降钙素基因相关肽在大鼠切牙和牙周组织中的表达

目的:研究降钙素基因相关肽(calcitonin gene-related petide,CGRP)在大鼠切牙成釉细胞、成牙本质细胞和牙周膜细胞中的定位表达。方法:取6周龄Wistar大鼠的下颌骨,常规脱钙,切片,并进行HE染色和免疫组织化学染色,显微镜下观察CGRP在各组织细胞中的定位和表达。结果:CGRP在牙周膜细胞中呈阳性表达,在分泌期成釉细胞和成牙本质细胞中呈强阳性表达。结论:CGRP在牙齿硬组织发育细胞中呈强阳性表达,提示CGRP在釉质和牙本质发育的过程具有一定的意义。     

釉原蛋白羧基末端肽加速细胞周期促进成釉细胞系ALC细胞增殖

ORCID: 0000-0003-4338-4123(刘敏) 中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程     

Indirect visualization of ameloblast modulation in the rat incisor using calcium-binding compounds

Abstract – Rats were injected with Calcein® and killed l h, and 1, 2 and 3 days alter injection. Incisors were stained with glyoxal-bis-(2-hydroxyanil) (GBHA) and the enamel surface examined in a fluorescence microscope with incident-light excitation. In maturing enamel Calcein produced five fluorescent double bands across the long axis of the tooth. GBHA produced a series of single red stripes, each of which was imposed on a double Calcein band l h after injection. At longer intervals after injection GBHA stripes were seen to be gradually displaced in the apical direction from the Calcein double bands. Since GBHA is known to stain enamel adjacent to smooth-ended ameloblasts this supports the view of a cyclic modulation of ameloblast morphology and function.     

Overexpression of transforming growth factor-β1 in teeth results in detachment of ameloblasts and enamel defects

Transforming growth factor- β 1 (TGF- β 1) is a key regulator of many cellular processes, including cell adhesion, the immune response and synthesis of extracellular matrix proteins. In the present study, we report the characterization of enamel defects in a transgenic mouse model overexpressing TGF- β 1 in odontoblasts and ameloblasts, its expression being driven by the promoter sequences of the dentin sialophosphoprotein gene. As reported earlier, these mice develop distinct dentin defects similar to those seen in human dentin dysplasia and dentinogenesis imperfecta. A further detailed examination of enamel in these mice revealed that from the early secretory stage, ameloblasts began to detach from dentin to form cyst-like structures. A soft X-ray analysis revealed that this cyst-like structure had a disorganized and partially mineralized matrix with an abnormal mineralization pattern and a globular appearance. In the molars, the enamel was not only pitted and hypoplastic, but enamel rods were completely lost. Thus, altered TGF- β 1 expression in the tooth seems to trigger detachment of ameloblasts and abnormal secretion and deposition of minerals in the cyst-like structures adjoining the dentin. We speculate that the altered expression of TGF- β 1 in teeth impacts the adhesion process of ameloblasts to dentin.     

牙齿再生——梦想与现实

牙齿及牙列缺失在临床上很常见，目前的修复方法均为非生物性的，尚不能满足人们的要求。实现真牙再生一直是一个梦想。牙齿再生分为全牙再生和部分牙齿再生，前者目前尚存在相当大的困难，但后者已有可喜进展，已在小鼠及大型动物小型猪上成功再生出生物牙根，有望成为全牙再生成功前良好的过渡。研究表明骨髓中部分细胞在一定条件下可以直接分化为成釉上皮样细胞及成牙本质细胞，有望成为牙齿再生的间充质来源的种子细胞。     

T-2毒素对大鼠切牙成釉细胞凋亡相关基因Bcl-2和Bax表达的影响

目的:研究不同剂量T-2毒素对大鼠切牙成釉细胞Bcl-2和Bax表达的影响。方法:选择30只SD大鼠,随机分为3组:对照组,实验组1和实验组2,T-2毒素灌胃剂量分别为每天每公斤体质量0、100、200 ng,每周灌胃6 d,连续灌胃4周后处死,取含牙的下颌骨,沿切牙长轴做5μm连续切片,SABC免疫组化检测成釉细胞Bcl-2和Bax蛋白表达,计算机图像采集积分光密度半定量分析Bcl-2和Bax蛋白表达量,蛋白表达量和积分光密度值成反比。结果:两实验组较对照组分泌期成釉细胞Bcl-2蛋白表达下降,Bax蛋白表达上升,Bax/Bcl-2表达的比值上升,各组间均有显著性差异(P<0.05)。结论:T-2毒素可使大鼠切牙分泌期成釉细胞Bcl-2蛋白表达下降,同时上调Bax蛋白表达。高剂量T-2毒素影响更明显。     

Influence of fluoride on secretory pathway of the secretory ameloblast in rat incisor tooth germs exposed to sodium fluoride

 Fluoride, which is an environmental toxicant, is a potent inducer of mottled enamel in humans and rats. To define the influence of fluoride on the secretory pathway in enamel fluorosis, mottled enamel was induced in the incisor tooth germs of rats by subcutaneous injections of sodium fluoride for 4 days, and then morphological and cytochemical changes of the secretory ameloblast were examined in the tooth germs with HRP-labeled lectin (Con A, GS-I, SBA and PNA) and En3 antibody labeling amelogenins. The accumulation of small vesicles on the route of the secretory pathway between the rER and the Golgi apparatus, disorder of Golgi stacks, and formation of abnormal large granules in distal cytoplasm were seen in the secretory ameloblast. Lectin staining patterns of the secretory ameloblast indicated the disturbance of the vesicular transport between the rER and the Golgi apparatus, and disorganization of the Golgi stack. Immunolabeling of the cell showed disruption of the sorting and fusion process on the secretory pathway. These results suggest that the fluoride disturbs the intracellular transport in the synthesis-secretory pathway of the ameloblast, and that this effect of fluoride on the synthesis-secretory pathway participates in the formation of enamel fluorosis. Received: 9 August 1995 / Accepted: 17 October 1995