Evidence map›Paper›PMID 32788914›Full record

ReviewEXCLI journal2020

Osteoporosis: Pathophysiology and therapeutic options.

Ursula Föger-Samwald, Peter Dovjak, Ursula Azizi-Semrad, Katharina Kerschan-Schindl, Peter Pietschmann

Abstract readReview
In one paragraph

Review in EXCLI journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

162 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. The role of CD8Frontiers in immunology · 2026
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102 more citing papers are in PubMed but not listed here.

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

5 authors.

Ursula Föger-SamwaldInstitute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Peter DovjakDepartment of Acute Geriatrics, Salzkammergut Klinikum Gmunden, Gmunden, Austria.
Ursula Azizi-SemradDepartment of Emergency Medicine, Medical University of Vienna, Vienna, Austria.
Katharina Kerschan-SchindlDepartment of Physical Medicine, Rehabilitation and Occupational Medicine, Medical University of Vienna, Vienna, Austria.
Peter PietschmannInstitute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis is a metabolic bone disease that, on a cellular level, results from osteoclastic bone resorption not compensated by osteoblastic bone formation. This causes bones to become weak and fragile, thus increasing the risk of fractures. Traditional pathophysiological concepts of osteoporosis focused on endocrine mechanisms such as estrogen or vitamin D deficiency as well as secondary hyperparathyroidism. However, research over the last decades provided exiting new insights into mechanisms contributing to the onset of osteoporosis, which go far beyond this. Selected mechanisms such as interactions between bone and the immune system, the gut microbiome, and cellular senescence are reviewed in this article. Furthermore, an overview on currently available osteoporosis medications including antiresorptive and bone forming drugs is provided and an outlook on potential future treatment options is given.

Indexed as

gut microbiomeosteoimmunologyosteoporosisosteoporosis treatmentpathophysiologysenescence

Identifiers

PMID32788914
PMCPMC7415937

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.