Evidence map›Paper›PMID 30671590›Full record

ReviewCalcified tissue international2019

Paget's Disease of Bone.

Luigi Gennari, Domenico Rendina, Alberto Falchetti, Daniela Merlotti

Abstract readReview
PubMed Publisher
In one paragraph

Review in Calcified tissue international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Latest developments in Paget's disease of bone.European journal of endocrinology · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Epigenetic Regulation ofInternational journal of molecular sciences · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

4 authors at 3 institutions in 1 country.

Luigi GennariDepartment of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy. luigi.gennari@unisi.it.ORCID http://orcid.org/0000-0001-6833-4232
Domenico RendinaDepartment of Medicine and Surgery, Federico II University, Naples, Italy.
Alberto FalchettiCentro Hercolani and Villa Alba (GVM), 40123 Bologna and EndOsMet, Villa Donatello Private Hospital, 50132, Florence, Italy.
Daniela MerlottiDepartment of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy.ORCID http://orcid.org/0000-0002-3338-6339
University of Siena · ITFederico II University Hospital · ITVilla Torri Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paget's disease of bone (PDB) is a chronic and focal bone disorder, characterized by increased osteoclast-mediated bone resorption and a subsequent compensatory increase in bone formation, resulting in a disorganized mosaic of woven and lamellar bone at one or more affected skeletal sites. As a result, bone pain, noticeable deformities, arthritis at adjacent joints, and fractures can occur. In a small proportion of cases neoplastic degeneration in osteosarcoma, or, less frequently, giant cell tumor has been also described at PDB sites. While recent epidemiological evidences clearly indicate a decrease in the prevalence and the severity of PDB, over the past 2 decades there have been consistent advances on the genetic mechanisms of disease. It is now clear that PDB is a genetically heterogeneous disorder, with mutations in at least two different genes (SQSTM1, ZNF687) and more common predisposing variants. As a counterpart to the genetic hypothesis, the focal nature of lesions, the decline in prevalence rates, and the incomplete penetrance of the disease among family members suggest that one or more environmental triggers may play a role in the pathophysiology of PDB. The exact nature of these triggers and how they might interact with the genetic factors are less understood, but recent experimental data from mice models suggest the implication of paramixoviral infections. The clinical management of PDB has also evolved considerably, with the development of potent aminobisphosphonates such as zoledronic acid which, given as a single intravenous infusion, now allows a long-term disease remission in the majority of patients.

Indexed as

AnimalsBone ResorptionClinical Trials as TopicDiphosphonatesDNA-Binding ProteinsGenetic Predisposition to DiseaseHumansMiceMutationOsteitis DeformansOsteoclastsOsteogenesisProtein DomainsRiskSequestosome-1 ProteinTranscription FactorsDiphosphonatesDNA-Binding ProteinsSequestosome-1 ProteinSQSTM1 protein, humanTranscription FactorsZNF687 protein, humanBisphosphonatesBone painPaget’s disease of boneSQSTM1 gene

Identifiers

PMID30671590
OpenAlexW2914444909

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.