目的·研究牙周炎（periodontitis，PD）对主动脉弓缩窄（transverse aortic constriction，TAC）诱导的小鼠心肌肥厚的作用和机制。方法·将25只 C57BL/6J小鼠随机分为假手术（Sham）组、TAC组及TAC+PD组。用丝线结扎加涂抹龈下菌斑的方法诱导PD模型，并在PD模型建立后做TAC手术。在假手术或TAC手术后4周，用心脏超声评估心脏功能，然后处死小鼠并取材，其样本用于实时定量聚合酶链式反应（qRT-PCR）、免疫组织化学检测、免疫荧光检测、16S rRNA基因测序。结果·TAC+PD组小鼠的牙槽骨吸收和牙龈组织炎症相关基因的表达均高于Sham组和TAC组，表明在TAC小鼠中成功建立了PD模型。与TAC组相比，TAC+PD组小鼠的左心室射血分数（EF）、左心室缩短分数（FS）值都显著降低，表明PD加重TAC导致的心功能受损。与TAC组相比，TAC+PD组小鼠的心脏质量/体质量比率（HW/BW）和心脏质量/胫骨长度比率（HW/TL）升高、肺质量/体质量比率（LW/BW）升高、心肌细胞横截面积增大、心肌肥厚相关的基因表达水平也显著升高，表明PD加重TAC诱导的心肌肥厚和心力衰竭。与TAC组相比，TAC+PD组小鼠的心肌纤维化程度上升、纤维化相关基因上调、脾脏胫骨长度比率（SW/TL）上升、炎症相关基因上调，表明PD加重了TAC诱导心肌细胞的纤维化和炎症反应。16S rRNA基因测序结果表明，TAC+PD组小鼠的口腔结扎丝线中链球菌属（Streptococcus）和韦荣球菌属（Veillonella）的相对丰度显著高于TAC组；TAC+PD组小鼠的心脏中罗尔斯通菌属（Ralstonia）和嗜糖假单胞菌属（Pelomonas）的相对丰度显著高于TAC组；而且TAC+PD组小鼠的心脏中罗尔斯通菌属和嗜糖假单胞菌属的相对丰度显著高于其口腔结扎丝线。结论·PD能够加重TAC术后小鼠心脏功能损害、心肌肥厚和心肌纤维化，并在一定程度上加重心脏的炎症反应，其作用机制可能与罗尔斯通菌属、嗜糖假单胞菌属等口腔微生物相关。

Objective ·To study the effects of periodontitis (PD) on transverse aortic constriction (TAC)-induced cardiac hypertrophy in mice and explore the mechanisms. Methods ·Twenty-five C57BL/6J mice were randomly divided into Sham operation (Sham) group, transverse aortic constriction (TAC) group, and periodontitis combined with TAC (TAC+PD) group. PD was induced by ligation of mouse molars and application of subgingival plaques of PD patients. TAC surgery was performed after the establishment of PD model. Cardiac function was assessed by echocardiography at 4 weeks after Sham or TAC surgery. The mice were then sacrificed and the samples were collected for quantitative realtime PCR (qRT-PCR), immunohistochemistry, immunofluorescence, and 16S rRNA gene sequencing. Results ·The mice in the TAC+PD group manifested significantly more resorption of the alveolar bone and higher expression of inflammatory genes in gingiva compared to Sham and TAC groups, demonstrating successful establishment of PD models in TAC mice. Compared to those in the TAC group, the mice in the TAC+PD group had significantly lower left ventricular ejection fraction (EF) and left ventricular shortening fraction (FS), illustrating that PD exacerbated TAC-induced cardiac dysfunction. Compared to those in the TAC group, the mice in the TAC+PD group had significantly bigger heart weight to body weight ratio (HW/BW) and heart weight to tibia length ratio (HW/TL), lung weight to body weight ratio (LW/BW), and cross-sectional area of cardiomyocytes, as well as higher expression of hypertrophy-related genes, demonstrating that PD exacerbated TAC-induced cardiac hypertrophy and heart failure. Compared to those in the TAC group, the mice in the TAC+PD group had significantly larger fibrotic areas and higher expression of fibrosis-related genes in the heart, bigger spleen weight to tibia length ratio (SW/TL) and higher expression of inflammatory genes in the heart, illustrating that PD exacerbated TAC-induced cardiac fibrosis and inflammation. Results of 16S rRNA gene sequencing showed that relative abundances of Streptococcus and Veillonella were significantly increased in the oral ligatures of mice in the TAC+PD group compared to the TAC group. Relative abundances of Ralstonia, and Pelomonas were significantly increased in the hearts of mice in the TAC+PD group. Comparison of oral microbiota and heart microbiota of the mice in the TAC+PD group revealed that relative abundances of Ralstonia and Pelomonas in hearts were significantly higher than those in oral ligatures. Conclusion ·PD aggravates TAC-induced cardiac dysfunction, cardiac hypertrophy, fibrosis, and inflammation in mice. The mechanisms may be related to alterations in oral microbiota, particularly bacterial genera including Ralstonia and Pelomonas.