title: Role of cortical bone in bone fragility.
abstract: OBJECTIVE
  Trabecular bone loss and vertebral fractures are historical hallmarks of osteoporosis. During the past 70 years, this view has dominated research aiming to understand the structural basis of bone fragility. We suggest this notion needs to be revised to recognize and include the role of cortical bone deterioration as an important determinant of bone strength throughout life.
  
  
  RESULTS
  About 80% of the fragility fractures involve the appendicular skeleton, at regions comprising large amounts of cortical bone. Up to 70% of the age-related bone loss at these locations is the result of intracortical remodeling that cavitates cortical bone producing porosity. It is now possible to accurately quantify cortical porosity in vivo and use this information to understand the pathogenesis of bone fragility throughout life, assist in identifying patients at risk for fracture, and use this as a potential marker to monitor the effects of treatment on bone structure and strength.
  
  
  CONCLUSIONS
  Cortical bone has an important role in determining bone strength. The loss of strength is the result of intracortical and endocortical remodeling imbalance that produces cortical porosity and thinning. Studies are needed to determine whether porosity is an independent predictor of fracture risk and whether a reduction in porosity serves as a surrogate of antifracture efficacy.
authors.affiliation: aLaboratoire Vibration Acoustique, Institut National des Sciences Appliquées de Lyon, Campus LyonTech la Doua, Villeurbanne bINSERM UMR1033, Université de Lyon, Lyon, France cDepartment of Endocrinology dDepartment of Medicine, Austin Health, University of Melbourne, Melbourne, Australia.
authors.forename: Yohann
authors.initials: Y
authors.lastname: Bala
authors.forename: Roger
authors.initials: R
authors.lastname: Zebaze
authors.forename: Ego
authors.initials: E
authors.lastname: Seeman
mesh_terms: D015519:Bone Density / Q000502:physiology*; D016723:Bone Remodeling / Q000502:physiology*; D006801:Humans; D010024:Osteoporosis / Q000503:physiopathology; D058866:Osteoporotic Fractures / Q000503:physiopathology*; D016062:Porosity