ArticleMechanisms of development2008
Shox2-deficiency leads to dysplasia and ankylosis of the temporomandibular joint in mice.
Article in Mechanisms of development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 77 citations in OpenAlex.
- LOXL2 deletion triggers TMJ osteoarthritis, while overexpression protects it from NF-κB-induced chondrocyte apoptosis.International journal of oral science · 2026Article
- Temporal constraints on enhancer usage shape the regulation of limb gene transcription.Nature communications · 2026Article
- Positional programs in early murine facial development and their role in human facial shape variability.Nature communications · 2025Article
- The subfunctionalization ofFrontiers in cell and developmental biology · 2025Article
- A gene desert required for regulatory control of pleiotropic Shox2 expression and embryonic survival.Nature communications · 2024Article
- LOXL2 promotes aggrecan and gender-specific anabolic differences to TMJ cartilage.Scientific reports · 2020Article
- The TMJ Disc Is a Common Ancestral Feature in All Mammals, as Evidenced by the Presence of a Rudimentary Disc During Monotreme Development.Frontiers in cell and developmental biology · 2020Article
- The Roles of Indian Hedgehog Signaling in TMJ Formation.International journal of molecular sciences · 2019Review
- Article
- Expressing human SHOX in Shox2SHOX KI/KI mice leads to congenital osteoarthritis‑like disease of the temporomandibular joint in postnatal mice.Molecular medicine reports · 2016Article
- A Joint Less Ordinary: Intriguing Roles for Hedgehog Signalling in the Development of the Temporomandibular Synovial Joint.Journal of developmental biology · 2016Review
- A Track Record on SHOX: From Basic Research to Complex Models and Therapy.Endocrine reviews · 2016Review
- Augmented Indian hedgehog signaling in cranial neural crest cells leads to craniofacial abnormalities and dysplastic temporomandibular joint in mice.Cell and tissue research · 2016Article
- Observing the development of the temporomandibular joint in embryonic and post-natal mice using various staining methods.Experimental and therapeutic medicine · 2016Article
- Mouse genetic models for temporomandibular joint development and disorders.Oral diseases · 2016Review
- Overexpression of Indian hedgehog partially rescues short stature homeobox 2-overexpression-associated congenital dysplasia of the temporomandibular joint in mice.Molecular medicine reports · 2015Article
- A common Shox2-Nkx2-5 antagonistic mechanism primes the pacemaker cell fate in the pulmonary vein myocardium and sinoatrial node.Development (Cambridge, England) · 2015Article
- Shox2 is required for the proper development of the facial motor nucleus and the establishment of the facial nerves.BMC neuroscience · 2015Article
- Article
- Altered FGF Signaling Pathways Impair Cell Proliferation and Elevation of Palate Shelves.PloS one · 2015Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The temporomandibular joint (TMJ) is a unique synovial joint whose development differs from the formation of other synovial joints. Mutations have been associated with the developmental defects of the TMJ only in a few genes. In this study, we report the expression of the homeobox gene Shox2 in the cranial neural crest derived mesenchymal cells of the maxilla-mandibular junction and later in the progenitor cells and undifferentiated chondrocytes of the condyle as well as the glenoid fossa of the developing TMJ. A conditional inactivation of Shox2 in the cranial neural crest-derived cells causes developmental abnormalities in the TMJ, including dysplasia of the condyle and glenoid fossa. The articulating disc forms but fuses with the fibrous layers of the condyle and glenoid fossa, clinically known as TMJ ankylosis. Histological examination indicates a delay in development in the mutant TMJ, accompanied by a significantly reduced rate of cell proliferation. In situ hybridization further demonstrates an altered expression of several key osteogenic genes and a delayed expression of the osteogenic differentiation markers. Shox2 appears to regulate the expression of osteogenic genes and is essential for the development and function of the TMJ. The Shox2 conditional mutant thus provides a unique animal model of TMJ ankylosis.
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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.