Evidence map›Paper›PMID 18757139›Full record

ReviewPathology, research and practice2008

Mechanisms modulating inflammatory osteolysis: a review with insights into therapeutic targets.

Shi Wei, Gene P Siegal

Abstract readReview
In one paragraph

Review in Pathology, research and practice, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. AggressiveThe Canadian veterinary journal = La revue veterinaire canadienne · 2026
    Article
  3. Article
  4. The mechanism and potential therapeutic target of piezo channels in pain.Frontiers in pain research (Lausanne, Switzerland) · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Ankle-brachial index and bone turnover in patients on dialysis.Journal of the American Society of Nephrology : JASN · 2015
    Article
  12. Article
  13. Article
  14. Article
  15. Lysine392, a K63-linked ubiquitination site in NEMO, mediates inflammatory osteoclastogenesis and osteolysis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2012
    Article
  16. Article
  17. Article
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

2 authors at 1 institution in 1 country.

Shi WeiDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL 35223, USA.
Gene P Siegal
University of Alabama at Birmingham · US

Funding

COG FOREIGN ACCRUALU10CA098543 · NCI · NATIONAL CHILDHOOD CANCER FOUNDATION · PI ADAMSON, PETER C. · 2003 to 2013
$335.5M
UAB Core Center for Musculoskeletal DisordersP30AR046031 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GILBERT, SHAWN ROBERT · 2001 to 2010
$5.6M
Canine model for evaluating CRAD efficacyR01CA093796 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SIEGAL, GENE P · 2002 to 2005
$1.1M
NCI NIH HHS CA098543NCI NIH HHS CA93796NCI NIH HHS R01 CA093796NCI NIH HHS U10 CA098543NIAMS NIH HHS AR046031NIAMS NIH HHS P30 AR046031
6 · The paper itself

Abstract

Inflammatory osteolysis is a relatively frequent and incapacitating complication of rheumatoid arthritis and multiple other inflammation-associated bone diseases. It is thought to operate through an ultimate common pathway of accelerated osteoclast recruitment and activation under the control of cytokines produced in the inflammatory environment. Over the past decade, there have been major advances in our understanding of the mechanisms of osteoclastogenesis. It is now clear that the interaction of receptor activator NF-kappaB (RANK) and its ligand, RANKL, plays a central role in osteoclast formation and activity. Therefore, understanding osteoclastogenesis offers new pathways for potential therapeutic intervention in inflammatory osteolysis. The success of anti-tumor necrosis factor-alpha and interleukin-1 therapy highlights the central role that these specific cytokines play in this disease. This review outlines our current understanding of the mechanisms mediating inflammatory osteolysis and highlights potential therapeutic strategies.

Indexed as

Genetic TherapyAnimalsAnti-Inflammatory AgentsBone ResorptionHumansInflammationInflammation MediatorsInterleukin-1OsteoclastsOsteolysisp38 Mitogen-Activated Protein KinasesReceptor Activator of Nuclear Factor-kappa BSignal TransductionTumor Necrosis Factor-alphaAnti-Inflammatory AgentsInflammation MediatorsInterleukin-1p38 Mitogen-Activated Protein KinasesReceptor Activator of Nuclear Factor-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID18757139
PMCPMC3747958
OpenAlexW2047277096

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.