title: The effects of antifracture therapies on the components of bone strength: assessment of fracture risk today and in the future.
abstract: OBJECTIVE
  To summarize the current knowledge regarding the impact of the most common antifracture medications on the various determinants of bone strength.
  
  
  METHODS
  Relevant English-language articles acquired from Medline from 1966 to January 2005 were reviewed. Searches included the keywords bone AND 1 of the following: strength, remodeling, microcrack, structure, mineralization, collagen, organic, crystallinity, osteocyte, porosity, diameter, anisotropy, stress risers, or connectivity AND alendronate, estrogen, etidronate, hormone replacement therapy, parathyroid hormone, risedronate, OR teriparatide. Abstracts from relevant conference proceedings were also reviewed for pertinent information.
  
  
  RESULTS
  Antiresorptive therapies increase bone strength through decreasing bone turnover. This lower bone turnover results in a higher mean mineralization and decreases the number of active resorption pits within bone at any given time. These resorption pits are speculated to be areas of focal weakness and a higher number of them would, if all other things were equal, result in greater fragility. Parathyroid hormone therapy increases the rate of bone remodeling, which introduces many resorption pits, but this source of strength loss is thought to be compensated by rapid increases in bone mass.
  
  
  CONCLUSIONS
  Both the antiresorptives, particularly bisphosphonates, and the parathyroid hormone therapy increase bone strength; however, the changes that are elicited to achieve this differ significantly.
authors.affiliation: Clinical Research Scientist, Department of Medicine, Laval University, Sainte Foy, Quebec, Canada. ebmedicine@gmail.com
authors.forename: K Shawn
authors.initials: KS
authors.lastname: Davison
authors.forename: Kerry
authors.initials: K
authors.lastname: Siminoski
authors.forename: J D
authors.initials: JD
authors.lastname: Adachi
authors.forename: David A
authors.initials: DA
authors.lastname: Hanley
authors.forename: David
authors.initials: D
authors.lastname: Goltzman
authors.forename: Anthony B
authors.initials: AB
authors.lastname: Hodsman
authors.forename: Robert
authors.initials: R
authors.lastname: Josse
authors.forename: Stephanie
authors.initials: S
authors.lastname: Kaiser
authors.forename: Wojciech P
authors.initials: WP
authors.lastname: Olszynski
authors.forename: Alexandra
authors.initials: A
authors.lastname: Papaioannou
authors.forename: Louis-George
authors.initials: LG
authors.lastname: Ste-Marie
authors.forename: David L
authors.initials: DL
authors.lastname: Kendler
authors.forename: Alan
authors.initials: A
authors.lastname: Tenenhouse
authors.forename: Jacques P
authors.initials: JP
authors.lastname: Brown
mesh_terms: D015519:Bone Density / Q000187:drug effects*; D050071:Bone Density Conservation Agents / Q000627:therapeutic use*; D016723:Bone Remodeling / Q000502:physiology*; D001842:Bone and Bones / Q000187:drug effects / Q000293:injuries*; D002113:Calcification, Physiologic / Q000502:physiology*; D005598:Fractures, Spontaneous / Q000517:prevention & control*; D006801:Humans; D012307:Risk Factors
chemical_list: D050071:Bone Density Conservation Agents