Bone’s material strength is determined by its organic and inorganic constituents.  Bone’s structural strength is determined by the amount of material and its spatial distribution. At the molecular level, triple helices of type 1 collagen are assembled as fibrils containing mineral platelets connected by helical noncollagenous proteins. These proteins uncoil in tension dissipating energy by breaking (‘sacrificing’) hydrogen bonds and storing energy as ‘hidden length’ which minimizes strain on mineral platelets, brittle structures which must not deform. Accumulation of advanced glycation end-products interferes with energy absorption by limiting lengthening predisposing to the alternative means of energy dissipation; the occurrence of intraosteonal diffuse microdamage.

The mineralized collagen fibrils are organised as concentric lamellae orientated in different directions forming hemiosteons in trabecular bone, and osteons in cortical bone. Cement lines delineate osteons from each other and from the more fully mineralized and glycated interstitial (interosteonal) matrix, the location of linear microdamage. Osteonal density (number/unit volume), cement lines, concentric lamellae and the central fluid filled canal form ‘edges’ or ‘discontinuities’ that limit the occurrence and progression of microcracks as more energy is needed to propagate a microcrack through a heterogeneous than homogeneous material.   

Bone remodelling renews these bone qualities until it becomes unbalanced; trabeculae perforate, cortices thin and cavitate. In women, the rate, and so surface extent, of remodeling increases, but at the single basic multicellular unit (BMU) level, resorption depth decreases so osteons become smaller, reduced formation by each BMU produces fewer lamellae and leaves a larger central canal.  Osteons are less fully mineralized due to the rapidity of remodeling. Unremodelled interosteonal matrix becomes more fully mineralized and glycated.

The plurality of these traits is better captured by the term bone ‘qualities’ than ‘quality’. To quantify the contribution of the deterioration in these many qualities to bone fragility, unmet challenges in image acquisition and analyses need to be recognised and addressed.  If this is achieved, it may be possible to identify individuals at risk for fracture, to target therapy, and monitor its success or failure with high sensitivity and specificity.