A discoidin domain receptor 1 knock-out mouse as a novel model for osteoarthritis of the temporomandibular joint

Boris Schminke, Hayat Muhammad, Christa Bode, Boguslawa Sadowski, Regina Gerter, Nikolaus Gersdorff, Ralf Bürgers, Efrat Monsonego-Ornan, Vicki Rosen, Nicolai Miosge*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

Discoidin domain receptor 1 (DDR-1)-deficient mice exhibited a high incidence of osteoarthritis (OA) in the temporomandibular joint (TMJ) as early as 9 weeks of age. They showed typical histological signs of OA, including surface fissures, loss of proteoglycans, chondrocyte cluster formation, collagen type I upregulation, and atypical collagen fibril arrangements. Chondrocytes isolated from the TMJs of DDR-1-deficient mice maintained their osteoarthritic characteristics when placed in culture. They expressed high levels of runx-2 and collagen type I, as well as low levels of sox-9 and aggrecan. The expression of DDR-2, a key factor in OA, was increased. DDR-1-deficient chondrocytes from the TMJ were positively influenced towards chondrogenesis by a three-dimensional matrix combined with a runx-2 knockdown or stimulation with extracellular matrix components, such as nidogen-2. Therefore, the DDR-1 knock-out mouse can serve as a novel model for temporomandibular disorders, such as OA of the TMJ, and will help to develop new treatment options, particularly those involving tissue regeneration.

Original languageAmerican English
Pages (from-to)1081-1096
Number of pages16
JournalCellular and Molecular Life Sciences
Volume71
Issue number6
DOIs
StatePublished - Mar 2014

Keywords

  • Chondrocyte signaling
  • Collagen receptor
  • Extracellular matrix
  • Osteoarthritis
  • Temporomandibular joint

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