Skip to main content

The link between different infection forms of Porphyromonas gingivalis and acute myocardial infarction: a cross-sectional study



Porphyromonas gingivalis (Pg) is one of the keystone pathogens involved in periodontitis. The present study aimed to observe the relationship among different infection forms of Pg, systemic inflammation, and acute myocardial infarction (AMI).


A total of 382 patients diagnosed with AMI and 78 patients without coronary heart disease (CHD) were included in the study. DNA from exfoliated oral cells, circulating cell-free DNA (cfDNA), and genomic DNA (gDNA) from blood samples were extracted. The qPCR method was employed to detect Pg infection. Clinical characteristics, inflammatory parameters, and severity of coronary artery lesions of the patients were analyzed and compared.


Both the oral colonization and distant invasion of Pg correlated positively with systemic inflammation. Multivariate logistic regression analysis suggested that Pg positivity in gDNA was correlated with the risk of AMI [Model 1 (odds ratio (OR) = 1.917, 95% confidence interval (CI) 1.108–3.315), Model 2 (OR = 1.863, 95% CI 1.064–3.262), and Model 3 (OR = 1.853, 95% CI 1.042–3.295); p < 0.05]. Pg positivity in cfDNA and gDNA was related to the severity of coronary artery lesions (cfDNA-positive cases, adjusted OR = 1.577, p < 0.05; gDNA-positive cases, adjusted OR = 1.976, p < 0.01).


The distant invasion and colonization of Pg were the risk factors of AMI. They also affected the severity of CHD, indicating that periodontitis severity and distant invasion of periodontal pathogens were related to CHD. The presence of Pg was likely able to drive systemic inflammation, suggesting that there was an inflammatory relationship between periodontitis and AMI.

Peer Review reports


Cardiovascular disease (CVD) is the leading cause of death worldwide [1]. Atherosclerosis is the pathological basis of CVD. In addition to traditional risk factors, chronic inflammatory process is one of the important CVD mechanisms [2]. Endothelial dysfunction caused by immune and inflammatory responses is the earliest and most significant process in atherosclerosis [3]. Therefore, chronic infectious diseases, such as periodontitis (PD), have recently become considered responsible for CVD [4,5,6]. In 1993, DeStefano et al. [7] discovered that PD is one of the risk factors for coronary heart disease (CHD). Since then, the impact of PD on CVD has become the focus of research studies. A growing number of studies have reported a positive correlation between PD and CVD [5]. Several clinical studies have observed the relationship between CVD and oral examination data for patients with PD, such as the number of retained teeth, bleeding on probing, periodontal pocket depth, etc. [8, 9]. However, the American Heart Association [4] has noted that previous data have been inconclusive regarding whether the relationship between PD and CVD is causal or coincidental. Therefore, it is in need of further evaluation.

Porphyromonas gingivalis (Pg) is the most important pathogen of PD. Based on animal experiments, it has been confirmed that Pg is closely related to the initiation and development of many systemic diseases, such as atherosclerosis, cancer, and Alzheimer’s disease [10,11,12]. Nevertheless, few clinical studies have been conducted to directly observe the effect of pathogens that cause PD in patients with CVD.

Thus, the purpose of the present study was to investigate the presence of Pg DNA in the oral cavity and blood samples of patients with acute myocardial infarction (AMI) and non-CHD patients, and analyze its relationship with the incidence of AMI, inflammatory markers, and severity of coronary artery disease, with the aim to optimize early risk stratification for CHD patients and guide clinical treatment.


Study population

In the present study, the inclusion criteria for the case group were patients diagnosed with AMI, those who underwent direct percutaneous coronary intervention, and individuals < 75 years of age (Fig. 1). The control group consisted of 78 patients < 75 years of age who were hospitalized due to precordial discomfort during the same period. In addition, coronary angiography was performed to exclude CHD (Fig. 2). The patients were fully informed about the study and participated voluntarily. Diagnostic criteria for AMI conformed to the present AMI guidelines [13]. Exclusion criteria included severe heart failure symptoms (NYHA III or Killip II or above); patients with other serious systemic diseases, such as malignant tumors and rheumatic immune system diseases, that affect life expectancy; patients with severe renal failure [serum creatinine > 2.0 mg/dL (176.8 μmol/L)], those undergoing hemodialysis, or individuals suffering from severe liver diseases before the operation; patients with poor compliance judged by the researcher or patients who could not complete the study as required; patients with severe cognitive dysfunction or those unable to communicate for other reasons.

