Evidence map›Paper›PMID 37117332›Full record

ArticleScientific reports2023

Smoking induces increased apoptosis in osteoblasts: changes in bone matrix organic components.

Júlia Benini Kohler, Alex Ferreira da Silva, Walleson Alves Farias, Barbara Fialho Carvalho Sampaio, Marco Aurélio Silveiro Neves, Leandro Gregorut Lima, Juliana Dias Lourenço, Alyne Riani Moreira, Alexandre Póvoa Barbosa, Iolanda de Fátima Lopes Calvo Tibério and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 19% 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, 9 citations in OpenAlex.

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  8. 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

12 authors at 2 institutions in 1 country.

Júlia Benini KohlerDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Alex Ferreira da SilvaDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Walleson Alves FariasDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Barbara Fialho Carvalho SampaioDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Marco Aurélio Silveiro NevesDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Leandro Gregorut LimaDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Juliana Dias LourençoDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Alyne Riani MoreiraDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Alexandre Póvoa BarbosaDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Iolanda de Fátima Lopes Calvo TibérioDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Walcy Rosolia TeodoroRheumatology Division of the Hospital das Clinicas FMUSP, School of Medicine, University of Sao Paulo, São Paulo, Brazil.
Fernanda Degobbi Tenorio Quirino Dos Santos LopesDepartment of Clinical Medicine, Laboratory of Experimental Therapeutics (LIM-20), School of Medicine, University of Sao Paulo, São Paulo, Brazil. fernandadtqsl@gmail.com.
Universidade de São Paulo · BRHospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical studies demonstrate the impact of smoking on bone tissue fragility and higher incidence of fractures. However, it is not totally understood which physiological mechanisms could be involved in these events. Previously, we showed important changes in bone tissue components in experimental model of cigarette smoke (CS) exposure. CS exposure induces worsening in bone mineralization and a decrease in collagen type I deposition, leading to bone fragility. Considering that the majority of clinical studies described bone structural changes by radiographic images, in this study we performed analyses "in situ" using tissue samples from smokers, former smokers and non-smokers to better understand how the increase in inflammatory mediators induced by smoking exposure could interfere in bone cells activity leading bone structural changes. We observed increased levels of IL-1β, IL-6 and TNF-α in bone tissue homogenates with a concomitant increase in osteoblast apoptosis in smokers and former smokers compared with non-smokers. Histological changes in both smokers and former smokers were characterized by reduction in collagen type I. Only in smokers, it was observed decrease in trabecular area, suggesting increased bone resorption and increase in collagen type V. These results showed that osteoblasts apoptosis in association with increased bone resorption leads bone structural changes in smokers.

Indexed as

Bone ResorptionCollagen Type IApoptosisBone MatrixHumansOsteoblastsSmokingCollagen Type I

Identifiers

PMID37117332
PMCPMC10147676
OpenAlexW4367298036

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.