Histological Analysis of Dentinogenesis Imperfecta in Slc39a13/Zip13 Knockout Mice
Histological Analysis of Dentinogenesis Imperfecta in Slc39a13/Zip13 Knockout Mice
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DOI：
10.2485/jhtb.23.163
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发表时间：
2014-04-01
影响因子：
0.4
通讯作者：
Asada, Yoshinobu
中科院分区：
文献类型：
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作者：
Munemasa, Takaaki;Idaira, Yayoi;Asada, Yoshinobu
本研究对牙本质基质的异常进行了研究，以阐明人牙本质发育不全（DI）的发病机制。对野生型（Zip 13+/+）和Slc39a/Zip 13敲除（KO）小鼠下颌磨牙的牙本质基质进行组织学检查。苏木精和伊红，以及银染色，用于光学显微镜。并对样品进行了背散射和透射电镜观察。采用I型胶原进行免疫组化。结果表明：光镜下，Zip13-KO小鼠牙本质基质呈层状，呈明显的增加线；透射电镜下，胶原纤维异常，胶原分子呈圆形；对i型胶原的免疫反应异常。Zip13-KO小鼠牙本质组织学特征与人类DI相似，提示Zip13-KO小鼠可作为研究人类DI机制的模型。
This study focused on the abnormality of dentin matrix to clarify the pathogenesis of human dentinogenesis imperfecta (DI). Dentin matrix of mandibular molars from wild type (Zip 13+/+) and Slc39a/Zip 13 knockout (KO) mice were examined histologically. Hematoxylin and eosin, as well as silver staining, were used for light microscopy. Samples were also observed under backscattered and transmission electron microscopy. Immunohistochemistry using type I collagen was also carried out. Results showed that Zip 13-KO mice exhibited 1) lamellated dentin matrix with accentuated incremental lines under the light microscope, 2) abnormal collagen fibers and round shape collagen molecules in transmission electron microscope, and 3) unusual immunoreaction to collagen type I. The similarity in the histological features of dentin in Zip 13-KO mice to human DI indicates that Zip13-KO mice may be used as models for investigating the mechanism of human DI.