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All materials undergo an aging process which is characterized essentially by changes of the rigidity (stiffness), of the ability to absorb the stresses (toughness) and then ultimately in the mechanical resistance (strength). Both cortical and trabecular bone undergo a continuous process of structural remodeling with the main aim to preserve their biomechanical properties. An imbalance in this process, which promotes bone resorption, results in a quantitative loss of bone tissue and in a qualitative alteration of the skeletal microarchitecture, as you can see in osteoporosis, rheumatoid arthritis or bone metastases. Cortical component has a prominent role on strength therefore loss of cortical bone that is prevalent in elderly may explain the higher frequency of fractures of bones composed mainly of cortical bone such as the proximal femur. Remodeling inhibition with denosumab improved structural strength without altering material properties, that can be primarily explained by the combined effects of increased trabecular and cortical bone mass, and reductions in trabecular eroded surfaces and particularly cortical porosity. Denosumab for its mechanism of action and pharmacokinetics results in a significant, early and continued increase in BMD with enhanced bone strength improving both cortical and trabecular bone.

The contribution of cortical and trabecular tissues to bone strength: insights from denosumab studies