Fig. 1
figure 1

The flow chart for enrollment in the case group

Fig. 2
figure 2

The flow chart for enrollment in the control group

The present study was approved by the ethical review committee of the First Affiliated Hospital of Henan University of Science and Technology, Luoyang, China (approval ID: 2022-03-B029). All patients included in the study were fully informed about the investigation and provided written consent of participation. The study protocol conformed to the ethical guidelines of the 1975 Declaration of Helsinki.

Clinical data collection

Complete patient medical record information was collected for all participants. All patients underwent coronary angiography, and all angiography procedures were performed using a Philips coronary angiography device (Integris BH, 5000; Philips, Netherlands). Selective coronary angiography was carried out utilizing the radial artery approach with a 6F catheter. Two independent operators determined the percentage of coronary artery stenosis. A syntax scoring system was used to evaluate the severity of coronary artery lesions.

Quantification of Pg DNA in the oral cavity and circulatory system

Prior to performing coronary angiography, oral samples were collected from the gingival tissues of the second and third molars in the four quadrants of the subjects’ oral cavities using disposable oral flocked swabs. Blood samples were obtained from the radial artery through a 6.0F sheath after radial artery puncture.

Oral samples were centrifuged at 12,000 rpm at room temperature and the supernatant was discarded. After adding 50 µL of Tris–EDTA (10-mM Tris, 1-M EDTA, pH 8.0) to the precipitate, it was resuspended in preparation for qPCR. Blood samples were centrifuged at 2500 rpm for 10 min to separate the serum and buffy coat. Circulating cell-free DNA (cfDNA) and genomic DNA (gDNA) were extracted from blood samples for qPCR according to the instructions for the kits (DP348-02, DP339; Tiangen Biotech Co., Ltd., Beijing, China).

The positive rate of Pg was determined using qPCR and specific primer probe sequences were as Kuboniwa et al. [14] reported. The designed primer sequences were as follows: P. gingivalis forward, 5′-ACCTTACCCGGGATTGAAATG-3′, P. gingivalis reverse, 5′-CAACCATGCAGCACCTACATA-GAA-3′; P. gingivalis probe, 5′-FAMATGACTGATGGTGAAAA-CCGTCTTCCCTTC-TARMA-3′. Both the primer and probe sequences were synthesized by GENEWIZ Biotechnology Co., Ltd, Suzhou. The PCR system consisted of the following: 10 μL of Ace qPCR Probe Master Mix (Q112-03; Vazyme Biotech Co., Ltd., Nanjing, China), 10-μmol forward (0.5 μL) and reverse (0.5 μL) primers, 0.2-pmoL TaqMan probe, and 2 μL of sample including 50 ng of DNA. DEPC water was added to achieve a total volume of 20 μL. The above system solution was added into the PCR strip tubes. The amplification was performed in the BioRad CFX96TM real-time PCR system at 95ºC for 10 min for a total of 40 PCR cycles (95 °C, 10 s; 60 °C, 60 s). The amplification results were analyzed using the CFX Maestro™ software.

Statistical analysis

Measurement data were expressed as means and standard deviations (\(\overline{x} \pm s\)). The differences between groups were compared using a t-test if the data satisfied the normal distribution and homogeneity test of variance requirements. Wilcoxon rank sum test was utilized if the data did not satisfy the normal distribution or homogeneity test of variance requirements. Count data were expressed using frequency (percentage), and the differences between the groups were compared by the Pearson’s χ2 test. Spearman’s rank analysis was carried out to identify the association between Pg and systemic inflammatory factors. The differences in inflammatory parameters of different infection forms of Pg in AMI patients were compared with a one-way analysis of variance. Multivariate logistic regression analysis was performed to evaluate the relationship among the different infection forms of Pg, AMI, and severity of coronary artery lesions. SPSS statistical software for Windows, version 22.0 (SPSS, Chicago, IL, USA) was employed to sort and analyze the data. All statistical tests were bilateral, with p < 0.05 considered to indicate statistical significance.


