ArticleAnatomical record (Hoboken, N.J. : 2007)2020
Anatomical similarity between the Sost-knockout mouse and sclerosteosis in humans.
Article in Anatomical record (Hoboken, N.J. : 2007), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Genetic factors underlying Mandibular prognathism: insights from recent human and animal studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- Wnt/β-Catenin Signaling in Craniomaxillofacial Osteocytes.Current osteoporosis reports · 2023Review
- Size changes in miR‑21 knockout mice: Geometric morphometrics on teeth, alveolar bone and mandible.Molecular medicine reports · 2021Article
- Molecular Basis for Craniofacial Phenotypes Caused by Sclerostin Deletion.Journal of dental research · 2021Article
- Caspase inhibitor attenuates the shape changes in the alveolar ridge following tooth extraction: A pilot study in rats.Journal of periodontal research · 2021Article
- Gene Expression and RNA Splicing Imputation Identifies Novel Candidate Genes Associated with Osteoporosis.The Journal of clinical endocrinology and metabolism · 2020Article
- Anatomical similarity between the Sost-knockout mouse and sclerosteosis in humans.Anatomical record (Hoboken, N.J. : 2007) · 2020Article
- Effects of Multi-Generational Soft Diet Consumption on Mouse Craniofacial Morphology.Frontiers in physiology · 2020Article
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sclerosteosis, a rare autosomal recessive genetic disorder caused by a mutation of the Sost gene, manifests in the facial skeleton by gigantism, facial distortion, mandibular prognathism, cranial nerve palsy, and, in extreme cases, compression of the medulla oblongata. Mice lacking sclerostin reflect some symptoms of sclerosteosis, but this is the first report of the effect on the facial skeleton. We used geometric morphometrics (GMM) to analyze the deformations of the murine facial skeleton from the wild-type to the Sost gene knockout. Landmark coordinates were obtained by surface reconstructions from micro-computed tomography. Centroid size, principal component scores in shape space and form space, and asymmetry were computed by the standard GMM formulas, and dental and skeletal jaw lengths were examined as ratios. We show here that, compared to wild type controls, mice lacking Sost have larger centroid size (effect size, p-value: 4.59, <.001), higher mean asymmetry (1.14, .065), dental and skeletal mandibular prognathism (1.36, .010 and 5.92, <.001), a smaller foramen magnum (-1.71, .015), and calvaria that are more highly curved (form space p = 4.09, .002; shape space p = 12.82, .002). These features of mice lacking sclerostin largely correspond to the changes of the facial skeleton observed in sclerosteosis. This alignment further supports claims that the Sost gene plays a fundamental role in bony facial development in rodents and humans alike.
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