Like we said...quality over quantity.

It is a well-established fact that as we grow older, our bones become more brittle and prone to fracturing. It is also well established that loss of mass is a major reason for older bones fracturing more readily than younger bones, hence medical treatments have focused on slowing down this loss. However, new research from scientists at the U.S. Department of Energy shows that at microscopic dimensions, the age-related loss of bone quality can be every bit as important as the loss of quantity in the susceptibility of bone to fracturing. Researchers showed that the advancement of age ushers in a degradation of the mechanical properties of human cortical bone over a range of different size scales. As a result, the bone's ability to resist fracture becomes increasingly compromised. This age-related loss of bone quality is independent of age-related bone mass loss.

Published in the Proceedings of the National Academy of Science (PNAS), the study explains that human cortical or compact bone is a composite of collagen molecules and nanocrystals of a mineralized form of calcium called hydroxyapatite (HA). Mechanical properties of stiffness, strength and toughness arise from both the characteristic structure at the nanoscale, and at multiple length scales through the hierarchical architecture of the bone. These length scales extend from the molecular level to the osteonal structures at near-millimeter levels. An osteon is the basic structural unit of compact bone, composed of a central canal surrounded by concentric rings of lamellae plates, through which bone remodels.

These features are present in healthy, young human bone and are responsible for its unique mechanical properties. However, with biological aging, the ability of these mechanisms to resist fracture deteriorates leading to a reduction in bone strength and fracture toughness. Working with bone samples that ranged in age between 34 and 99 years, they found that biological aging increases non-enzymatic cross-linking between the collagen molecules, which suppresses plasticity at nanoscale dimensions, meaning that collagen fibrils can no longer slide with respect to one another as a way to absorb energy from an impact. With age, remodeling of the bone can lead the osteons to triple in number, which means the channels become more closely packed and less effective at deflecting the growth of cracks. This growing ineffectiveness must be accommodated at higher structural levels by increased micro cracking. In turn, the increased micro cracking compromises the formation of crack bridges, which provide one of the main sources of extrinsic toughening in bone at length scales in the range of tens to hundreds of micrometers. Thus, age-related changes occur across many levels of the structure to increase the risk of fracture with age.

Bonnie - we have said for years that osteoporosis meds focus on just building quantity of bone, not quality. As this study shows, quality is just, if not more important, than quantity.