{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T08:56:21Z","timestamp":1792659381663,"version":"4.5.0"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2016,11,10]],"date-time":"2016-11-10T00:00:00Z","timestamp":1478736000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100011781","name":"Shriners Hospitals for Children","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100011781","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100007338","name":"Barnes-Jewish Hospital Foundation","doi-asserted-by":"publisher","award":["DK067145"],"award-info":[{"award-number":["DK067145"]}],"id":[{"id":"10.13039\/100007338","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,4,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>In 1985, we briefly reported infant sisters with a unique, lethal, autosomal recessive disorder designated congenital sclerosing osteomalacia with cerebral calcification. In 1986, this condition was entered into Mendelian Inheritance In Man (MIM) as osteomalacia, sclerosing, with cerebral calcification (MIM 259660). However, no attestations followed. Instead, in 1989 Raine and colleagues published an affected neonate considering unprecedented the striking clinical and radiographic features. In 1992, \u201cRaine syndrome\u201d entered MIM formally as osteosclerotic bone dysplasia, lethal (MIM #259775). In 2007, the etiology emerged as loss-of-function mutation of FAM20C that encodes family with sequence similarity 20, member C. FAM20C is highly expressed in embryonic calcified tissues and encodes a kinase (dentin matrix protein 4) for most of the secreted phosphoproteome including FGF23, osteopontin, and other regulators of skeletal mineralization. Herein, we detail the clinical, radiological, biochemical, histopathological, and FAM20C findings of our patients. Following premortem tetracycline labeling, the proposita's non-decalcified skeletal histopathology after autopsy indicated no rickets but documented severe osteomalacia. Archival DNA revealed the sisters were compound heterozygotes for a unique missense mutation and a novel deletion in FAM20C. Individuals heterozygous for the missense mutation seemed to prematurely fuse their metopic suture and develop a metopic ridge sometimes including trigonocephaly. Our findings clarify FAM20C's role in hard tissue formation and mineralization, and show that Raine syndrome is congenital sclerosing osteomalacia with cerebral calcification. \u00a9 2016 American Society for Bone and Mineral Research.<\/jats:p>\n                  <jats:p>Abstract<\/jats:p>\n                  <jats:p>In 1985, we briefly characterized \u201ccongenital sclerosing osteomalacia with cerebral calcification\u201d (CSOCC) in infant sisters. Later, Raine syndrome (RNS) became known, with FAM20C deactivation discovered in 2007. FAM20C is a kinase for the secreted phosphoproteome, including FGF23 and SIBLINGs that regulate mineralization. We find the sisters carried two unique mutations in FAM20C. Skeletal histopathology indicated severe osteomalacia yet no rickets. Our findings clarify FAM20C's role in osteogenesis and hard tissue mineralization, and show RNS is CSOCC.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.3034","type":"journal-article","created":{"date-parts":[[2016,11,10]],"date-time":"2016-11-10T15:52:50Z","timestamp":1478793170000},"page":"757-769","source":"Crossref","is-referenced-by-count":47,"title":["Raine Syndrome (OMIM #259775), Caused By <i>FAM20C<\/i> Mutation, Is Congenital Sclerosing Osteomalacia With Cerebral Calcification (OMIM 259660)"],"prefix":"10.1093","volume":"32","author":[{"given":"Michael P","family":"Whyte","sequence":"first","affiliation":[{"name":"Division of Bone and Mineral Diseases, Department of Internal MedicineWashington University School of Medicine at Barnes-Jewish HospitalSt. LouisMOUSA"},{"name":"Center for Metabolic Bone Disease and Molecular ResearchShriners Hospital for ChildrenSt. LouisMOUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William H","family":"McAlister","sequence":"additional","affiliation":[{"name":"Department of Pediatric Radiology, Mallinckrodt Institute of RadiologyWashington University School of Medicine at St. Louis Children's HospitalSt. LouisMOUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael D","family":"Fallon","sequence":"additional","affiliation":[{"name":"Department of Surgical PathologyUniversity of Pennsylvania School of MedicinePhiladelphiaPAUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary Ella","family":"Pierpont","sequence":"additional","affiliation":[{"name":"Department of PediatricsUniversity of Minnesota School of Medicine, and Children's Hospitals and Clinics of MinnesotaMinneapolisMNUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vinieth N","family":"Bijanki","sequence":"additional","affiliation":[{"name":"Center for Metabolic Bone Disease and Molecular ResearchShriners Hospital for ChildrenSt. LouisMOUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shenghui","family":"Duan","sequence":"additional","affiliation":[{"name":"Division of Bone and Mineral Diseases, Department of Internal MedicineWashington University School of Medicine at Barnes-Jewish HospitalSt. LouisMOUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ghada A","family":"Otaify","sequence":"additional","affiliation":[{"name":"Department of Clinical Genetics, Division of Human Genetics and Genome ResearchCentre of Excellence of Human Genetics, National Research CentreCairoEgypt"},{"name":"Division of Bone and Mineral Diseases, Department of Internal MedicineWashington University School of Medicine at Barnes-Jewish HospitalSt. LouisMOUSA"},{"name":"Center for Metabolic Bone Disease and Molecular ResearchShriners Hospital for ChildrenSt. LouisMOUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William S","family":"Sly","sequence":"additional","affiliation":[{"name":"E.A. Doisey Department of BiochemistrySt. Louis University School of MedicineSt. LouisMOUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven","family":"Mumm","sequence":"additional","affiliation":[{"name":"Division of Bone and Mineral Diseases, Department of Internal MedicineWashington University School of Medicine at Barnes-Jewish HospitalSt. LouisMOUSA"},{"name":"Center for Metabolic Bone Disease and Molecular ResearchShriners Hospital for ChildrenSt. LouisMOUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2016,11,10]]},"reference":[{"key":"2024021014202983500_jbmr3034-bib-0001","first-page":"A82","article-title":"Congenital sclerosing osteomalacia with cerebral calcification: a new, recessively-inherited, syndrome which radiographically mimics carbonic anhydrase II deficiency","volume":"37","author":"Whyte","year":"1985","journal-title":"(Abstract). 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