1) Established histomorphometry methods showed no distinction between fracture and nonfracture groups with the same bone volume. [ 3 ]

BUT a novel bespoke histology method [ 1 ] identified trabecular disconnection as 4 × more prevalent in fracture than nonfracture groups with the same bone volume. [ 3 ]

2) Trabecular disconnection relates primarily to tensile cross-strut microdamage [ 6 ], which unlike vertical strut damage rarely stimulates callus [ 13 ]. In embryogenesis, de novo cross-struts derive from a scaffold of Sharpey fibres while vertical struts derive from a cartilage model [ 27 ].

3) Trabecular disconnection is reduced by bisphosphonate drugs. [ 24 ]

4) Trabecular disconnection is age-related and its mapping pinpoints “hotspot” clusters of weakness that are sex- and sector-specific. [ 5 ]

5) Trabecular disconnection in predictable “hotspots” may release “floating bone segments” and function as “crumple zones” of controlled deformation. [ 5 ]

6) Trabecular disconnection “hotspots” are a biomechanical frontier, the gatekeeper to which may be periosteal Sharpey’s fibres (collagen Type III/VI); these regulate cross-strut microdamage, their uncalcified intraosseous presence protecting from osteoclasis. [ 16 ]

BUT periosteal Sharpey’s fibre arrays calcify and fragment with age; they expand with exercise and retract in oestrogen-deficiency; they atrophy prior to bone loss in osteoporosis and become hypertrophic in osteoarthritis. [ 17 - 19 ]