Basic clinical data

A total of 382 patients with a mean age of 57.51 ± 9.92 years diagnosed with AMI (295 cases with ST-segment elevation myocardial infarction, 87 cases with non-ST-segment elevation myocardial infarction) were included in the case group. Then, 78 non-CHD patients with a mean age of 56.85 ± 8.96 years and confirmed non-CHD status using coronary angiography were included in the control group. There were statistically significant differences (p < 0.05, Table 1) in proportion of male patients [275 (72%) vs. 47 (60%)], previous history of CHD [54 (14%) vs. 0 (0%)], diabetes status [152 (40%) vs. 20 (26%)], and current smoking status [104 (27%) vs. 12 (15%)] in the AMI group compared to the control group. Indices, such as total cholesterol, low-density lipoprotein, high-density lipoprotein, and inflammatory indexes, represented statistical differences between the non-CHD group and AMI group (Table 1). Most AMI patients were directly transferred to the interventional operating room. Therefore, the clinical data in the present study did not include information such as height and weight.

Table 1 Comparison of baseline characteristics between the AMI group and the control group

Comparison of Pg DNA positivity

There was no significant difference in Pg DNA positivity in the oral cavity between the AMI and non-CHD groups [209 cases (55%) vs. 34 cases (44%), p > 0.05]. The positive rate of Pg in the blood samples was statistically different between the two groups [cfDNA-positive in 177 cases (46%) vs. 26 cases (33%), p < 0.05; gDNA-positive in 152 cases (40%) vs. 20 cases [26%], p < 0.05; Table 1].

Association between different infection forms of Pg and systemic inflammation

Spearman’s rank correlation analysis was performed to identify the association between different infection forms of Pg and systemic inflammatory factors (Table 2). In addition, patients in the AMI group were divided into groups based on the presence of Pg. The inflammatory indexes in AMI patients with Pg infection were significantly high (Fig. 3), especially in patients with Pg positivity in gDNA (Table 3).

Table 2 Spearman’s rank correlation for different infection forms of Pg with the values of inflammatory parameters
Fig. 3
figure 3

Effect of Pg on inflammatory indexes of AMI group. A Showed that WCC, NEUT, and hsCRP levels were higher in patients positive for Pg in the oral cavity, p < 0.05. B Showed that WCC, NEUT, hsCRP, and ESR levels were higher in patients positive for Pg in cfDNA, p < 0.05. C Showed that WCC, NEUT, FIB, hsCRP, ESR and PCT levels were higher in patients positive for Pg in gDNA, p < 0.05. WCC white cell count, NEUT neutrophil count, hsCRP high sensitivity C-reactive protein, ESR erythrocyte sedimentation rate, FIB fibrinogen, PCT procalcitonin

Table 3 The effect of different infection forms of Pg on the values of inflammatory parameters in AMI patients

Association between Pg infection and AMI

Univariate and multivariable logistic regression were performed with the occurrence of AMI (No: 0; Yes: 1) was used as the dependent variable, and Pg positivity was used as the variable to be adjusted first. The results showed that Pg positivity in gDNA was an independent risk factor for AMI [Model 1 (odds ratio (OR) = 1.917, 95% confidence interval (CI) 1.108–3.315), Model 2 (OR = 1.863, 95% CI 1.064–3.262), and Model 3 (OR = 1.853, 95% CI 1.042–3.295) (p < 0.05); Table 4].

Table 4 Correlation between Pg infection and risk of AMI occurrence

Association between Pg infection and severity of coronary artery lesions

The severity of coronary artery lesions in AMI patients was divided into a mild (Syntax score < 23) and a moderate-severe (Syntax score ≥ 23) groups. In univariate logistic regression analysis, the results indicated that Pg positivity in the circulatory system was related to the severity of coronary artery. The same result was obtained when the confounding factors were adjusted (Table 5).

