Evidence map›Paper›PMID 24526374›Full record

ArticleHormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme2014

Testosterone regulates bone response to inflammation.

J P Steffens, B S Herrera, L S Coimbra, D N Stephens, C Rossa, L C Spolidorio, A Kantarci, T E Van Dyke

Abstract read
In one paragraph

Article in Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 3 pooled it
2.8field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 3 syntheses or guidelines pooled it, 40 citations in OpenAlex.

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  8. The Metabolic Syndrome, a Human Disease.International journal of molecular sciences · 2024
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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

8 authors at 2 institutions in 1 country.

J P SteffensDepartment of Physiology and Pathology, School of Dentistry at Araraquara - UNESP, São Paulo State University, -Araraquara, SP, Brazil.
B S HerreraDepartment of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA, USA.
L S CoimbraDepartment of Physiology and Pathology, School of Dentistry at Araraquara - UNESP, São Paulo State University, -Araraquara, SP, Brazil.
D N StephensDepartment of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA, USA.
C RossaDepartment of Physiology and Pathology, School of Dentistry at Araraquara - UNESP, São Paulo State University, -Araraquara, SP, Brazil.
L C SpolidorioDepartment of Physiology and Pathology, School of Dentistry at Araraquara - UNESP, São Paulo State University, -Araraquara, SP, Brazil.
A KantarciDepartment of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA, USA.
T E Van DykeDepartment of Applied Oral Sciences, Center for Periodontology, The Forsyth Institute, Cambridge, MA, USA.
Centro Universitário de Araraquara · BRUniversidade Estadual Paulista (Unesp) · BR

Funding

Neutrophils and Periodontitis in DiabetesR01DE015566 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI VAN DYKE, THOMAS ELLIOTT · 2005 to 2014
$4.2M
Pathological basis of MRS and DTI changes in neurodegenerative dementiaR01AG040042 · NIA · MAYO CLINIC ROCHESTER · PI KANTARCI, KEJAL · 2011 to 2015
$1.6M
Hypoxia and PMN Function in PeriodontitisR21DE020906 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI KANTARCI, IBRAHIM ALPDOGAN · 2011 to 2012
$478k
NIA NIH HHS R01 AG040042NIDCR NIH HHS DE015566NIDCR NIH HHS DE020906NIDCR NIH HHS R01 DE015566NIDCR NIH HHS R21 DE020906
6 · The paper itself

Abstract

This study evaluated the alveolar bone response to testosterone and the impact of Resolvin D2 (RvD2) on testosterone-induced osteoblast function. For the in vivo characterization, 60 male adult rats were used. Treatments established sub-physiologic (L), normal (N), or supra-physiologic (H) concentrations of testosterone. Forty rats were subjected to orchiectomy; 20 rats received periodical testosterone injections while 20 rats received testicular sham-operation. Four weeks after the surgeries, 10 rats in each group received a subgingival ligature around the lower first molars to induce experimental periodontal inflammation and bone loss. In parallel, osteoblasts were differentiated from neonatal mice calvariae and treated with various doses of testosterone for 48 h. Cell lysates and conditioned media were used for the determination of alkaline phosphatase, osteocalcin, RANKL, and osteoprotegerin. Micro-computed tomography linear analysis demonstrated that bone loss was significantly increased for both L and H groups compared to animals with normal levels of testosterone. Gingival IL-1β expression was increased in the L group (p<0.05). Ten nM testosterone significantly decreased osteocalcin, RANKL, and OPG levels in osteoblasts; 100 nM significantly increased the RANKL:OPG ratio. RvD2 partially reversed the impact of 10 nM testosterone on osteocalcin, RANKL, and OPG. These findings suggest that both L and H testosterone levels increase inflammatory bone loss in male rats. While low testosterone predominantly increases the inflammatory response, high testosterone promotes a higher osteoblast-derived RANKL:OPG ratio. The proresolving mediator RvD2 ameliorates testosterone-derived downregulation of osteocalcin, RANKL, and OPG in primary murine osteoblasts suggesting a direct role of inflammation in osteoblast function.

Indexed as

Alkaline PhosphataseAnimalsBone and BonesCells, CulturedCytokinesDocosahexaenoic AcidsDown-RegulationInflammationMaleMiceOsteoblastsOsteocalcinOsteoprotegerinPeriodontal DiseasesRANK LigandRatsAlkaline PhosphataseCytokinesDocosahexaenoic AcidsOsteocalcinOsteoprotegerinRANK Ligandresolvin D2Testosterone

Identifiers

PMID24526374
PMCPMC4522923
OpenAlexW1972929597

What OpenQuestion holds

Textmetadata
LicenceTDM
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.