Evidence map›Paper›PMID 26439240›Full record

Trial reportOsteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA2016

Clonidine increases bone resorption in humans.

E J Limonard, T Schoenmaker, T J de Vries, M W Tanck, A C Heijboer, E Endert, E Fliers, V Everts, P H Bisschop

Open access · hybridAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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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

9 authors at 4 institutions in 1 country.

E J LimonardDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD, Amsterdam, Netherlands.
T SchoenmakerDepartment of Periodontology, Academic Centre for Dentistry Amsterdam, University of Amsterdam and VU University, MOVE Research Institute, Gustav Mahlerlaan 3004, 1081 LA, Amsterdam, Netherlands.
T J de VriesDepartment of Periodontology, Academic Centre for Dentistry Amsterdam, University of Amsterdam and VU University, MOVE Research Institute, Gustav Mahlerlaan 3004, 1081 LA, Amsterdam, Netherlands.
M W TanckDepartment of Clinical Epidemiology, Biostatistics and Bioinformatics, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD, Amsterdam, Netherlands.
A C HeijboerDepartment of Clinical Chemistry, Endocrine Laboratory, VU University Medical Center, PO Box 7057, 1007 MB, Amsterdam, Netherlands.
E EndertDepartment of Clinical Chemistry, Laboratory of Endocrinology, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD, Amsterdam, Netherlands.
E FliersDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD, Amsterdam, Netherlands.
V EvertsDepartment of Oral Cell Biology, Academic Centre for Dentistry Amsterdam, University of Amsterdam and VU University, MOVE Research Institute, Gustav Mahlerlaan 3004, 1081 LA, Amsterdam, Netherlands.
P H BisschopDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD, Amsterdam, Netherlands. p.h.bisschop@amc.uva.nl.
University of Amsterdam · NLAcademic Medical Center · NLAcademic Center for Dentistry Amsterdam · NLAmsterdam UMC Location VUmc · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

summaryInhibition of sympathetic signaling to bone reduces bone resorption in rodents. In contrast, we show that pharmacological reduction of the sympathetic tone increases bone resorption in humans in vivo. This effect does not appear to be mediated via a direct pharmacological effect on the osteoclast.

introductionInhibition of sympathetic signaling to bone reduces bone resorption in rodents. It is uncertain whether a similar role for the sympathetic nervous system exists in humans. The sympathetic tone can be reduced by clonidine, which acts via alpha-2-adrenergic receptors in the brainstem. Our objective was to determine the effect of clonidine on bone turnover in humans.

methodsThe acute effect of a single oral dose of 0.3 mg clonidine on serum bone turnover markers (C-terminal cross-linking telopeptides of collagen type I (CTx), a marker for bone resorption, and procollagen type 1 N propeptide (P1NP), a marker for bone formation) was determined in a randomized crossover design in 12 healthy volunteers, aged 18-70 years. In addition, we assessed the effect of clonidine on the number of tartrate-resistant acid phosphatase-positive multinucleated cells (TRAcP(+) MNCs) and bone resorption.

resultsCTx concentrations increased after clonidine treatment compared to the control condition (p = 0.035). P1NP concentrations were not affected by clonidine (p = 0.520). In vitro, clonidine had no effect on the number of TRAcP(+) MNCs (p = 0.513) or on bone resorption (p = 0.996).

conclusionsWe demonstrated that clonidine increases bone resorption in humans in vivo. This effect does not appear to be mediated via a direct effect on the osteoclast.

Indexed as

AdolescentAdultAgedAntihypertensive AgentsBiomarkersBone RemodelingBone ResorptionCells, CulturedClonidineCollagen Type ICross-Over StudiesFemaleHumansMaleMiddle AgedOsteoclastsAntihypertensive AgentsBiomarkersClonidineCollagen Type Icollagen type I trimeric cross-linked peptidePeptide FragmentsPeptidesProcollagenprocollagen Type I N-terminal peptideTartrate-Resistant Acid PhosphataseAlpha-2-adrenergic receptorBone turnoverOsteoclastSympathetic nervous system

Identifiers

PMID26439240
PMCPMC4767867
OpenAlexW1865104220

What OpenQuestion holds

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LicenceCC BY-NC
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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.