Struttin' Your Stuff
A filigree of slender, mineral-rich struts gives bone much of
its strength.
By Adam Summers ~ Illustrations by Sally
J. Bensusen
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.
Adam Summers is an assistant professor of ecology and evolutionalry
biology at the University of California, Irvine.