Evidence map›Paper›PMID 24771986›Full record

ReviewMediators of inflammation2014

Advanced glycation end products play adverse proinflammatory activities in osteoporosis.

Roberta Sanguineti, Alessandra Puddu, François Mach, Fabrizio Montecucco, Giorgio Luciano Viviani

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07329543 (Association of Advanced Glycation End-Product Burden With Response to Antiresorptive Therapy and Residual Fracture Risk in Osteoporosis), which is not on this map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 6% 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.

NCT07329543 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Association of Advanced Glycation End-Product Burden With Response to Antiresorptive Therapy and Residual Fracture Risk in Osteoporosis: A Prospective Cohort Study

TypeobservationalSponsorBursa City HospitalRan2026 to 2027Enrolled240ConditionsOsteoporosis, Postmenopausal Osteoporosis
3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Association between type 1 diabetes mellitus and reduced bone mineral density in children: a meta-analysis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2021
    Pooled it
  3. Review
  4. Review
  5. Review
  6. Obesity, diabetes and risk of bone fragility: How BMAT behavior is affected by metabolic disturbances and its influence on bone health.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Bone collagen quality in lumbar fusion patients: the association between volumetric bone mineral density and advanced glycation endproducts.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2023
    Article
  13. Review
  14. Article
  15. Article
  16. Carnosine and bone (Review).Molecular medicine reports · 2023
    Review
  17. Degradation of Bone Quality in a Transgenic Mouse Model of Alzheimer's Disease.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  18. Article
  19. Review
  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

5 authors at 3 institutions in 2 countries.

Roberta SanguinetiDepartment of Internal Medicine, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, Italy.ORCID 0000-0002-3130-9372
Alessandra PudduDepartment of Internal Medicine, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, Italy.ORCID 0000-0002-9084-2636
François MachDivision of Cardiology, Foundation for Medical Researches, Faculty of Medicine, Geneva University Hospitals, 64 Avenue de la Roseraie, 1211 Geneva, Switzerland.
Fabrizio MontecuccoDivision of Cardiology, Foundation for Medical Researches, Faculty of Medicine, Geneva University Hospitals, 64 Avenue de la Roseraie, 1211 Geneva, Switzerland ; First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa School of Medicine, IRCCS Azienda Ospedaliera Universitaria San Martino-IST Istituto Nazionale per la Ricerca sul Cancro, 6 Viale Benedetto XV, 16132 Genoa, Italy ; Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, 4 Gabrielle-Perret-Gentil, 1205 Geneva, Switzerland.ORCID 0000-0003-0823-8729
Giorgio Luciano VivianiDepartment of Internal Medicine, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, Italy.
University of Genoa · ITFoundation for laboratory medicine · CHUniversity Hospital of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis is a major public health burden that is expected to further increase as the global population ages. In the last twenty years, advanced glycation end products (AGEs) have been shown to be critical mediators both in the pathogenesis and development of osteoporosis and other chronic degenerative diseases related to aging. The accumulation of AGEs within the bone induces the formation of covalent cross-links with collagen and other bone proteins which affects the mechanical properties of tissue and disturbs bone remodelling and deterioration, underlying osteoporosis. On the other hand, the gradual deterioration of the immune system during aging (defined as immunosenescence) is also characterized by the generation of a high level of oxidants and AGEs. The synthesis and accumulation of AGEs (both localized within the bone or in the systemic circulation) might trigger a vicious circle (in which inflammation and aging merged in the word "Inflammaging") which can establish and sustain the development of osteoporosis. This narrative review will update the molecular mechanisms/pathways by which AGEs induce the functional and structural bone impairment typical of osteoporosis.

Indexed as

AgingBiomarkersBone and BonesBone RemodelingDiphosphonatesGlycation End Products, AdvancedHumansInflammationOsteoporosisOxidantsOxidative StressBiomarkersDiphosphonatesGlycation End Products, AdvancedOxidants

Identifiers

PMID24771986
PMCPMC3977495
OpenAlexW2142996665

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.