Table 5 Correlation between Pg and severity of coronary artery lesions in AMI patients


The present study for the first time evaluated the different infection forms of Pg by detecting the presence of Pg DNA using the qPCR method and analyzed its relationship with AMI. The main study findings were as follows: (1) Pg correlated positively with systemic inflammation regardless of the Pg infection mode, and systemic inflammatory molecular levels increased significantly; (2) Pg positivity in the circulatory system (cfDNA and gDNA) was an independent risk factor for first-time AMI and was related to the severity of coronary artery, with a possible clinical significance for optimizing risk stratification in CHD patients; and (3) the study findings further strengthened the possibility of an independent relationship between PD and CVD manifestations.

The present study supported the idea that the main mechanism for PD affecting the development of atherosclerosis was the direct invasion of endothelial cells by periodontal pathogens [6]. Furthermore, cfDNA consisted of extracellular DNA fragments present in the serum that may be derived from both normal and diseased cells. Pg positivity in cfDNA indicated that Pg invaded the circulatory system. In addition, Pg positivity in gDNA indicated that Pg colonized the circulatory system with persistent presence in the cells, further resulting in a lasting inflammatory state. The study results also showed a positive association between gDNA Pg positivity and AMI, which remained following adjustment for the differences in clinical characteristics between patients and controls. This reinforces the possibility of an independent relationship between PD and the risk for CVD presently expressed as AMI, which depends on whether the distant invasion and colonization of endothelial cells by periodontal pathogens were involved.

On one hand, Pg can leave oral epithelial cells via the endocytic recycling pathway and infect other cells or enter the circulatory system [15]. Live Pg can be detected in human aortic endothelial cells [16], human pancreatic tumor cells [17], and human myeloid dendritic cells [18]. Pg DNA can be detected in atherosclerotic plaques [19]. Repeated intravenous injection of Pg can aggravate the progression of atherosclerosis in mice, and the size of aortic lesions inoculated with Pg was twice as large as that of the control group [10]. On the other hand, Dietrich et al. [8] have found that patients with severe PD had an increased risk of the first coronary artery event compared to patients without PD or those with mild PD. In the PAROKRANK study [9] has found that the risk of the first AMI increased significantly in patients with moderate to severe PD. It has been speculated that this was because patients with severe PD were more likely to transfer microorganisms from dental pockets into the bloodstream by chewing and via dental treatments causing bacteremia and systemic inflammation [20]. Another finding of the present study illustrated that Pg positivity in cfDNA and gDNA samples from AMI patients was positively correlated with the severity of coronary artery disease (Table 5), which again demonstrated that direct invasion of periodontal pathogens was related to the development of atherosclerosis. Such studies indicate that Pg can enter the circulatory system and directly act on the lesion site to promote the development of atherosclerosis. So far, it has not been determined how the bacteria existing in cells influence atherosclerosis. However, in vitro experiments have shown that Pg could trigger the formation of foam cells or result in their persistent presence in the cells, causing a secondary inflammatory state and leading to endothelial dysfunction [21]. In addition, it inhibits cell apoptosis [22], suggesting the inflammatory relationship between Pg and atherosclerosis, which is consistent with the present study results.

The present study showed that Pg correlated positively with systemic inflammation regardless of the Pg infection mode (Table 2). The same results were observed in patients with AMI (Fig. 3), especially in individuals with Pg positivity in gDNA (Table 3). These results supported another hypothesis that periodontal pathogens affect the occurrence and development of atherosclerosis, increasing systemic inflammatory molecular levels through indirect pathways.

CHD is an inflammatory disease, and inflammation plays an important role in the development and manifestations of CHD [23]. Determining the levels of inflammatory markers may be important for assessing the risk of CHD [24,25,26]. PD can stimulate a systemic inflammatory response, resulting in a long-term increase in the levels of different cytokines, which are also related to atherosclerotic vascular diseases [27]. However, most previous studies have focused on the relationship between periodontal parameters, inflammatory factors, and CVD [28, 29]. In the present study, the effects of different infection forms of the PD pathogen Pg on systemic inflammatory factors were directly observed in the human body. It was discovered that Pg could increase systemic inflammatory factors whether it was colonized in the oral cavity or invaded a distant area. At the same time, patients with Pg-positive gDNA and AMI had more severe systemic inflammatory reactions, further supporting the direct effect of periodontal pathogens.

