The clinical contribution of cortical porosity to fragility fractures

Abstract

Cortical bone is not compact; rather it is penetrated by many Haversian and Volkmann canals for blood supply. The lining of these canals are the intracortical bone surfaces available for bone remodeling. Increasing intracortical bone remodeling increases cortical porosity. However, cortical bone loss occurs more slowly than trabecular loss due to the fact that less surface per unit of bone matrix volume is available for bone remodeling. Nevertheless, most of the bone loss over time is cortical because cortical bone constitutes 80% of the skeleton, and the relative proportion of trabecular bone diminishes with advancing age. Higher serum levels of bone turnover markers are associated with higher cortical porosity of the distal tibia and the proximal femur. Greater porosity of the distal radius is associated with higher odds for forearm fracture, and greater porosity of the proximal femur is associated with higher odds for non-vertebral fracture in postmenopausal women. Measurement of cortical porosity contributes to fracture risk independent of areal bone mineral density and Fracture Risk Assessment Tool. On the other hand, antiresorptive treatment reduces porosity at the distal radius and at the proximal femoral shaft. Thus, porosity is a substantial determinant of the bone fragility that underlies the risk of fractures and may be a target for fracture prevention.