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Root anomalies and dentin dysplasia in autosomal recessive hyperphosphatemic familial tumoral calcinosis (HFTC).
Vieira, Alexandre R; Lee, Moses; Vairo, Filippo; Loguercio Leite, Julio Cesar; Munerato, Maria Cristina; Visioli, Fernanda; D'Ávila, Stéphanie Rodrigues; Wang, Shih-Kai; Choi, Murim; Simmer, James P; Hu, Jan C-C.
Afiliação
  • Vieira AR; Departments of Oral Biology and Pediatric Dentistry, Center for Craniofacial and Dental Genetics, School of Dental Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA; Department of Human Genetics, Graduate School of Public Health; Clinical and Translational Science Institute, Universi
  • Lee M; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
  • Vairo F; Medical Genetics Service, Hospital de Clínicas de Porto Alegre, RS, Brazil.
  • Loguercio Leite JC; Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul, RS, Brazil.
  • Munerato MC; Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul, RS, Brazil.
  • Visioli F; Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul, RS, Brazil.
  • D'Ávila SR; Department of Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul, RS, Brazil.
  • Wang SK; Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, Michigan, USA.
  • Choi M; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea. Electronic address: Murimchoi@snu.ac.kr.
  • Simmer JP; Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, Michigan, USA.
  • Hu JC; Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, Michigan, USA.
Article em En | MEDLINE | ID: mdl-26337219
Hyperphosphatemic familial tumoral calcinosis (HFTC, OMIM #211900) is an autosomal recessive metabolic disorder characterized by hyperphosphatemia, tooth root defects, and the progressive deposition of calcium phosphate crystals in periarticular spaces, soft tissues, and sometimes bone.(1) In this HFTC case report, we document the dental phenotype associated with a homozygous missense mutation (g.29077 C>T; c.484 C>T; p.Arg162*) in GALNT3 (OMIM 6017563), a gene encoding UDP-GalNAc transferase 3 that catalyzes the first step of O-linked oligosaccharide biosynthesis in the Golgi. The medical and dental pathology is believed to be caused primarily by high serum phosphate levels (hyperphosphatemia), which, in turn, is caused by failure of GALNT3 to glycosylate the phosphate regulator protein FGF23, impairing its ability inhibit reabsorption of filtered phosphate in the kidneys.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Raiz Dentária / Calcinose / Hiperostose Cortical Congênita / N-Acetilgalactosaminiltransferases / Displasia da Dentina / Hiperfosfatemia Idioma: En Ano de publicação: 2015 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Raiz Dentária / Calcinose / Hiperostose Cortical Congênita / N-Acetilgalactosaminiltransferases / Displasia da Dentina / Hiperfosfatemia Idioma: En Ano de publicação: 2015 Tipo de documento: Article