In summary, Pg had an independent influence on the occurrence of AMI and the severity of CHD. It could affect the development of CHD through direct invasion and triggering systemic inflammatory reactions. Although there is insufficient evidence to clarify the potential benefits of periodontal treatment for secondary prevention of CVD [5, 30], PD is widespread, and some studies suggest that it may be a changeable risk factor for CVD. Therefore, we should pay attention to the periodontal health of patients with CVD and take appropriate preventive and therapeutic measures. In fact, when clinicians are faced with patients with AMI, it is difficult to obtain detailed periodontal test data for patients at the first time, such as the number of retained teeth, bleeding on probing, and so on. However, determining whether patients are infected with related pathogenic bacteria and the level of related inflammatory mediators may play a guiding role in further clinical interventions.

There were some limitations in this study. First, this was a cross-sectional, single-center study with relatively small sample size. Therefore, it could not determine the causality between Pg and AMI. Second, other inflammatory processes might coexist in AMI patients. Third, due to the sample size, the effect of Pg on inflammatory molecular levels in non-CHD patients was not investigated. Finally, the present study results showed no significant difference in Pg DNA positivity in the oral cavity between the two groups [209 cases (55%) vs. 34 cases (44%), p > 0.05], which contradicted previous study results [31, 32]. This may be explained by the use of a specific and possibly less efficient oral sampling method. In addition, periodontal diagnosis was not performed in the study. Therefore, there may be some bias in the results and further study is needed.


PD pathogen invasion and colonization in the circulatory system was one of the risk factors of first-time AMI and was related to the severity of coronary artery lesions. The systemic inflammation was more evident in AMI patients with Pg positivity in the circulatory system, which may suggest a potential inflammatory link between PD and AMI. Two conclusions can be drawn from the present study. First, Pg positivity in the circulatory system was significantly and positively correlated with AMI. Second, Pg promoted systemic inflammation response. Future multicenter, prospective, and randomized clinical trials are necessary to determine whether the treatment of PD and removal of its pathogenic bacteria can help prevent the occurrence or recurrence of CVD.

Availability of data and materials

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.


Pg :

Porphyromonas gingivalis


Circulating free DNA


Genomic DNA


Coronary heart disease


Acute myocardial infarction


Cardiovascular disease




  1. Nowbar AN, Howard JP, Finegold JA, Asaria P, Francis DP. 2014 global geographic analysis of mortality from ischaemic heart disease by country, age and income: statistics from World Health Organisation and United Nations. Int J Cardiol. 2014;174:293–8.

    Article  Google Scholar 

  2. Zimmer S, Grebe A, Latz E. Danger signaling in atherosclerosis. Circ Res. 2015;116:323–40.

    Article  Google Scholar 

  3. Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000;20:1262–75.

    Article  Google Scholar 

  4. Lockhart PB, Bolger AF, Papapanou PN, Osinbowale O, Trevisan M, Levison ME, et al. Periodontal disease and atherosclerotic vascular disease: does the evidence support an independent association?: a scientific statement from the American Heart Association. Circulation. 2012;125:2520–44.

    Article  Google Scholar 

  5. Sanz M, Marco Del Castillo A, Jepsen S, Gonzalez-Juanatey JR, D’Aiuto F, Bouchard P, et al. Periodontitis and cardiovascular diseases: consensus report. J Clin Periodontol. 2020;47:268–88.

    Article  Google Scholar 

  6. Zardawi F, Gul S, Abdulkareem A, Sha A, Yates J. Association between periodontal disease and atherosclerotic cardiovascular diseases: revisited. Front Cardiovasc Med. 2021;7:625579.

    Article  Google Scholar 

  7. DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM. Dental disease and risk of coronary heart disease and mortality. BMJ. 1993;306:688–91.

    Article  Google Scholar 

  8. Dietrich T, Sharma P, Walter C, Weston P, Beck J. The epidemiological evidence behind the association between periodontitis and incident atherosclerotic cardiovascular disease. J Clin Periodontol. 2013;40(Suppl 14):S70–84.

    Google Scholar 

  9. Rydén L, Buhlin K, Ekstrand E, de Faire U, Gustafsson A, Holmer J, et al. Periodontitis increases the risk of a first myocardial infarction: a report from the PAROKRANK study. Circulation. 2016;133:576–83.

