The present study aimed to investigate the mechanism(s) through which endoplasmic reticulum stress (ERS)-induced apoptosis, in the role of periodontitis, affects vascular calcification. Rat models of periodontitis, vascular calcification, periodontitis-vascular calcification, and a normal group were established. Cardiovascular tissues were obtained, and hematoxylin–eosin staining was applied to demonstrate the morphological changes in vascular tissues. Immunohistochemical staining was applied to analyze apoptosis in cardiovascular tissues. The expression levels of apoptotic factor cysteinyl aspartate specific proteinase 3 (Caspase-3), ERS-induced apoptotic factors glucose-regulated protein 78 (GRP78), 94 (GRP94), and ERS-induced apoptosis pathways Caspase-12, C/EBP homologous protein (CHOP), and c-Jun N-terminal kinase (JNK) were analyzed and compared. Hematoxylin–eosin staining revealed that the arterial layers in the normal group were structurally intact. The structural damage to the aortic wall gradually aggravated from the periodontitis group to the vascular calcification group to the combined group. The immunohistochemistry results showed Caspase-3, GRP78, GRP94, and ERS-induced apoptosis pathways in the cardiovascular tissues cells in the periodontitis group, vascular calcification group, and combined group. The Caspase-3, GRP78, GRP94, and CHOP expression levels in the combined group were significantly higher than that in the normal group (P < 0.05); however, the Capase-12 and JNK expression levels in the four groups exhibited no significant differences (P > 0.05). Apoptosis induced by ERS is involved in the effect of periodontitis on vascular calcification and might be mainly achieved through the activation of the CHOP transcription pathway.

本研究旨在探讨内质网应激（ERS）诱导的细胞凋亡在牙周炎中影响血管钙化的机制。建立大鼠牙周炎、血管钙化、牙周炎-血管钙化模型及正常组。获得心血管组织，并应用苏木精-伊红染色来显示血管组织的形态变化。应用免疫组织化学染色分析心血管组织的细胞凋亡。凋亡因子半胱氨酰天冬氨酸特异性蛋白酶3(Caspase-3)、ERS诱导的凋亡因子葡萄糖调节蛋白78(GRP78)、94(GRP94)以及ERS诱导的凋亡通路Caspase-12、C/EBP同源物的表达水平分析并比较了 c-Jun N 末端激酶 (JNK) 和 c-Jun N 末端激酶 (JNK)。苏木精-伊红染色显示正常组的动脉层结构完整。主动脉壁结构损伤从牙周炎组到血管钙化组再到联合组逐渐加重。免疫组化结果显示牙周炎组、血管钙化组和联合组心血管组织细胞中存在Caspase-3、GRP78、GRP94和ERS诱导的凋亡通路。联合组Caspase-3、GRP78、GRP94、CHOP表达水平均显着高于正常组（P < 0.05）；但四组中 Capase-12 和 JNK 表达水平无显着差异（P > 0.05）。 ERS诱导的细胞凋亡参与了牙周炎对血管钙化的影响，可能主要是通过激活CHOP转录途径来实现的。