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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 publication




Journal article


Cell Mol Life Sci

Publication Date





1081 - 1096


Animals, Bone and Bones, Cells, Cultured, Chondrocytes, Chondrogenesis, Collagen Type I, Core Binding Factor Alpha 1 Subunit, Discoidin Domain Receptor 1, Disease Models, Animal, Extracellular Matrix, Membrane Glycoproteins, Mice, Mice, Knockout, Osteoarthritis, Proteoglycans, RNA Interference, RNA, Small Interfering, Receptor Protein-Tyrosine Kinases, Receptors, Collagen, Signal Transduction, Temporomandibular Joint, Temporomandibular Joint Disorders