Biomechanics of Bone: Determinants of Skeletal Fragility and Bone Quality

Abstract

Bone fragility can be defined by biomechanical parameters, including ultimate force (a measure of strength), ultimate displacement (reciprocal of brittleness) and work to failure (energy absorption). Bone fragility is influenced by bone size, shape, architecture and tissue 'quality'. Many osteoporosis treatments build bone mass but also change tissue quality. Antiresorptive therapies, such as bisphosphonates, substantially reduce bone turnover, impairing microdamage repair and causing increased bone mineralization, which can increase the brittleness of bone. Anabolic therapies, such as parathyroid hormone (PTH-(1-84)) or teriparatide (PTH-( 1-34)), increase bone turnover and porosity, which offset some of the positive effects on bone strength. Osteoporosis therapies may also affect bone architecture by causing the redistribution of bone structure. Restructuring of bone during treatment may change bone fragility, even in the absence of drug effects on bone mineral density (BMD). This effect may explain why some drugs can affect fracture incidence disproportionately to changes in BMD. For instance, in a recent clinical trial, PTH-(1-34) therapy caused a dose-related increase in spinal BMD without any dose-dependent effect on the observed decrease in spinal fracture incidence. This apparent disassociation between spinal BMD and bone fragility is probably due to effects of PTH-(1-34) on bone architecture within vertebral bodies. While it has been shown that BMD is highly heritable, bone mineral distribution and architecture are also under strong genetic influence. Recent findings suggest that different genes regulate trabecular and cortical structures within lumbar vertebrae, producing a wide range of bone architectural designs. These findings suggest that there is no single optimal bone architecture; instead many different architectural solutions produce adequate bone strength.

Age-related changes in the plasticity and toughness of human cortical bone at multiple length scales

“…Additionally, variability in both mineralization (48)(49)(50) and the local mineral content (51-53) due to disease or osteoporosis treatments are known to affect the mechanical properties and may play a role in aging. We believe that the age-related increase in microdamage originates at the fibrillar level; however, changes in the location (42) or nature (54,55) of microcracking with age may further reveal how this role of microcracking contributes to the toughness.…”

A demineralized calf vertebra model as an alternative to classic osteoporotic vertebra models for pedicle screw pullout studies

“…Hydroxyapatite crystals constitute the mineral components of bone [2,3,7,21]. The mechanical properties of the vertebra (stiffness, strain, ultimate load, etc.,) are related to the extent of mineralization of the bone matrix [7,22]. Currey [5] demonstrated that observed torsional strength is proportional to and most depended on mineral content.…”

Use of multiple acoustic wave modes for assessment of long bones: Model study

“…That is why the knowledge about changes in elastic properties and the effective thickness of the cortex are of equal diagnostic value for better assessment of different types of osteopenia and detecting osteoporosis development in long bones at earlier stages. Thinning of the cortex is one of the main indicators of decreasing total bone strength and capacity to withstand fracturing [12]. The elastic properties also can be altered by appearance of inner pores and accumulation of microcracks, as well as by degree of mineralization, i.e.…”