Evidence map›Paper›PMID 24453178›Full record

ArticleJournal of dental research2014

TMJ degeneration in SAMP8 mice is accompanied by deranged Ihh signaling.

Y Ishizuka, Y Shibukawa, M Nagayama, R Decker, T Kinumatsu, A Saito, M Pacifici, E Koyama

Abstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of dental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. The Roles of Indian Hedgehog Signaling in TMJ Formation.International journal of molecular sciences · 2019
    Review
  8. Roles of Ihh signaling in chondroprogenitor function in postnatal condylar cartilage.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. 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

8 authors at 3 institutions in 2 countries.

Y IshizukaDepartment of Periodontology, Tokyo Dental College, Tokyo, Japan.
Y Shibukawa
M Nagayama
R Decker
T Kinumatsu
A Saito
M Pacifici
E Koyama
Tokyo Dental College · JPChildren's Hospital of Philadelphia · USAsahi University · JP

Funding

Mechanisms of Synovial Joint FormationR01AR062908 · NIAMS · CHILDREN'S HOSP OF PHILADELPHIA · PI ENOMOTO-IWAMOTO, MOTOMI, PACIFICI, MAURIZIO · 2011 to 2020
$4.5M
Mechanisms of Synovial Joint FormationR01AG025868 · NIA · THOMAS JEFFERSON UNIVERSITY · PI PACIFICI, MAURIZIO · 2005 to 2009
$1.8M
Mechansisms directing synovial joint morphogenesisF32AR064071 · NIAMS · CHILDREN'S HOSP OF PHILADELPHIA · PI DECKER, REBEKAH STACEY · 2013 to 2015
$179k
NIAMS NIH HHS 1F32AR064071-01NIAMS NIH HHS AR062908NIAMS NIH HHS F32 AR064071NIAMS NIH HHS R01 AR062908NIA NIH HHS R01 AG025868
6 · The paper itself

Abstract

The temporomandibular joint (TMJ) functions as a load-bearing diarthrodial joint during mastication, and its continuous use and stress can lead to degeneration over age. Using senescence-accelerated (SAMP8) mice that develop early osteoarthritis-like changes in synovial joints at high frequency, we analyzed possible molecular mechanisms of TMJ degeneration and tested whether and how malocclusion may accelerate it. Condylar articular cartilage in young SAMP8 mice displayed early-onset osteoarthritic changes that included reductions in superficial/chondroprogenitor cell number, proteoglycan/collagen content, and Indian hedgehog (Ihh)-expressing chondrocytes. Following malocclusion induced by tooth milling, the SAMP8 condyles became morphologically defective, displayed even lower proteoglycan levels, and underwent abnormal chondrocyte maturation compared with malocclusion-treated condyles in wild-type mice. Malocclusion also induced faster progression of pathologic changes with increasing age in SAMP8 condyles as indicated by decreased PCNA-positive proliferating chondroprogenitors and increased TUNEL-positive apoptotic cells. These changes were accompanied by steeper reductions in Ihh signaling and by expression of matrix metalloproteinase 13 at the chondro-osseous junction in SAMP8 articular cartilage. In sum, we show for the first time that precocious TMJ degeneration in SAMP8 mice is accompanied by--and possibly attributable to--altered Ihh signaling and that occlusal dysfunction accelerates progression toward degenerative TMJ disease in this model.

Indexed as

Age FactorsAnimalsApoptosisCarrier ProteinsCartilage, ArticularChondrocytesCollagenCollagen Type ICollagen Type IICollagen Type XDisease Models, AnimalDisease ProgressionHedgehog ProteinsKruppel-Like Transcription FactorsMalocclusionMandibular CondyleCarrier ProteinsCollagenCollagen Type ICollagen Type IICollagen Type XGli1 protein, mouseGli2 protein, mouseHedgehog ProteinsHhip protein, mouseihh protein, mouseKruppel-Like Transcription FactorsMatrix Metalloproteinase 13Membrane GlycoproteinsMmp13 protein, mousePatched ReceptorsProliferating Cell Nuclear AntigenProteoglycansReceptors, Cell SurfaceZinc Finger Protein GLI1Zinc Finger Protein Gli2degenerative joint diseaseIndian hedgehogosteoarthritissenescence-accelerated mousesuperficial celltemporomandibular joint

Identifiers

PMID24453178
PMCPMC3929979
OpenAlexW2133447217

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.