Evidence map›Paper›PMID 28062525›Full record

ArticleBone & joint research2017

Parathyroid hormone 1-34 and skeletal anabolic action: The use of parathyroid hormone in bone formation.

L Osagie-Clouard, A Sanghani, M Coathup, T Briggs, M Bostrom, G Blunn

Open access · goldAbstract read
In one paragraph

Article in Bone & joint research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Romosozumab versus teriparatide and risk of all-cause mortality in patients with osteoporosis: a real-world propensity score-matched cohort study.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
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  12. Employing Indirect Adenosine 2Journal of functional biomaterials · 2023
    Article
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  15. Review
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  17. Article
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  19. Article
  20. The Development of Molecular Biology of Osteoporosis.International journal of molecular sciences · 2021
    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

6 authors at 3 institutions in 2 countries.

L Osagie-ClouardInstitute of Orthopaedics and Musculoskeletal Sciences, University College London, Royal National Orthopaedic Hospital, Stanmore, Middlesex HA7 4LP, London, UK l.osagie@ucl.ac.uk.
A SanghaniInstitute of Orthopaedics and Musculoskeletal Sciences, University College London, Royal National Orthopaedic Hospital, Stanmore, Middlesex HA7 4LP, London, UK.
M CoathupInstitute of Orthopaedics and Musculoskeletal Sciences, University College London, Royal National Orthopaedic Hospital, Stanmore, Middlesex HA7 4LP, London, UK.
T BriggsInstitute of Orthopaedics and Musculoskeletal Sciences, University College London, Royal National Orthopaedic Hospital, Stanmore, Middlesex HA7 4LP, London, UK.
M BostromHospital for Special Surgery, New York, New York, USA.
G BlunnInstitute of Orthopaedics and Musculoskeletal Sciences, University College London, Royal National Orthopaedic Hospital, Stanmore, Middlesex HA7 4LP, London, UK.
Royal National Orthopaedic Hospital · GBUniversity College London · GBHospital for Special Surgery · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intermittently administered parathyroid hormone (PTH 1-34) has been shown to promote bone formation in both human and animal studies. The hormone and its analogues stimulate both bone formation and resorption, and as such at low doses are now in clinical use for the treatment of severe osteoporosis. By varying the duration of exposure, parathyroid hormone can modulate genes leading to increased bone formation within a so-called 'anabolic window'. The osteogenic mechanisms involved are multiple, affecting the stimulation of osteoprogenitor cells, osteoblasts, osteocytes and the stem cell niche, and ultimately leading to increased osteoblast activation, reduced osteoblast apoptosis, upregulation of Wnt/β-catenin signalling, increased stem cell mobilisation, and mediation of the RANKL/OPG pathway. Ongoing investigation into their effect on bone formation through 'coupled' and 'uncoupled' mechanisms further underlines the impact of intermittent PTH on both cortical and cancellous bone. Given the principally catabolic actions of continuous PTH, this article reviews the skeletal actions of intermittent PTH 1-34 and the mechanisms underlying its effect. CITE THIS ARTICLE: L. Osagie-Clouard, A. Sanghani, M. Coathup, T. Briggs, M. Bostrom, G. Blunn. Parathyroid hormone 1-34 and skeletal anabolic action: The use of parathyroid hormone in bone formation. Bone Joint Res 2017;6:14-21. DOI: 10.1302/2046-3758.61.BJR-2016-0085.R1.

Indexed as

AnabolicBone formationParathyroid hormone

Identifiers

PMID28062525
PMCPMC5227055
OpenAlexW2569948192

What OpenQuestion holds

Textmetadata
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.