Osteoporosis (OP) is characterized by a reduction in bone quality, which is associated with inadequacies in bone marrow mesenchymal stromal cells (BMSCs).
These findings suggest that the AGE-RAGE system as a whole may affect bone quality, which is not determined by BMD.
Bone quality, which is a significant determinant of the survival rate of an implant, depends on the bone mineral density as well as the spatial structure of trabecular bone.
This conventional measurement was inadequate to evaluate volumetric bone density and bone quality which are important determinants for bone strength and bone health status as defined in the 2000 NIH consensus statement.
This definition is widely used today, but does not take into account bone microarchitecture and/or bone quality, which are much more difficult to define.
Further, inherent limitations exist with DXA, particularly the inability to measure true vertebral volumetric BMD - a parameter which may have demonstrated greater deficits in trabecular BMD between the groups - and indices of bone quality which are equally important as aBMD in mediating bone strength.
Bone strength depends not only on the quantity of bone mineral (BMD) but also on the quality, which is characterized by several factors including collagen content (and quality).
However, these measurements do not always provide an accurate fracture prediction, arguably because DXA does not grapple with 'bone quality', which is a combined result of microarchitecture, texture, bone tissue properties, past loading history, material chemistry and bone physiology in reaction to disease.
Therefore, the osteoporosis after SCI is mainly caused by the loss of trabecular bone quality, which can be characterized by decreased mechanical properties, altered chemical composition, and disarrangement of the bone tissue microarchitecture [ 6].
Results of bone material level properties using nanoindentation highlight the major deleterious effects of a low protein diet on humerus cortical bone quality, which have been already observed in previous studies [ 6].
This suggests two problems: an inherent limitation of measurement of aBMD with dual-energy x-ray absorptiometry (DXA) for clinical assessment of bone-fracture risk, and that glucocorticoids lead to deterioration of bone quality, which cannot be measured with the DXA measurements.
