Evidence map›Paper›PMID 25683519›Full record

ReviewJournal of biomechanics2015

American Society of Biomechanics Journal of Biomechanics Award 2013: cortical bone tissue mechanical quality and biological mechanisms possibly underlying atypical fractures.

Joseph R Geissler, Devendra Bajaj, J Christopher Fritton

Abstract readReview
In one paragraph

Review in Journal of biomechanics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Rebound-associated vertebral fractures after discontinuation of denosumab-from clinic and biomechanics.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2016
    Article
  12. Article
  13. Review
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Joseph R GeisslerDepartment of Orthopaedics, New Jersey Medical School, Rutgers University, 205 S. Orange Avenue, Newark, NJ 07103, USA; Joint Program in Biomedical Engineering, Rutgers Biomedical and Health Sciences, and the New Jersey Institute of Technology, Newark, NJ, USA. Electronic address: geissljr@rutgers.edu.
Devendra BajajDepartment of Orthopaedics, New Jersey Medical School, Rutgers University, 205 S. Orange Avenue, Newark, NJ 07103, USA. Electronic address: devendrabajaj@gmail.com.
J Christopher FrittonDepartment of Orthopaedics, New Jersey Medical School, Rutgers University, 205 S. Orange Avenue, Newark, NJ 07103, USA; Joint Program in Biomedical Engineering, Rutgers Biomedical and Health Sciences, and the New Jersey Institute of Technology, Newark, NJ, USA. Electronic address: chris.fritton@rutgers.edu.

Funding

Dynamic Analysis of Bone Tissue Biopsies after Treatment with BisphosphonatesR21AR063351 · NIAMS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI FRITTON, JAMES CHRISTOPHER · 2012 to 2013
$370k
NIAMS NIH HHS AR063351NIAMS NIH HHS R21 AR063351
6 · The paper itself

Abstract

The biomechanics literature contains many well-understood mechanisms behind typical fracture types that have important roles in treatment planning. The recent association of "atypical" fractures with long-term use of drugs designed to prevent osteoporosis has renewed interest in the effects of agents on bone tissue-level quality. While this class of fracture was recognized prior to the introduction of the anti-resorptive bisphosphonate drugs and recently likened to stress fractures, the mechanism(s) that lead to atypical fractures have not been definitively identified. Thus, a causal relationship between these drugs and atypical fracture has not been established. Physicians, bioengineers and others interested in the biomechanics of bone are working to improve fracture-prevention diagnostics, and the design of treatments to avoid this serious side-effect in the future. This review examines the mechanisms behind the bone tissue damage that may produce the atypical fracture pattern observed increasingly with long-term bisphosphonate use. Our recent findings and those of others reviewed support that the mechanisms behind normal, healthy excavation and tunnel filling by bone remodeling units within cortical tissue strengthen mechanical integrity. The ability of cortical bone to resist the damage induced during cyclic loading may be altered by the reduced remodeling and increased tissue age resulting from long-term bisphosphonate treatment. Development of assessments for such potential fractures would restore confidence in pharmaceutical treatments that have the potential to spare millions in our aging population from the morbidity and death that often follow bone fracture.

Indexed as

Awards and PrizesBiomechanical PhenomenaBone and BonesBone RemodelingDiphosphonatesFractures, BoneHumansOsteoporosisSocieties, ScientificUnited StatesDiphosphonatesAntiresorptivesBone remodelingOsteoblastsOsteoclastsOsteocytesOsteoporosis

Identifiers

PMID25683519
PMCPMC4380555

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.