    Article  Google Scholar 

  10. Xie M, Tang Q, Nie J, Zhang C, Zhou X, Yu S, et al. BMAL1-downregulation aggravates Porphyromonas Gingivalis-induced atherosclerosis by encouraging oxidative stress. Circ Res. 2020;126:e15–29.

    Article  Google Scholar 

  11. Wu JS, Zheng M, Zhang M, Pang X, Li L, Wang SS, et al. Porphyromonas gingivalis promotes 4-nitroquinoline-1-oxide-induced oral carcinogenesis with an alteration of fatty acid metabolism. Front Microbiol. 2018;9:2081.

    Article  Google Scholar 

  12. Dominy SS, Lynch C, Ermini F, Benedyk M, Marczyk A, Konradi A, et al. Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors. Sci Adv. 2019;5:eaau3333.

    Article  Google Scholar 

  13. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, et al. Executive Group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth Universal Definition of Myocardial Infarction. Circulation. 2018;138:e618–51.

    Google Scholar 

  14. Kuboniwa M, Amano A, Kimura KR, Sekine S, Kato S, Yamamoto Y, et al. Quantitative detection of periodontal pathogens using real-time polymerase chain reaction with TaqMan probes. Oral Microbiol Immunol. 2004;19:168–76.

    Article  Google Scholar 

  15. Takeuchi H, Furuta N, Morisaki I, Amano A. Exit of intracellular Porphyromonas gingivalis from gingival epithelial cells is mediated by endocytic recycling pathway. Cell Microbiol. 2011;13:677–91.

    Article  Google Scholar 

  16. Yamatake K, Maeda M, Kadowaki T, Takii R, Tsukuba T, Ueno T, et al. Role for gingipains in Porphyromonas gingivalis traffic to phagolysosomes and survival in human aortic endothelial cells. Infect Immun. 2007;75(5):2090–100.

    Article  Google Scholar 

  17. Gnanasekaran J, Binder Gallimidi A, Saba E, Pandi K, Eli Berchoer L, Hermano E, et al. Intracellular Porphyromonas gingivalis promotes the tumorigenic behavior of pancreatic carcinoma cells. Cancers (Basel). 2020;12:2331.

    Article  Google Scholar 

  18. El-Awady AR, Miles B, Scisci E, Kurago ZB, Palani CD, Arce RM, et al. Porphyromonas gingivalis evasion of autophagy and intracellular killing by human myeloid dendritic cells involves DC-SIGN-TLR2 crosstalk. PLoS Pathog. 2015;10:e1004647.

    Article  Google Scholar 

  19. Szulc M, Kustrzycki W, Janczak D, Michalowska D, Baczynska D, Radwan-Oczko M. Presence of periodontopathic bacteria DNA in atheromatous plaques from coronary and carotid arteries. Biomed Res Int. 2015;2015:825397.

    Article  Google Scholar 

  20. Forner L, Larsen T, Kilian M, Holmstrup P. Incidence of bacteremia after chewing, tooth brushing and scaling in individuals with periodontal inflammation. J Clin Periodontol. 2006;33(6):401–7.

    Article  Google Scholar 

  21. Roth GA, Moser B, Huang SJ, Brandt JS, Huang Y, Papapanou PN, et al. Infection with a periodontal pathogen induces procoagulant effects in human aortic endothelial cells. J Thromb Haemost. 2006;4:2256–61.

    Article  Google Scholar 

  22. Bélanger M, Rodrigues PH, Dunn WA Jr, Progulske-Fox A. Autophagy: A highway for Porphyromonas gingivalis in endothelial cells. Autophagy. 2006;2:165–70.

    Article  Google Scholar 

  23. Libby P. Inflammation and cardiovascular disease mechanisms. Am J Clin Nutr. 2006;83:456S-460S.

    Article  Google Scholar 

  24. Stumpf C, Sheriff A, Zimmermann S, Schaefauer L, Schlundt C, Raaz D, et al. C-reactive protein levels predict systolic heart failure and outcome in patients with first ST-elevation myocardial infarction treated with coronary angioplasty. Arch Med Sci. 2017;13:1086–93.

