Evidence map›Paper›PMID 33538965›Full record

ReviewCurrent osteoporosis reports2021

Osteoarthritis: Insights Offered by the Study of Bone Mass Genetics.

A Hartley, C L Gregson, L Paternoster, J H Tobias

Open access · hybridAbstract readReview
In one paragraph

Review in Current osteoporosis reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 3 pooled it
1.7field-weighted citation impact, top 16% of its field
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

8 citing papers in PubMed, 3 syntheses or guidelines pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Epigenetic Patterns in Musculoskeletal Disease: Methylation ofCurrent issues in molecular biology · 2026
    Article
  5. Article
  6. Review
  7. [Finite element analysis of the impact of bone mass and volume of low-density area under tibial plateau on lower limb alignment].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2024
    Article
  8. Article
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

4 authors at 2 institutions in 1 country.

A HartleyMusculoskeletal Research Unit, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK.
C L GregsonMusculoskeletal Research Unit, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK.
L PaternosterMRC Integrated Epidemiology Unit, Bristol Medical School, University of Bristol, Bristol, UK.
J H TobiasMusculoskeletal Research Unit, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK. Jon.Tobias@bristol.ac.uk.ORCID 0000-0002-7475-3932
University of Bristol · GBAt Bristol · GB

Funding

Medical Research Council MC_UU_00011/1Versus Arthritis 20000Wellcome TrustWellcome Trust 20378/Z/16/Z
6 · The paper itself

Abstract

purpose of reviewThis paper reviews how bone genetics has contributed to our understanding of the pathogenesis of osteoarthritis. As well as identifying specific genetic mechanisms involved in osteoporosis which also contribute to osteoarthritis, we review whether bone mineral density (BMD) plays a causal role in OA development. RECENT

findingsWe examined whether those genetically predisposed to elevated BMD are at increased risk of developing OA, using our high bone mass (HBM) cohort. HBM individuals were found to have a greater prevalence of OA compared with family controls and greater development of radiographic features of OA over 8 years, with predominantly osteophytic OA. Initial Mendelian randomisation analysis provided additional support for a causal effect of increased BMD on increased OA risk. In contrast, more recent investigation estimates this relationship to be bi-directional. However, both these findings could be explained instead by shared biological pathways. Pathways which contribute to BMD appear to play an important role in OA development, likely reflecting shared common mechanisms as opposed to a causal effect of raised BMD on OA. Studies in HBM individuals suggest this reflects an important role of mechanisms involved in bone formation in OA development; however further work is required to establish whether the same applies to more common forms of OA within the general population.

Indexed as

Bone DensityGenetic Predisposition to DiseaseHumansOsteoarthritisBone mineral densityGeneticsHigh bone massOsteoarthritis

Identifiers

PMID33538965
PMCPMC8016765
OpenAlexW3128364939

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.