You've heard of remodeling your kitchen. How about remodeling your bones? According to Carol Gay, a professor of cellular biology, bones are in constant repair, involved in a process she calls "bone remodeling."
Technically called resorption, the process begins in the parathyroid gland. This gland in your neck measures the concentration of calcium ions necessary for nerve stimulation and muscle contraction. Normally, your body has only 10 milligrams of calcium ions per 100 milliliters of blood, like a pinch of sugar in a cup of tea. But if the gland senses even a one percent drop in calcium concentration, it sends a parathyroid hormone to stimulate cells called osteoclasts (osteo means bone, and clast means resorbing, or dissolving).
"It has been suspected that there were bone resorbing cells for over 100 years," comments Gay. Looking at a cross-section of bone under a microscope, scientists in the 1870's saw osteoclasts at work. Under the high-powered microscope Gay uses, an osteoclast coming in contact with a bone begins to look like the blade of a saw, weppj of bone as big as itself, then floats off, leaving a pit or pocket in the bone.
Cartilage cells grown for joint replacment. Bright staining matrix surrounds dark cells.
In come the osteoblasts (blast means forming), which cluster along the bone, gradually filling in the pocket. But while an osteoclast needs only a few days to form the pit (just like it's easy to rip out old kitchen cabinets), osteoblasts require months to refill it. And the bone's carpenters might walk out on the job: "Sometimes," Gay explains, "osteoblasts don't completely refill the pit, weakening the bone. This leads to osteoporosis." A porous bone, full of these pits, is easy to fracture, especially in the spine, hip, and wrists, and it heals very slowly. To help develop prevention measures, Gay is testing osteoclasts grown in culture, to see what hormones stimulate or inhibit the resorption process.
She and colleague, Roland Leach, professor of poultry science, for instance, have noticed a similarity between the parathyroid hormone that triggers the remodeling process and a related protein that starts and regulates the growth in cartilage tissue.
"The long bones in the body develop from a cartilage model," Gay explains. During fetal development, the skeleton is all cartilage, and as the baby grows, cartilage is replaced by bone. Adults only have a small amount of cartilage left at the ends of bones, forming joints.
"Chondrocytes are the cells found in cartilage," explains Leach. "These cells are responsible for maintaining a sponge-like matrix which surrounds them. When you walk your joints are squishing." If those joints wear out, osteoarthritis—a painful inflammation commonly treated surgically with joint replacement—is often the result.
Leach studies cartilage cell metabolism to learn how we might craft replacements for hips and other joints using natural cartilage. "Cartilage cells in the body aren't in direct contact with one another," he explains. "On a human scale, they would be at a distance of about ten miles, with tissue connecting them, like a highway." Only when the cells multiply do they come in contact. By generating cells in culture, and then spreading them apart to build a rigid "highway" matrix, researchers might "grow" cartilage—the key to natural joint replacement.
Knowing how this process works at the cellular level may alert physicians to problems before they begin. Just like we update our kitchens every few years, we might someday remodel our bones to better suit our lifestyles.
Carol Gay, Ph.D., is professor of cell biology in the Eberly College of Science, 468 A North Frear Bldg, University Park, PA, 16802; 814-865-6722; cvg1@psu.edu. Roland Leach, Ph.D., is professor of poultry science in the College of Agricultural Sciences, 205 Henning Building, 865-5802; lnr@psu.edu. Their research is funded by BARD Bi-National Agricultural Research.