Evaluation of a mouse odontoma model and elucidation of the developmental mechanisms of odontoma

已知聚（adp -核糖）聚合酶（Parp1）通过转录控制在细胞死亡和细胞分化中起作用。在本研究中，对遗传背景为ICR/129Sv的Parp1-/-和野生型Parp1^<+/+>小鼠的脱钙下颌骨（包括门牙）进行了基础饮食维持2年的组织学分析。共分析雄性Parp1^<-/->小鼠10个样本和雄性Parp1^<+/+>小鼠13个样本。在Parp1^<-/->小鼠的所有样本中，牙本质均表现出明显的增殖，在牙髓腔内观察到不规则排列的成牙细胞。相比之下，Parp1^<+/+>小鼠样本中的成牙细胞在牙髓一侧排列整齐，未观察到牙釉质异常。为了阐明PARP1在人牙瘤发生发展中的作用，我们对7例复合型和6例复合型人牙瘤标本进行了免疫组化分析。结果显示，PARP1在牙瘤的牙胚样组织、牙釉质上皮、未成熟牙本质和未成熟牙釉质中表达。此外，在成牙细胞和成釉细胞对应的上皮成分中也检测到其表达。这些发现表明PARP1有助于构成牙瘤的细胞的分化。此外，PARP1在没有细胞核的鬼细胞的细胞质中表达。这些鬼细胞的细胞质也被M30CytoDEATH抗体强烈免疫染色，该抗体针对细胞角蛋白18在凋亡过程中产生的切割位点。由于鬼细胞被认为是一种积累硬角蛋白的退行性细胞，并且一些早期凋亡事件似乎已经发生，这些观察结果表明，经历凋亡的鬼细胞中PARP1的表达促进了这些细胞在牙瘤中的形成。少

Poly (ADP-ribose) polymerase (Parp1) is known to play roles in cell death and cell differentiation through transcriptional control. In the present study, decalcified mandibles, including the incisors, from Parp1-/- and wild-type Parp1^<+/+> mice with a genetic background of ICR/129Sv maintained on a basal diet for 2 years were subjected to histological analyses. A total of 10 samples from male Parp1^<-/-> mice and 13 samples from male Parp1^<+/+> mice were analyzed. In all samples from the Parp1^<-/-> mice, the dentin showed remarkable proliferation and irregularly lined odontoblasts were observed on the inside of the dental pulp cavity. In contrast, the odontoblasts in the samples from the Parp1^<+/+> mice were regularly lined up on the side of the dental pulp and no abnormalities of the enamel were observed. To elucidate the involvement of PARP1 in the development of human odontoma, samples obtained from 7 complex type and 6 compound type human odontoma cases were analyzed immunohist … More ochemically for their expressions of PARP1. The results revealed that PARP1 was expressed in tooth germ-like tissue, reduced enamel epithelium, immature dentin and immature enamel in the odontomas. Moreover, its expression was detected in odontoblasts and the epithelial component corresponding to ameloblasts. These findings indicate that PARP1 contributes to the differentiation of the cells that constitute odontomas. In addition, PARP1 was expressed in the cytoplasm of ghost cells that did not possess a nucleus. The cytoplasm of these ghost cells was also strongly immunostained by the M30CytoDEATH antibody raised against the cleavage site of cytokeratin 18 produced during the process of apoptosis. Since ghost cells are considered to represent a type of degenerative cells that accumulate hard keratins, and some early apoptosis events seem to have occurred, these observations indicate that PARP1 expression in ghost cells undergoing apoptosis contributed to the formation of these cells in odontomas. Less