title: The effect of antiresorptives on bone quality.
abstract: BACKGROUND
  Currently, antiresorptive therapy in the treatment and prevention of osteoporosis includes bisphosphonates, estrogen replacement, selective estrogen receptor modulators (raloxifene), and denosumab (a human antibody that inactivates RANKL). The original paradigm driving the development of antiresorptive therapy was that inhibition of bone resorption would allow bone formation to continue and correct the defect. However, it is now clear increases in bone density account for little of the antifracture effect of these treatments.
  
  
  OBJECTIVE
  We examined the antifracture benefit of antiresorptives deriving from bone quality changes.
  
  
  METHODS
  We searched the archive of nearly 30,000 articles accumulated over more than 40 years in our research center library using a software program (Refman™). Approximately 250 publications were identified in locating the 69 cited here.
  
  
  RESULTS
  The findings document antiresorptive agents are not primarily anabolic. All cause a modest increase in bone density due to a reduction in the bone remodeling space; however, the majority of their efficacy is due to suppression of the primary cause of osteoporosis, ie, excessive bone remodeling not driven by mechanical need. All of them improve some element(s) of bone quality.
  
  
  CONCLUSIONS
  Antiresorptive therapy reduces risk of fracture by improving bone quality through halting removal of bone tissue and the resultant destruction of microarchitecture of bone and, perhaps to some extent, by improving the intrinsic material properties of bone tissue. Information presented here may help clinicians to improve selection of patients for antiresorptive therapy by avoiding them in cases clearly not due to excessive bone remodeling.
authors.affiliation: Osteoporosis Research Center, Creighton University, 601 N 30th Street #5766, Omaha, NE 68131, USA. rrecker@creighton.edu
authors.forename: Robert R
authors.initials: RR
authors.lastname: Recker
authors.forename: Laura
authors.initials: L
authors.lastname: Armas
mesh_terms: D000911:Antibodies, Monoclonal / Q000187:drug effects / Q000494:pharmacology; D061067:Antibodies, Monoclonal, Humanized; D050071:Bone Density Conservation Agents / Q000494:pharmacology* / Q000627:therapeutic use; D016723:Bone Remodeling / Q000502:physiology; D001842:Bone and Bones / Q000187:drug effects* / Q000502:physiology; D000069448:Denosumab; D004164:Diphosphonates / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D008593:Menopause / Q000502:physiology; D053245:RANK Ligand / Q000187:drug effects / Q000494:pharmacology; D020845:Selective Estrogen Receptor Modulators / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D053245:RANK Ligand; D020845:Selective Estrogen Receptor Modulators; D000069448:Denosumab