Evidence map›Paper›PMID 16303111›Full record

ReviewCurrent osteoporosis reports2005

Osteoprotegerin as a potential therapy for osteoporosis.

Neveen A T Hamdy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current osteoporosis reports, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 12 citations in OpenAlex.

  1. Genetics and Epigenetics of Bone Remodeling and Metabolic Bone Diseases.International journal of molecular sciences · 2022
    Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Neveen A T HamdyDepartment of Endocrinology & Metabolic Diseases, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands. n.a.t.hamdy@lumc.nl
Leiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The discovery and characterization of the RANKL/RANK/OPG signaling pathway and the identification of its role in the pathogenesis of bone loss have provided the rationale for the development of drugs with the ability to modulate RANK-induced osteoclastogenesis. In vivo studies have identified interfering with the RANKL/RANK interaction as a potential therapeutic target in the management of osteoporosis. Two agents capable of blocking the binding of RANKL to RANK have been so far tested in clinical studies--osteoprotegerin (Fc-OPG fusion molecule) and the RANKL-antibody (AMG 162). Both have been found to have profound inhibitory effects on bone resorption, with AMG 162 appearing to be overall superior to OPG. Data are still very scarce, however, and much remains to be uncovered before novel strategies capable of modulating the RANKL/OPG signaling pathway could be safely and effectively used in the management of osteoporosis.

Indexed as

AnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedBone Density Conservation AgentsDenosumabHumansOsteoporosisOsteoprotegerinRANK LigandSignal TransductionAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedBone Density Conservation AgentsDenosumabOsteoprotegerinRANK Ligand

Identifiers

PMID16303111
OpenAlexW3022185281

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.