SAFETY FACTORS IN BONE STRENGTH

Functional in vivo strain data are examined in relation to bone materi al properties in an attempt to evaluate the relative importance of ost eoporotic bone loss versus fatigue damage accumulation as factors unde rlying clinical bone fragility. Specifically, does the skeleton have a sufficiently large safety factor (ratio of bone failure strain to max imum functional strain) to require that fatigue damage accumulation is the main factor contributing to increased risk of fracture in the eld erly? Existing methods limit in vivo strain measurements to the surfac es of cortical bone. Peak principal compressive strains measured at co rtical sites during strenuous activity in various mammalian and avian species range from -1700 to -5200 muepsilon, averaging -2500 muepsilon (-0.0025 strain). Much of this threefold variation reflects differenc es in the intensity of physical activity, as well as differences among species and bones that have been studied. Peak strains can also vary as much as tenfold at different cortical sites within the same bone. N o data exist for cortical bone strain during strenuous activity in hum ans, but it is likely that human bones experience a similar range of p eak strain levels. Compact bone fails in longitudinal compression at s trains as high as -14,000 to -21,000 muepsilon, but begins to yield at strains between -6000 and -8000 muepsilon. Given that yielding involv es rapid accumulation of microdamage within the bone, it seems prudent to base skeletal safety factors on the yield strain, rather than the ultimate failure strain of bone tissue. Safety factors to yield failur e therefore range from 1.4 to 4. 1. This safety factor range is likely diminished further by age-related increases in mineralization and sec ondary remodeling that reduce the strength and energy-absorbing capaci ty of bone. Although no one safety factor applies to all skeletal site s within an individual, it seems clear that osteoporotic bone loss of 40 to 50% of normal constitutes a causative factor of clinical bone fr agility, particularly if bone loss is high at sites of high functional strain. Theoretical consideration of the statistical distribution of bone strength in relation to functional loading events within a popula tion over a lifetime of use further supports this interpretation, by i ndicating an increased probability of fracture with increasing age. Fa tigue damage accumulation will serve to exacerbate these trends. Bone loss and fatigue damage accumulation therefore, should be viewed as mu tually reinforcing agents of bone fragility. Improved correlation of p eak functional strain patterns with localized bone loss and bone turno ver dynamics at sites of high fracture risk, together with assessment of microdamage, is needed to resolve the relative contribution of thes e factors to osteoporotic bone fragility.