Evidence map›Paper›PMID 27001307›Full record

ArticleMolecular and cellular biology2016

Intercellular Communication between Keratinocytes and Fibroblasts Induces Local Osteoclast Differentiation: a Mechanism Underlying Cholesteatoma-Induced Bone Destruction.

Yoriko Iwamoto, Keizo Nishikawa, Ryusuke Imai, Masayuki Furuya, Maki Uenaka, Yumi Ohta, Tetsuo Morihana, Saori Itoi-Ochi, Josef M Penninger, Ichiro Katayama and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 26% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Cholesteatoma has an altered microbiota with a higher abundance ofLaryngoscope investigative otolaryngology · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Bone turnover in chronic otitis media with bone destruction.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2020
    Article
  15. Article
  16. Osteoclasts Modulate Bone Erosion in Cholesteatoma via RANKL Signaling.Journal of the Association for Research in Otolaryngology : JARO · 2019
    Article
  17. The role of bone resorption in the etiopathogenesis of acquired middle ear cholesteatoma.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2017
    Review
  18. Biology of recurrent cholesteatoma in a Romanian young patient - a case report.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    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

12 authors at 2 institutions in 2 countries.

Yoriko IwamotoDepartment of Otorhinolaryngology-Head and Neck Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan Department of Immunology and Cell Biology, Graduate School of Medicine and Frontier Biosciences, Osaka University, Osaka, Japan WPI-Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Keizo NishikawaDepartment of Immunology and Cell Biology, Graduate School of Medicine and Frontier Biosciences, Osaka University, Osaka, Japan WPI-Immunology Frontier Research Center, Osaka University, Osaka, Japan JST, CREST, Tokyo, Japan.
Ryusuke ImaiDepartment of Otorhinolaryngology-Head and Neck Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan Department of Dermatology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Masayuki FuruyaDepartment of Immunology and Cell Biology, Graduate School of Medicine and Frontier Biosciences, Osaka University, Osaka, Japan WPI-Immunology Frontier Research Center, Osaka University, Osaka, Japan Department of Orthopedic Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Maki UenakaDepartment of Immunology and Cell Biology, Graduate School of Medicine and Frontier Biosciences, Osaka University, Osaka, Japan WPI-Immunology Frontier Research Center, Osaka University, Osaka, Japan.
Yumi OhtaDepartment of Otorhinolaryngology-Head and Neck Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Tetsuo MorihanaDepartment of Otorhinolaryngology-Head and Neck Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Saori Itoi-OchiDepartment of Dermatology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Josef M PenningerInstitute of Molecular Biotechnology, Austrian Academy of Sciences, Vienna, Austria.
Ichiro KatayamaDepartment of Dermatology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Hidenori InoharaDepartment of Otorhinolaryngology-Head and Neck Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan.
Masaru IshiiDepartment of Immunology and Cell Biology, Graduate School of Medicine and Frontier Biosciences, Osaka University, Osaka, Japan WPI-Immunology Frontier Research Center, Osaka University, Osaka, Japan JST, CREST, Tokyo, Japan mishii@icb.med.osaka-u.ac.jp.
Osaka University · JPAustrian Academy of Sciences · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone homeostasis is maintained by a balance in activity between bone-resorbing osteoclasts and bone-forming osteoblasts. Shifting the balance toward bone resorption causes osteolytic bone diseases such as rheumatoid arthritis and periodontitis. Osteoclast differentiation is regulated by receptor activator of nuclear factor κB ligand (RANKL), which, under some pathological conditions, is produced by T and B lymphocytes and synoviocytes. However, the mechanism underlying bone destruction in other diseases is little understood. Bone destruction caused by cholesteatoma, an epidermal cyst in the middle ear resulting from hyperproliferation of keratinizing squamous epithelium, can lead to lethal complications. In this study, we succeeded in generating a model for cholesteatoma, epidermal cyst-like tissue, which has the potential for inducing osteoclastogenesis in mice. Furthermore, an in vitro coculture system composed of keratinocytes, fibroblasts, and osteoclast precursors was used to demonstrate that keratinocytes stimulate osteoclast differentiation through the induction of RANKL in fibroblasts. Thus, this study demonstrates that intercellular communication between keratinocytes and fibroblasts is involved in the differentiation and function of osteoclasts, which may provide the molecular basis of a new therapeutic strategy for cholesteatoma-induced bone destruction.

Indexed as

AnimalsCell CommunicationCell DifferentiationCells, CulturedCholesteatomaCoculture TechniquesDisease Models, AnimalFibroblastsKeratinocytesMiceOsteoclastsRANK LigandRANK LigandTnfsf11 protein, mouse

Identifiers

PMID27001307
PMCPMC4959317
OpenAlexW2311965376

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.