    Article  Google Scholar 

  25. Lu Y, Zhou S, Dreyer RP, Spatz ES, Geda M, Lorenze NP, et al. Sex differences in inflammatory markers and health status among young adults with acute myocardial infarction: results from the VIRGO (variation in recovery: role of gender on outcomes of young acute myocardial infarction patients) study. Circ Cardiovasc Qual Outcomes. 2017;10:e003470.

    Article  Google Scholar 

  26. Ang L, Behnamfar O, Palakodeti S, Lin F, Pourdjabbar A, Patel MP, et al. Elevated baseline serum fibrinogen: effect on 2-year major adverse cardiovascular events following percutaneous coronary intervention. J Am Heart Assoc. 2017;6:e006580.

    Article  Google Scholar 

  27. Caúla AL, Lira-Junior R, Tinoco EM, Fischer RG. The effect of periodontal therapy on cardiovascular risk markers: a 6-month randomized clinical trial. J Clin Periodontol. 2014;41:875–82.

    Article  Google Scholar 

  28. Wojtkowska A, Zapolski T, Wysokińska-Miszczuk J, Wysokiński AP. The inflammation link between periodontal disease and coronary atherosclerosis in patients with acute coronary syndromes: case-control study. BMC Oral Health. 2021;21:5.

    Article  Google Scholar 

  29. Górski B, Nargiełło E, Opolski G, Ganowicz E, Górska R. The association between dental status and systemic lipid profile and inflammatory mediators in patients after myocardial infarction. Adv Clin Exp Med. 2016;25:625–30.

    Article  Google Scholar 

  30. Liu W, Cao Y, Dong L, Zhu Y, Wu Y, Lv Z, et al. Periodontal therapy for primary or secondary prevention of cardiovascular disease in people with periodontitis. Cochrane Database Syst Rev. 2019;12:CD009197.

    Google Scholar 

  31. Griffen AL, Becker MR, Lyons SR, Moeschberger ML, Leys EJ. Prevalence of Porphyromonas gingivalis and periodontal health status. J Clin Microbiol. 1998;36:3239–42.

    Article  Google Scholar 

  32. Curia MC, Pignatelli P, D’Antonio DL, D’Ardes D, Olmastroni E, Scorpiglione L, et al. Oral Porphyromonas gingivalis and Fusobacterium nucleatum abundance in subjects in primary and secondary cardiovascular prevention, with or without heterozygous familial hypercholesterolemia. Biomedicines. 2022;10:2144.

    Article  Google Scholar 

Download references


We would like to acknowledge the hard and dedicated work of all the staff that implemented the intervention and evaluation components of the study. The authors would like to thank the Project on Key Medical Discipline (Specialty) Construction of Tianjin.


Tianjin Key Medical Discipline (Specialty) Construction Project (TJYXZDXK-029A). Joint Construction Project of Henan Medical Science and Technology Research Plan in 2019(LHGJ20190561). Luoyang Special Scientific Research on Medical and Health in 2020(2001029A).

Author information

Authors and Affiliations



Concept—YW; design—YW, KW; supervision—YW, KW; fundings—GL, LD, KW; materials—LD, YW; data collection and/or processing—YW, YW; analysis and/or interpretation—LD, SW, GL; literature search—KW, SW; writing—YW, SW, GL; critical review—LD, GL. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Guangping Li.

Ethics declarations

Competing interests

The authors declare no competing interests.

Ethics approval and consent to participate

This study was approved by the ethical review committee of the First Affiliated Hospital of Henan University of Science and Technology (Luoyang, China) (approval ID: 2022-03-B029; date: 24.03.2022). Informed consent was obtained from all individual participants included in the study. The study protocol conforms to the ethical guidelines of the 1975 Declaration of Helsinki.

Consent for publication

Not applicable.

Competing interest

The authors declare no competing interest.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Wu, Y., Wang, Y., Du, L. et al. The link between different infection forms of Porphyromonas gingivalis and acute myocardial infarction: a cross-sectional study. BMC Oral Health 23, 63 (2023).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI:


  • Acute myocardial infarction
  • Atherosclerosis
  • Inflammation
  • Periodontitis
  • Porphyromonas gingivalis