Abstract:
Abstract for poster P25 presented at Bone Research Society, Winchester 28/6/2018 All that fractures is not bone: microscopic anatomy of vertebral bodies.
Objectives:
To understand interface between cortical shell and cancellous bone in human vertebral bodies, age changes, and probable mechanical significance. Archival material, 3-4 mm mid-body vertical slices, 80 L2 embedded PMMA: blocks polished, carbon coated, 20 kV qBSE SEM; high contrast resolution x-ray microtomography (XMT: 44 hour scans); iodine vapour staining and further BSE SEM, uncoated. Some 10µm laser ablation machined sections from block surfaces for polarised light microscopy (PLM). 50 L4 macerated for 3D BSE SEM. Mineral concentration: cortex contains lamellar bone and more highly mineralised tissues: ligament, dense fibrous periosteum, or Sharpey fibre bone. 2D SEM with iodine staining, PLM: uncalcified osteoid, ligament, fibrous periosteum, and Sharpey fibres can be distinguished. 3D SEM: inimitable branching bundle morphology of bone collagen lamellae was displayed on all (re)modelled surfaces of trabeculae and endocortex, modified where penetrated by any Sharpey fibres at ectocortex. However, the greatest part of the most exterior cortex is composed of strictly parallel ─ non-branching ─ collagen, either mostly longitudinal ─ ligament ─ or decussating layers of dense fibrous periosteum. Ligament tissue becomes incorporated in the bone organ by calcification extending into it from the mineralising front of bone tissue proper. Owing to endocortical resorbtion, sections of the entire shell thickness can be composed of non-bone. Calcified tissues in vertebral cortical shells include matrices which are, emphatically, not bone: they have a different structure, their collagen is not made by osteoblasts, and generally reach a higher level of mineralisation than bone: they will be assessed as ’thicker bone’ with CT. Further, these phases cannot be recognised from bone by clinical imaging, and it is highly improbable that they will be distinguished using decalcification and staining LM histology. If lamellar structure is ideal, then the anterior cortex in particular is not. The proportion of calcified ligament tissue masquerading as bone dramatically increases in anterior collapse, often in hand with thickening of this cortex. It remains to be elucidated whether failure is favoured by this less auspicious and perhaps more fragile structure. A vicious circle?