A filigree of slender, mineral-rich struts gives bone much of its strength.
Story by Adam Summers - Illustrations by Sally J. Bensusan
At about thirty years of age, the human skeleton is as heavy and strong as it will ever get. Then comes the downhill slide that for many people ends in osteoporosis (severe bone loss), crushed vertebrae, and fractured hips and wrists. But through studies of the internal architecture of bones and the ways they can fail, orthopedic biomechanics is setting a course for preventive measures and new treatments.
A typical bone consists of a hard outer shell surrounding a cavity filled with soft marrow tissue. Made of what is called cortical bone, the outer shell is remarkably thin. In the thighbone, or femur, for example—the longest, strongest bone in your body, running from the hip to the knee—the shell's thickness ranges from just two to eight millimeters. For most of the femur's length, the cavity is filled with fatty yellow marrow. At both ends, however, the last few inches of cavity are occupied by a meshwork of thin, mineralized struts called trabecular bone. The pores of this bone are filled with red marrow, which produces blood cells. Surprisingly, this bony filigree, which may fill in 30 percent of the open space, is responsible for most of the bone's overall strength.
The struts of trabecular bone are only about half as thick as pencil lead; their structural importance comes from their orientation and interconnections. The beauty of the arrangement of trabecular bone was noted in 1866 by a Swiss engineer, Karl Cullman, who happened upon the bisected head of a femur in a colleague's lab. "Why, that's my crane!" he is said to have exclaimed, and indeed, the pattern of struts in the bone would have looked remarkably like the pattern of girders in the heavy-duty crane Cullman had just designed for a loading dock. Further investigations of bones ranging from heels and wrists to vertebrae have revealed that struts tend to follow the lines of stress to which the bones are normally subjected. For example, most of the struts in the human heel are oriented so that they dissipate the impact associated with walking, while the orientation of the struts in the wing of a vulture counteracts the bones' tendency to bend during flapping.
Our bones develop from soft cartilage. Evidence of these cartilaginous beginnings can be seen in the soft spot in the center of a baby's skull or in the way a child tends to bounce where an adult would break—or at least hurt mightily. Most of our cartilage is gradually replaced by bone, which becomes more and more mineralized (and thus heavier) until reaching a peak in early middle age. Then, for reasons probably having to do with changing hormone levels, the rest of the body starts to extract calcium stored in the bones. (Our bodies use calcium as a signaling ion. Every time a muscle contracts, for example, huge numbers of calcium ions move through cell membranes. As we age, our bodies become less efficient at maintaining a constant level of calcium in the system and must mobilize it from the bones.) This natural process is especially rapid in postmenopausal women, leading in many cases to significant reductions in bone density and eventually to osteoporosis. An elderly woman with advanced osteoporosis might have just 50 percent of the bone mass she had in her early thirties.
We lose trabecular bone twice as fast as cortical bone. Recently, Tony Keaveny, a bioengineer at the University of California, Berkeley, uncovered an interesting wrinkle in trabecular bone loss. It turns out that not all struts are created—or rather, lost—equally. The most durable are those positioned to withstand the loads to which a bone is most often subjected. This helps explain why a hip that is still strong enough to carry the burden of everyday movements is far less able to withstand the stress of a fall.
Once enough bone mass has been lost, however, all trabecular struts—regardless of their orientation—are prone to failure. Keaveny has pioneered an unusual method for determining just how failure happens. With a high-resolution CAT scanner, he makes a computer model—accurate down to 0.015 inch—of a section of trabecular bone. Using a supercomputer, he "pushes on the model bone until it breaks." These simulations have led him to conclude that when trabecular bone is subjected to stress from the usual directions, failure (breakage) is primarily due to crushing. On the other hand, stresses that come from other directions force the struts to bend, reducing their effectiveness.
How might these insights aid efforts to repair bones weakened by mineral loss? Keaveny points out that while replacing an entire osteoporotic bone is impractical, strengthening or augmenting its trabecular struts might be possible. In their tissue-culture facility, he and his colleagues start with a sterile block of trabecular bone—the scaffolding—which they submerge in a solution of nutrients, osteoblasts (bone-building cells), and various growth factors. For the next several weeks to months, the researchers monitor the tissue culture with CAT scans and, if all goes well, track the development of new, mineralized material. Computer simulations can test how much strength the new growth has added. This combination of engineering, tissue culture, and basic biology has raised the possibility that one day, an injection of cells and growth factors may stimulate old bones to thicken their thinning struts.
Meanwhile, research shows that exercise helps make bones stronger and denser. So, baby boomers, to keep osteoporosis at bay, take the stairs, not the elevator, and keep lifting those weights.