Root anomalies and dentin dysplasia in autosomal recessive hyperphosphatemic familial tumoral calcinosis (HFTC).

TitleRoot anomalies and dentin dysplasia in autosomal recessive hyperphosphatemic familial tumoral calcinosis (HFTC).
Publication TypeJournal Article
Year of Publication2015
AuthorsVieira, AR, Lee, M, Vairo, F, Leite, JCesar Logu, Munerato, MCristina, Visioli, F, D'Ávila, SRodrigues, Wang, S-K, Choi, M, Simmer, JP, Hu, JC-C
JournalOral Surg Oral Med Oral Pathol Oral Radiol
Volume120
Issue6
Paginatione235-9
Date Published2015 Dec
ISSN2212-4411
KeywordsAdolescent, Calcinosis, Dentin Dysplasia, Humans, Hyperostosis, Cortical, Congenital, Hyperphosphatemia, Male, Mutation, Missense, N-Acetylgalactosaminyltransferases, Pedigree, Phenotype, Radiography, Panoramic, Tooth Root
Abstract

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.

DOI10.1016/j.oooo.2015.05.006
Alternate JournalOral Surg Oral Med Oral Pathol Oral Radiol
PubMed ID26337219
PubMed Central IDPMC4640955
Grant ListR01 DE015846 / DE / NIDCR NIH HHS / United States
U54 HG006504 / HG / NHGRI NIH HHS / United States
DE015846 / DE / NIDCR NIH HHS / United States