title: Implications of architecture for the pathogenesis and prevention of vertebral fracture.
abstract: Rapid loss of cancellous bone after menopause occurs by a mechanism that removes some structural elements completely, leaving those that remain more widely separated and less well connected. Slow loss of cancellous bone continues by a mechanism that reduces the thickness of the structural elements that survive the initial phase of rapid loss. Both processes have advanced further in patients with vertebral compression fracture due to osteoporosis, than in healthy subjects of similar age; whether this is because they began sooner, proceeded more rapidly or continued for longer is unknown. This overall concept, first developed about ten years ago, has now been confirmed by a variety of different methods including node-strut analysis, star volume and the change in curvature with profile dilation. Because part of the architectural contribution to compressive strength is captured by non-invasive densitometric methods, and the contribution of cortical bone to compressive strength is significant, it has been difficult to demonstrate an independent architectural component of bone fragility by in vitro comparison of structural measurements with biomechanical testing. Nevertheless, three independent clinical studies, comparing subjects with and without vertebral fracture, have each strongly suggested an independent architectural contribution to fracture risk. Complete removal of structural elements is initiated by focal perforation of trabecular plates, but the mechanism of perforation remains controversial.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Bone and Mineral Research Laboratory, Henry Ford Hospital, Detroit, MI 48202.
authors.forename: A M
authors.initials: AM
authors.lastname: Parfitt
mesh_terms: D000367:Age Factors; D000375:Aging / Q000502:physiology; D016723:Bone Remodeling / Q000502:physiology*; D001862:Bone Resorption / Q000517:prevention & control*; D001842:Bone and Bones / Q000473:pathology*; D006801:Humans; D008954:Models, Biological; D016103:Spinal Fractures / Q000209:etiology* / Q000517:prevention & control