and lack of weight bearing exercise. Secondary causes of osteoporosis include a broad range of diseases and medications. Culprit medications may include corticosteroids, anticonvulsants, heparin, aluminum and thyroxine. Medical conditions associated with secondary osteoporosis include hyperparathyroidism, hyperthyroidism, diabetes, chronic renal failure, scoliosis, gonadal insufficiency, multiple myeloma, lymphoma, chronic obstructive pulmonary disease, rheumatoid arthritis, sarcoidosis, and malabsorption syndromes among several others.
The bone mineral density of any patient is the product of their own personal history and part of a predictable lifelong process of skeletal development and deterioration. The accepted WHO guidelines for osteopenia and osteoporosis compare peak adult bone mass (PABM) to a population of postmenopausal Caucasian women from the United Kingdom and the United States. About a third of all postrnenopausal women meet the WHO criteria for osteoporosis and half of these women will already harbor objective evidence of osteoporotic fractures. The WHO criteria simply provide a yardstick for comparison and allow for the identification of individuals at increased risk of osteoporotic fractures. The applicability of the WHO criteria to other ethnic groups or even premenopausal women has been the source of some debate. There are concerns regarding the possibility of excessive diagnosis, treatment and expense in otherwise low risk individuals. The incidence of osteoporotic fracture inpremenopausal females is indeed quite low and the lack of support for short-term interventions is not unexpected. Nevertheless , the 30 or 40 year-old female with low bone mineral density is likely to eventually be the same 50 or 60 year-old individual who is at considerable risk from her now even lower BMD. The intervening years are ones of steady declines in bone mineral density in all clinical studies without exception.
In general, women lose about 1% of their spinal bone density per year. Thus the natural history of bone mineral density supports the need for screening at a stage when actual fracture risk is quite low. The potential benefits from early intervention are significant and it is important to note that even small changes in bone density can have dramatic benefits on the risk of fracture and long term complications. (Table 1)
Indeed, far from being viewed as a geriatric disease, osteoporosis has its roots in childhood and adolescence. Family practitioners and pediatricians increasingly rec ognize their responsibility to promote bone health at the stage oflife when the peak adult bone mass (PABM) can be readily affected. Children are susceptible to many conditions that interfere with normal bone development such as eating disorders and nutritional deficiencies . It is estimated that only ten percent of young girls ages 9 to 17receive adequate dietary calcium intake and many lack regular weight bearing exercise. Furthermore , chronic medications such as steroids and anticonvulsants may have profound effects on bone development and eventual adult peak bone mass.
Beyond the universal recommendations of the National Osteoporosis Foundation (Table 4) there are now several therapeutic options for intervention. They include estrogen, progesterone, hormone replacement, raloxifene, tamoxifen, phytoestrogens, alendronate, risedronate, etidronate, and calcitonins with many more to come. Patients and their physicians need not passively await a future of isolation, deformity and disability from osteoporosis. Aggressive patient education and preventive measures should lessen the incidence and severity of osteoporosis in our communities.
Physicians should do what they do best - look into the future of their patients and take an active role in ensuring it is a long and healthy one.
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May 2000 / Jacksonville Medicine