| Literature DB >> 29175271 |
Ghada A Otaify1, Michael P Whyte2, Gary S Gottesman3, William H McAlister4, J Eric Gordon5, Abby Hollander6, Marisa V Andrews7, Samir K El-Mofty8, Wei-Shen Chen8, Deborah V Veis9, Marina Stolina10, Albert S Woo11, Panagiotis Katsonis12, Olivier Lichtarge12, Fan Zhang3, Marwan Shinawi13.
Abstract
Gnathodiaphyseal dysplasia (GDD; OMIM #166260) is an ultra-rare autosomal dominant disorder caused by heterozygous mutation in the anoctamin 5 (ANO5) gene and features fibro-osseous lesions of the jawbones, bone fragility with recurrent fractures, and bowing/sclerosis of tubular bones. The physiologic role of ANO5 is unknown. We report a 5-year-old boy with a seemingly atypical and especially severe presentation of GDD and unique ANO5 mutation. Severe osteopenia was associated with prenatal femoral fractures, recurrent postnatal fractures, and progressive bilateral enlargement of his maxilla and mandible beginning at ~2months-of-age that interfered with feeding and speech and required four debulking operations. Histopathological analysis revealed benign fibro-osseous lesions resembling cemento-ossifying fibromas of the jaw without psammomatoid bodies. A novel, de novo, heterozygous, missense mutation was identified in exon 15 of ANO5 (c.1553G>A; p.Gly518Glu). Our findings broaden the phenotypic and molecular spectra of GDD. Fractures early in life with progressive facial swelling are key features. We assessed his response to a total of 7 pamidronate infusions commencing at age 15months. Additional reports must further elucidate the phenotype, explore any genotype-phenotype correlation, and evaluate treatments.Entities:
Keywords: Autosomal dominant; Bisphosphonates; Cemento-ossifying fibroma; Cherubism; Diaphyseal sclerosis; Fracture; Psammomatoid bodies
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Year: 2017 PMID: 29175271 PMCID: PMC5987759 DOI: 10.1016/j.bone.2017.11.012
Source DB: PubMed Journal: Bone ISSN: 1873-2763 Impact factor: 4.398