BOSTON—In the mid-19th century, thousands of children in England and northern Europe were marked by abnormally large heads, twisted long bones, and enlarged wrists and ankles. These children had rickets—the softening of bones that leads to bone fractures and deformities—because sunlight deprivation and their bread-and-water diets didn’t provide enough calcium and vitamin D.
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Explore This IssueJuly 2008
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Rickets is still a problem today in developing countries. But, in the U.S., bone diseases like rickets, avascular necrosis (AVN), and osteoporosis are relatively rare in children. An estimated 30% to 40% of adults over 60 have osteoporosis, and incidence increases with age. But, as C. Egla Rabinovich, MD, co-chief of pediatric rheumatology at Duke University School of Medicine in Durham, N.C., noted, pediatric osteoporosis doesn’t even have its own Wikipedia page.
Recent evidence, however, suggests that the epidemiological roots of osteoporosis and avascular necrosis lie in childhood, according to speakers at a session called “Bone Health in Children and Adolescents with Rheumatic Disease,” at the ACR/ARHP Annual Scientific Meeting in Boston last November. The three experts—Dr. Rabinovich; Matthew Warman, MD, professor of orthopedic surgery at Children’s Hospital Boston; and Julian M. Aldridge, MD, assistant professor of surgery in the division of orthopedic surgery at Duke University Medical Center—also discussed what makes healthy bones, how this process is disrupted in children with bone diseases, and the controversy surrounding treatment options for children.
What Makes Healthy Bones?
In both children and adults, bones are constantly changing. Mesenchymal stem cells (MSCs) in the bone marrow constantly produce new osteoblasts while hematopoietic stem cells (HSCs) give rise to osteoclasts that resorb the old tissue.
But the process is even more dynamic in children than in adults because their bones are growing. During childhood—and particularly in infancy and adolescence—the process of formation by osteoblasts predominates, which leads to a net increase in bone mass and size. Our peak bone mass occurs right after puberty, and usually remains stable until at least age 30. After that, bone resorption by osteoclasts happens more rapidly, gradually increasing with age.
This situation makes childhood and adolescence critical times for optimizing bone growth, acquiring calcium, and, as Dr. Rabinovich put it, is “our best window of opportunity for preventing osteoporosis.” It’s also why pediatric osteoporosis is often called a “silent” disease, because the bone fractures it causes may not show up for many decades.
The session began with an overview of bone biology in children. Dr. Warman stressed first that doctors must remember that bone growth depends on both genetic and environmental factors. The trait for height, for instance, “has been increasing about an inch a generation since the late 1800s,” he said. “Our genes have actually not changed that much since then; therefore, determination of height is clearly has a strong environmental contribution.”