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We aim to determine the clinical and radiographic manifestation, mutational features, and genotype\u2013phenotype relationships by characterization of 4 patients with MCDS and literature review. The four patients presented with short stature or waddling gait, flattened vertebrae, and irregular femoral epiphyses. We identified two novel\n                    <jats:italic>COL10A1<\/jats:italic>\n                    variants (c.1925\u00a0T\u2009&gt;\u2009A, c.1903C\u2009&gt;\u2009G) and reported the first case harboring both a de novo nonsense (c.2001\u00a0T\u2009&gt;\u2009G, p.Tyr667Ter) in the non-collagenous 1 (NC1) domain and a missense (c.1438A\u2009&gt;\u2009T, p.Ile480Leu) in the helix domain. Genotype\u2013phenotype analysis of 124 cases previously reported and 4 new cases revealed that NC1 domain mutations were associated with an earlier onset of MCDS than non-NC1 mutations (median 12 vs. 72\u00a0months,\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20090.0014). Patients carrying a missense mutation in\n                    <jats:italic>COL10A1<\/jats:italic>\n                    showed significantly lower height Z-scores (\u2212\u20093.62\u2009\u00b1\u20091.95 vs.\u2009\u2212\u20091.99\u2009\u00b1\u20091.28,\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20090.013) at first and more metaphyseal irregularities in the distal radius\/ulna than those with truncating mutations (\n                    <jats:italic>P<\/jats:italic>\n                    \u2009=\u20090.019). Structural modeling indicated that NC1 mutations may disrupt collagen X structure via electrostatic alterations or steric clashes. These findings expand the mutational spectrum of MCDS and establish that\n                    <jats:italic>COL10A1<\/jats:italic>\n                    genotype correlates with severity of MCDS, which will help to identify patients with severe phenotypes through molecular testing and to develop effective treatment strategies for MCDS.\n                  <\/jats:p>","DOI":"10.1007\/s00223-025-01457-8","type":"journal-article","created":{"date-parts":[[2025,12,27]],"date-time":"2025-12-27T15:37:21Z","timestamp":1766849841000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Clinical, Molecular Characteristics, and Genotype\u2013Phenotype Relationships of Metaphyseal Chondrodysplasia Type Schmid"],"prefix":"10.1007","volume":"117","author":[{"given":"Lingyang","family":"Meng","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jing","family":"Hu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lei","family":"Sun","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qian","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ou","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Jiang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaoping","family":"Xing","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Weibo","family":"Xia","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7270-4902","authenticated-orcid":false,"given":"Mei","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2025,12,27]]},"reference":[{"key":"1457_CR1","volume-title":"GeneReviews\u00ae","author":"CM Richmond","year":"2019","unstructured":"Richmond CM, Savarirayan R (2019) Schmid metaphyseal chondrodysplasia. 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