Dental pulp can initiate its damage repair after an injury of the pulp–dentin complex by rearrangement of odontoblasts and formation of newly differentiated odontoblast-like cells. Connexin 43 (Cx43) is one of the gap junction proteins that participates in multiple tissue repair processes. However, the role of Cx43 in the repair of the dental pulp remains unclear. This study aimed to determine the function of Cx43 in the odontoblast arrangement patterns and odontoblastic differentiation. Human teeth for in vitro experiments were acquired, and a pulp injury model in Sprague-Dawley rats was used for in vivo analysis. The odontoblast arrangement pattern and the expression of Cx43 and dentin sialophosphoprotein (DSPP) were assessed. To investigate the function of Cx43 in odontoblastic differentiation, we overexpressed or inhibited Cx43. The results indicated that polarized odontoblasts were arranged along the pulp–dentin interface and had high levels of Cx43 expression in the healthy teeth; however, the odontoblast arrangement pattern was slightly changed concomitant to an increase in the Cx43 expression in the carious teeth. Regularly arranged odontoblast-like cells had high levels of the Cx43 expression during the formation of mature dentin, but the odontoblast-like cells were not regularly arranged beneath immature osteodentin in the pulp injury models. Subsequent in vitro experiments demonstrated that Cx43 is upregulated during odontoblastic differentiation of the dental pulp cells, and inhibition or overexpression of Cx43 influence the odontoblastic differentiation. Thus, Cx43 may be involved in the maintenance of odontoblast arrangement patterns, and influence the pulp repair outcomes by the regulation of odontoblastic differentiation.

在牙髓-牙本质复合体受伤后，牙髓可通过成牙本质细胞的重排和新分化的成牙本质细胞样细胞的形成而开始其损伤修复。连接蛋白43（Cx43）是参与多个组织修复过程的间隙连接蛋白之一。但是，Cx43在修复牙髓中的作用仍不清楚。这项研究旨在确定Cx43在成牙本质细胞排列模式和成牙本质细胞分化中的功能。获得用于体外实验的人类牙齿，并将Sprague-Dawley大鼠的牙髓损伤模型用于体内分析。评估成牙本质细胞排列模式以及Cx43和牙本质唾液磷蛋白（DSPP）的表达。为了研究Cx43在成牙本质细胞分化中的功能，我们过表达或抑制了Cx43。结果表明极化的成牙本质细胞沿牙髓-牙本质界面排列，并在健康牙齿中具有高水平的Cx43表达。然而，成牙本质细胞排列模式略有改变，同时导致龋齿中Cx43表达的增加。规则排列的成牙本质细胞样细胞在成熟牙本质的形成过程中具有高水平的Cx43表达，但在牙髓损伤模型中，成牙本质细胞样细胞没有规则地排列在未成熟的骨齿质下方。随后的体外实验表明，Cx43在牙髓细胞的牙本质成牙细胞分化以及抑制或过度表达过程中被上调。成牙本质细胞排列方式略有改变，同时导致龋齿中Cx43表达的增加。规则排列的成牙本质细胞样细胞在成熟牙本质的形成过程中具有高水平的Cx43表达，但在牙髓损伤模型中，成牙本质细胞样细胞没有规则地排列在未成熟的骨齿质下方。随后的体外实验表明，Cx43在牙髓细胞的牙本质成牙细胞分化以及抑制或过度表达过程中被上调。成牙本质细胞排列方式略有改变，同时导致龋齿中Cx43表达的增加。规则排列的成牙本质细胞样细胞在成熟牙本质的形成过程中具有高水平的Cx43表达，但在牙髓损伤模型中，成牙本质细胞样细胞没有规则地排列在未成熟的骨齿质下方。随后的体外实验表明，Cx43在牙髓细胞的牙本质成牙细胞分化以及抑制或过度表达过程中被上调。但是在牙髓损伤模型中，成牙本质细胞样细胞没有规则地排列在未成熟的骨齿质素下方。随后的体外实验表明，Cx43在牙髓细胞的牙本质成牙细胞分化以及抑制或过度表达过程中被上调。但是在牙髓损伤模型中，成牙本质细胞样细胞没有规则地排列在未成熟的骨齿质素下方。随后的体外实验表明，Cx43在牙髓细胞的牙本质成牙细胞分化以及抑制或过度表达过程中被上调。Cx43影响成牙本质细胞分化。因此，Cx43可能参与成牙本质细胞排列模式的维持，并通过调节成牙本质细胞分化来影响牙髓修复结果。