Evidence map›Paper›PMID 22691115›Full record

ArticleAlcoholism, clinical and experimental research2012

Acute alcohol exposure impairs fracture healing and deregulates β-catenin signaling in the fracture callus.

Kristen L Lauing, Philip M Roper, Rachel K Nauer, John J Callaci

Abstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
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

30 citing papers in PubMed, 53 citations in OpenAlex.

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  14. Review
  15. Molecular pathogenesis of fracture nonunion.Journal of orthopaedic translation · 2018
    Review
  16. Article
  17. Development of controlled drug delivery systems for bone fracture-targeted therapeutic delivery: A review.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2018
    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

4 authors at 1 institution in 1 country.

Kristen L LauingBurn and Shock Trauma Institute, Loyola University Stritch School of Medicine, Maywood, Illinois 60153, USA. klauing@lumc.edu
Philip M Roper
Rachel K Nauer
John J Callaci
Loyola University Chicago · US

Funding

Training in Neuroimmunoendocrine Effects of AlcoholT32AA013527 · NIAAA · LOYOLA UNIVERSITY CHICAGO · PI CHOUDHRY, MASHKOOR A · 2002 to 2021
$4.4M
Classifying Binge Alcohol-Induced Bone DamageR01AA016138 · NIAAA · LOYOLA UNIVERSITY CHICAGO · PI CALLACI, JOHN J. · 2006 to 2009
$987k
The effects of acute binge alcohol exposure on the canonical Wnt signaling pathwaF31AA019613 · NIAAA · LOYOLA UNIVERSITY CHICAGO · PI LAUING, KRISTEN LEIGH · 2010 to 2011
$56k
NIAAA NIH HHS F31 AA019613NIAAA NIH HHS R01 AA016138NIAAA NIH HHS T32 AA013527PHS HHS T32 013527
6 · The paper itself

Abstract

backgroundAlcohol abuse is a risk factor for bone damage and fracture-related complications. Through precise β-catenin signaling, canonical Wnt signaling plays a key role in fracture repair by promoting the differentiation of new bone and cartilage cells. In this study, we examined the effects of alcohol on the Wnt pathway in injured bone using a murine model of alcohol-induced impaired fracture healing.

methodsMale C57Bl/6 or T cell factor (TCF)-transgenic mice were administered 3 daily intraperitoneal doses of alcohol or saline. One hour following the final injection, mice were subjected to a stabilized, mid-shaft tibial fracture. Injured and contralateral tibias were harvested at 6, 9, or 14 days post-fracture for the analysis of biomechanical strength, callus tissue composition, and Wnt/β-catenin signaling.

resultsAcute alcohol treatment was associated with a significant decrease in fracture callus volume, diameter, and biomechanical strength at day 14 post-fracture. Histology revealed an alcohol-related reduction in cartilage and bone formation at the fracture site, and that alcohol inhibited normal cartilage maturation. Acute alcohol exposure caused a significant 2.3-fold increase in total β-catenin protein at day 6 and a significant decrease of 53 and 56% at days 9 and 14, respectively. lacZ staining in β-galactosidase-expressing TCF-transgenic mice revealed spatial and quantitative differences in Wnt-specific transcriptional activation at day 6 in the alcohol group. Days 9 and 14 post-fracture showed that acute alcohol exposure decreased Wnt transcriptional activation, which correlates with the modulation of total β-catenin protein levels observed at these time points.

conclusionsAcute alcohol exposure resulted in significant impairment of fracture callus tissue formation, perturbation of the key Wnt pathway protein β-catenin, and disruption of normal Wnt-mediated transcription. These data suggest that the canonical Wnt pathway is a target for alcohol in bone and may partially explain why impaired fracture healing is observed in alcohol-abusing individuals.

Indexed as

Animalsbeta CateninBony CallusEthanolFracture HealingMaleMiceMice, Inbred C57BLMice, TransgenicTibial FracturesWnt Signaling Pathwaybeta CateninEthanol

Identifiers

PMID22691115
PMCPMC3443513
OpenAlexW2121112046

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.