Quality, Not Quantity, Determines Fracture

Scientists at Lawrence Berkeley National Laboratory have found evidence that bone quality plays a bigger role in fractures than bone quantity does. The researchers maintain that as people age, their bones lose the ability to resist the formation and growth of cracks, eventually leading to breaks.

It is widely believed that elderly people are more susceptible to injury because they have less bone mass than younger people, making their bones more likely to fracture. Yet, recent attempts have failed to find a direct relationship between changes in bone mineral density and the risk of bone fracture.

"We think bone quality is a more significant factor than bone mass when determining why bones fracture as people age," said Robert Ritchie, a scientist at Berkeley Lab and chairman of the UC Berkeley Department of Materials Science and Engineering. "Bone mass is probably only about 10 percent of the problem, but according to the drugs out there used to treat bone fractures, it's perceived to be 100 percent of the problem."

According to Ritchie, one in two women and one in four men over the age of 60 will suffer an age-related bone fracture in their lifetime. Doctors associate this statistic with the fact that bone mineral density decreases with age, but fail to consider other factors that may lead to this potentially fatal problem.

Ritchie and his colleagues were able to identify these other factors using Berkeley Lab facilities that yield extremely high resolution images such as the Advanced Light Source, where X-rays enable tomographic studies of materials. Tomagraphic studies assist in making 3-D objects of 2-D images.

Ritchie and his team used these tools to examine human cortical bone from cadavers of people aged 20, 40 to 50, and 90 to 100. Because bone is structurally unique at even the most microscopic scales, the scientists were examining collagen fibers that measured 50 to 70 nanometers in diameter. One nanometer is equivalent to one billionth of a meter.

The scientists found that the resistance of bone to the initiation of cracks fell by 40 percent over the age range examined. Among people age 70 and above, cortical bone completely lost the ability to resist the growth of an existing crack.

Using 3-D X-ray computed tomography images obtained at the Advanced Light Source and the Stanford Linear Accelerator Center, Ritchie found that the bones of younger people had large, unbroken regions of bone between their cracks, known as bridges, which act as support rods for the bone.

The amount of bridges found in the elderly was far less than younger people, making it easier for one tiny crack to connect to another, which could ultimately lead to a larger fracture.

Ritchie also found that microcracks appeared to initiate at the boundaries of osteons, or concentric rings of collagen fibrils that surround blood vessels in bone.

As a person gets older, their bones have excessive remodeling-the number of osteons in their bone increases. This means the more osteons there are, the closer they will be to the cracks, which is why there aren't as many bridges in older people.

Because their research is new and is still in the process of being developed, Ritchie and his colleagues are optimistic about its potential while maintaining a sense of realism about their project.

"We hope we will be able to predict bone disorders early. But if any drug treatments come out of our research, it is still a long way off," says Ritchie. "The real issue I'm concerned with is to understand the mechanism of bone fractures so we can understand what aspects are most important for the future."

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