Division of Bone and Mineral Diseases, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Center for Metabolic Bone Disease and Molecular Research, Shriners Hospital for Children, St. Louis, MO 63110, USA; Department of Clinical Genetics, Division of Human Genetics and Genome Research, Centre of Excellence of Human Genetics, National Research Centre, Cairo, Egypt.
Division of Bone and Mineral Diseases, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; Center for Metabolic Bone Disease and Molecular Research, Shriners Hospital for Children, St. Louis, MO 63110, USA.
Bone. 2018 Feb;107:161-171. doi: 10.1016/j.bone.2017.11.012. Epub 2017 Nov 21.
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.
颌骨牙骨质发育不良(GDD;OMIM #166260)是一种极为罕见的常染色体显性遗传病,由ANO5 基因的杂合突变引起,其特征为颌骨纤维-骨病变、骨脆性伴反复骨折、管状骨弯曲/硬化。ANO5 的生理作用尚不清楚。我们报告了一例 5 岁男孩,患有看似非典型且特别严重的 GDD 和独特的 ANO5 突变。严重的骨质疏松症与产前股骨骨折、产后反复骨折以及从约 2 月龄开始双侧上颌骨和下颌骨进行性增大有关,这干扰了喂养和言语功能,需要进行 4 次切除术。组织病理学分析显示良性纤维-骨病变,类似于颌骨的骨化性纤维瘤,无砂粒体样体。在 ANO5 的外显子 15 中发现了一种新的、从头发生的、杂合的、错义突变(c.1553G>A;p.Gly518Glu)。我们的发现拓宽了 GDD 的表型和分子谱。生命早期的骨折伴进行性面部肿胀是关键特征。我们评估了他从 15 月龄开始总共接受了 7 次帕米膦酸盐输注的反应。需要进一步的报告来阐明表型,探讨任何基因型-表型相关性,并评估治疗方法。