ArticleHuman molecular genetics2016
Meckel's and condylar cartilages anomalies in achondroplasia result in defective development and growth of the mandible.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Healthcare and Psychosocial Needs in Achondroplasia Across the Lifespan: Developmental Functioning, Multidisciplinary Care, and Family-Centered Outcomes.Healthcare (Basel, Switzerland) · 2026Review
- Signalling Pathways and Mechanical Forces Interact in Craniofacial Development and Homeostasis.International dental journal · 2026Review
- Dkk1 inhibition restores mandibular growth in an achondroplasia mouse model.Biology open · 2026Article
- Embryonic cranial cartilage defects in the Fgfr3Anatomical record (Hoboken, N.J. : 2007) · 2025Article
- An atlas of early human mandibular endochondral and osteogenic paracrine signaling regions of Meckel's cartilage.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genetic factors underlying Mandibular prognathism: insights from recent human and animal studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- FGFR antagonists restore defective mandibular bone repair in a mouse model of osteochondrodysplasia.Bone research · 2025Article
- Axolotl mandible regeneration occurs through mechanical gap closure and a shared regenerative program with the limb.Disease models & mechanisms · 2024Article
- Insights into Craniofacial Development and Anomalies: Exploring Fgf Signaling in Zebrafish Models.Current osteoporosis reports · 2024Review
- Overexpression ofFrontiers in cell and developmental biology · 2024Article
- Targeting FGFR3 signaling and drug repurposing for the treatment of SLC26A2-related chondrodysplasia in mouse model.Journal of orthopaedic translation · 2024Article
- Reconstruction of the temporomandibular joint using a vascularized medial femoral condyle osteocartilaginous flap: an experimental investigation in miniature pigs.BMC oral health · 2023Article
- Hypochondroplasia gain-of-function mutation in FGFR3 causes defective bone mineralization in mice.JCI insight · 2023Article
- Craniofacial growth and function in achondroplasia: a multimodal 3D study on 15 patients.Orphanet journal of rare diseases · 2023Article
- What to Expect of Feeding Abilities and Nutritional Aspects in Achondroplasia Patients: A Narrative Review.Genes · 2023Review
- Genetic Interaction ofJournal of developmental biology · 2022Article
- PRDM paralogs antagonistically balance Wnt/β-catenin activity during craniofacial chondrocyte differentiation.Development (Cambridge, England) · 2022Article
- The Mandibular and Hyoid Arches-From Molecular Patterning to Shaping Bone and Cartilage.International journal of molecular sciences · 2021Review
- Advantages and Disadvantages of Different Treatment Methods in Achondroplasia: A Review.International journal of molecular sciences · 2021Review
- Craniofacial and Craniocervical Features in Cartilage-Hair Hypoplasia: A Radiological Study of 17 Patients and 34 Controls.Frontiers in endocrinology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activating FGFR3 mutations in human result in achondroplasia (ACH), the most frequent form of dwarfism, where cartilages are severely disturbed causing long bones, cranial base and vertebrae defects. Because mandibular development and growth rely on cartilages that guide or directly participate to the ossification process, we investigated the impact of FGFR3 mutations on mandibular shape, size and position. By using CT scan imaging of ACH children and by analyzing Fgfr3
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