Osteoporosis: A pediatric perspective

While osteoporosis is usually considered a disease of the elderly, it could as accurately be considered a disease of childhood with manifestations in the elderly. More than 90% of peak bone mass is accrued by age 18 years. Bone mass increases in a linear manner during childhood until puberty (Figure 1). During puberty the rate of bone mass accrual increases until the late teenage years, at which time it levels off until peak bone mass is achieved (1). Once peak bone mass is achieved (in the late teens to early 20s), little can be done to further increase bone mass. Peak bone mass is thought to account for more than half the variability in adult bone mass; thus, adult fracture risk is dependent on childhood bone metabolism (2). Targeting interventions toward optimization of peak bone mass during childhood and adolescence therefore represents an important public health approach. Early intervention takes advantage of the unique window of opportunity to maximize bone mass accrual and peak bone mass, and theoretically decrease fracture risk for life. A vertebral compression fracture, or any other pathologic fracture, in childhood is something all patients, parents, and physicians hope to avoid. The price of childhood osteoporosis is arguably greater than that of osteoporosis that develops during adulthood since it carries the potential for many more years of disability. Avoiding childhood osteoporosis is an important goal. Rushing to treat “osteoporosis” in children using adult definitions and drug protocols is, however, potentially dangerous. The report by Roth and colleagues in this issue of Arthritis & Rheumatism (3) illustrates the difficulty of diagnosing bone metabolism disorders in childhood. The most commonly used technology for the diagnosis of osteoporosis is measurement of bone mineral density (BMD) using dual x-ray absorptiometry (DXA). DXA scanning is frequently used because it is accurate, reproducible, fast, and delivers a low radiation dose. Unfortunately, however, as noted by Roth et al, DXA scans are limited by their ability to obtain only a 2-dimensional measure of the 3-dimensional bone. Two bones of identical “true density,” but of differing size, will yield different BMD readings; the smaller bone will have a lower reading compared with the larger bone (4). In addition, specialized software in the DXA machine is needed to make appropriate comparisons in pediatric populations. Without this software, a child’s BMD result is compared with that of a normal young adult’s peak bone mass. The resultant T score is an underestimate of actual bone mass accrual. With the correct software, the BMD result is compared with that of an age-appropriate reference value, with a resultant and more accurate Z score. Most physicians with expertise in childhood osteoporosis have had the experience of having a child referred for “osteoporosis” where the BMD was measured and compared with adult normative data, with the reported T score in the osteoporotic range. In fact, the child’s BMD may have actually been normal when appropriately compared with age-matched pediatric normative data. There are available normative data for the lumbar spine and total body, but DXA machines do not have pediatric norms for the hip. Newer technologies, such as calcaneal ultrasound measurement, are not yet fully validated in diagnosis of adult osteoporosis and do not have large databases in order to determine normative values in children (5). Measurement of BMD in children is further complicated by the wide variation of age at onset and progression of puberty. This leads to a wide variation in the age at attainment of peak bone mass. The presence of a chronic disease, such as juvenile arthritis, is thought to delay pubertal onset and development. It has been estimated that one-third to one-half of the total mineralization in the lumbar spine in adult women is accumulated during the 3 years around the onset of puberty C. Egla Rabinovich, MD, MPH: Duke University Medical Center, Durham, North Carolina. Address correspondence and reprint requests to C. Egla Rabinovich, MD, MPH, Division of Pediatric Rheumatology, Duke University Medical Center, 044 Bell Building, Box 3212 DUMC, Durham, NC 27710. E-mail: rabin001@mc.duke.edu. Submitted for publication September 3, 2003; accepted in revised form December 17, 2003.