Computational Structural Modelling to Assess the Effect of Diabetes on Bone Microarchitecture and Mechanical Properties

Diabetes has been linked to a reduction in bone turnover due to osteocyte apoptosis, decreasing rates of bone apposition by osteoblasts and bone resorption by osteoclasts to differing extents [1]. The combined effect of this disruption to mechanoregulation of bone architecture may lead both to a reduction in bone mineral density (BMD) and increased bone porosity due to thinning of cortical and trabecular bone, and to the retention of fatigued bone with reduced mechanical properties due to the accumulation of microcracks, compromising the structural integrity of affected joints. As well as directly influencing bone turnover, diabetes induced neuropathy is believed to alter muscle and joint contact forces acting on bone due to altered movement patterns and a reduction in proprioception. The presented study adapts a novel finite element modelling approach to predicting bone microarchitecture and bone adaptation in which trabecular bone is represented using beam elements and cortical bone is represented using shell elements [2] to assess the effect on joint integrity of altering bone mechanotransduction (through altering the target strain and strain range that bone adapts to); rates of bone apposition and resorption; and altered loading. The developed structural models allow joints and whole bones to be modelled at a level of refinement approaching that of micro-CT, providing an improved representation in comparison to CT derived continuum models which are not capable of fully representing the microarchitecture of bone. The developed models also allow for an assessment of altered fracture risk following bone adaptation [4]. The developed models suggest an increased response to a change in bone mechanotransduction in comparison to a change in loading, with trabecular and cortical thinning occurring with an increase in the mechanical stimulus required for mechanoregulation. This may be due to the exponential relationship between apparent and tissue level bone stiffness. The findings suggest that while exercise regimes play a role in maintaining bone health with a diagnosis of diabetes, this is likely due to a greater extent to the role of exercise in diabetes control, maintaining a healthy mechanotransduction response, than to exercise in directly maintaining muscle and joint contact forces. However, altered loading, including erratic loading due to a reduction in proprioception because of neuropathy, may still be a risk factor for developing osteoarthritis.