Evidence map›Paper›PMID 23518238›Full record

ArticleArchives of oral biology2013

Osteoarthritis in temporomandibular joint of Col2a1 mutant mice.

M L Ricks, J T Farrell, D J Falk, D W Holt, M Rees, J Carr, T Williams, B A Nichols, L C Bridgewater, P R Reynolds and 2 more

Abstract read
In one paragraph

Article in Archives of oral biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Neural crest-specific disruption of Evc2 provides an animal model to study the temporomandibular joint development and homeostasis in response to jaw loading.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
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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 1 institution in 1 country.

M L RicksDepartment of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA.
J T Farrell
D J Falk
D W Holt
M Rees
J Carr
T Williams
B A Nichols
L C Bridgewater
P R Reynolds
D L Kooyman
R E Seegmiller
Brigham Young University · US

Funding

Common mechanisms of Osteoarthritis in three mouse modelsR15AR056861 · NIAMS · BRIGHAM YOUNG UNIVERSITY · PI SEEGMILLER, ROBERT E · 2009 to 2010
$275k
Pathogenesis of Osteoarthritis in Col2a1 Mutant MiceR15AR047568 · NIAMS · BRIGHAM YOUNG UNIVERSITY · PI SEEGMILLER, ROBERT E · 2002 to 2002
$146k
NIAMS NIH HHS 1-R15-AR056861-01A1NIAMS NIH HHS R15 AR047568NIAMS NIH HHS R15 AR056861
6 · The paper itself

Abstract

objectiveCol2a1 gene mutations cause premature degeneration of knee articular cartilage in disproportionate micromelia (Dmm) and spondyloepiphesial dysplasia congenita (sedc) mice. The present study analyses the temporomandibular joint (TMJ) in Col2a1 mutant mice in order to provide an animal model of TMJ osteoarthritis (OA) that may offer better understanding of the progression of this disease in humans.

designDmm/+ mice and controls were compared at two, six, nine and 12 months. Craniums were fixed, processed to paraffin sections, stained with Safranin-O/Fast Green, and analysed with light microscopy. OA was quantified using a Mankin scoring procedure. Unfolded protein response (UPR) assay was performed and immunohistochemistry (IHC) was used to assay for known OA biomarkers.

resultsDmm/+ TMJs showed fissuring of condylar cartilage as early as 6 months of age. Chondrocytes were clustered, leaving acellular regions in the matrix. Significant staining of HtrA1, Ddr2 and Mmp-13 was observed in Dmm/+ mice (p<0.01). We detected upregulation of the UPR in knee but not TMJ.

conclusionsDmm/+ mice are subject to early-onset OA in the TMJ. We observed upregulation of biomarkers and condylar cartilage degradation concomitant with OA. An upregulated UPR may exacerbate the onset of OA. The Dmm/+ mouse TMJ is a viable model for the study of the progression of OA in humans.

Indexed as

Age of OnsetAnalysis of VarianceAnimalsBiomarkersCartilageCollagen Type IIDisease Models, AnimalDisease ProgressionGene ExpressionHigh-Temperature Requirement A Serine Peptidase 1Matrix Metalloproteinase 13MiceMice, Mutant StrainsOsteoarthritisPolymerase Chain ReactionProteoglycansBiomarkersCollagen Type IIHigh-Temperature Requirement A Serine Peptidase 1HtrA1 protein, mouseMatrix Metalloproteinase 13ProteoglycansSerine EndopeptidasesCol2a1Ddr2Disproportionate micromelia (Dmm)OsteoarthritisTemporomandibular joint

Identifiers

PMID23518238
PMCPMC3716833
OpenAlexW1969496813

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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.