Objective:To observe apical sealing ability of two kinds of nanomaterial. Methods:40 straight human maxillary anterior teeth were randomly divided into four experimental groups of 8 samples each and two control groups of 4 samples each. The root canals were prepared using step-back technique and obturated with gutta-percha and one of the sealers by the lateral condensation technique. Group 1: Filled with zinc oxide-eugenol sealer and gutta-percha (ZOE); group 2: Filled with hydroxyapatite sealer and gutta-percha (HA); group 3: Filled with nano-zinc-oxide sealer and gutta-percha (NZO); group 4: Filled with nanohydroxyapatite sealer and gutta-percha (NHA). The teeth were placed into microleakage model. Glucose leakage from the coronal to apical was measured by the concentration of glucose in apical reservoir at 1, 2, 4, 7, 10, 15, 20, 25 and 30 days with GOD (glucose oxidase ) method. The apical sealing ability of the materials were assessed according to the concentration of glucose leakage. Results:The glucose leakage of four kinds of materials differed significantly (P

OBJECTIVETo identify deletion of large fragment in COL1A1/2 genes among patients with osteogenesis imperfecta (OI).

METHODSGenomic DNA was extracted from peripheral blood samples by a standard SDS-proteinase K-phenol/chloroform method. Multiplex ligation-dependent probe amplification (MLPA) was performed to detect gross deletions of the COL1A1/2 genes among 46 patients affected with OI, in whom no mutation was detected in the sequences of the COL1A1/2 genes.

RESULTSHeterozygous deletions of the entire COL1A1 gene and exon 20 of the COL1A2 gene were detected in probands A and B, respectively, and no gross deletion was found in the remaining 44 samples. The MLPA result of proband A was confirmed by fluorescence quantitative PCR (Q-PCR) in his family. A further conjunction point analysis through gap-PCR and DNA sequencing revealed deletion of exons 17 to 23 in the COL1A2 gene, and a 637 bp-insertion from chromosome 5 in the proband B.

CONCLUSIONTwo gross deletions have been found in the genes coding for collagen type I in the Chinese OI population, and the deletion of exons 17 to 23 in the COL1A2 gene is a novel mutation. This work not only has expanded the mutation spectrum of the COL1A1/2 gene, but also provided a support for prenatal genetic diagnosis for the families.

Adolescent ; Adult ; Child ; Child, Preschool ; Collagen Type I ; genetics ; Female ; Gene Deletion ; Humans ; Male ; Middle Aged ; Multiplex Polymerase Chain Reaction ; Osteogenesis Imperfecta ; genetics