Evidence map›Paper›PMID 16924451›Full record

ArticleZeitschrift fur Rheumatologie2006

[New pathophysological relevant metabolic pathways in osteoporosis. Future innovative therapies?].

E Neumann

Abstract readEnglish Abstract
PubMed Publisher
In one paragraph

Article in Zeitschrift fur Rheumatologie, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 50% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

1 author at 1 institution in 1 country.

E NeumannAbteilung für Innere Medizin mit Schwerpunkt Rheumatologie der Justus-Liebig-Universität Giessen, Abteilung für Rheumatologie und Klinische Immunologie, Kerckhoff-Klinik, Bad Nauheim. e.neumann@kerckhoff-klinik.de
University of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis is characterized by low bone mass and by changes in the microarchitecture of the bone. This leads to reduced bone stability and altered suscebtibility to fractures. Bone remodelling in healthy persons is characterized by a balance between bone resorption and bone formation. At the cellular level, bone remodelling is regulated by osteoclast and osteoblast activity. During bone loss, there is an imbalance, osteoclast activity being more pronounced. Therefore, the influende of estrogens, Wnt and the RANK/ RANKL/OPG system on osteoclastogenesis and osteoclast activity has been investigated. The RANK/RANKL/OPG-System is actively involved in the differentiation and function of osteoclasts and seems to play a central part in most pathophysiological mechanisms that are active in osteoporosis.

Indexed as

Bone DensityBone Density Conservation AgentsBone RemodelingHumansOsteoblastsOsteoclastsOsteoporosisOsteoprotegerinRANK LigandReceptor Activator of Nuclear Factor-kappa BBone Density Conservation AgentsOsteoprotegerinRANK LigandReceptor Activator of Nuclear Factor-kappa BTNFRSF11A protein, humanTNFSF11 protein, human

Identifiers

PMID16924451
OpenAlexW184473900

What OpenQuestion holds

Textmetadata
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.