Next Article in Journal
Adaptive Sliding Mode Control Integrating with RBFNN for Proton Exchange Membrane Fuel Cell Power Conditioning
Next Article in Special Issue
Evaluation of Salivary Mucin, Amylase, Protein Profile, and Periodontal Parameters among Hypertensive and Diabetic Patients
Previous Article in Journal
Building a Territorial Working Group to Reduce Gender Gap in the Field of Artificial Intelligence
Previous Article in Special Issue
TNF-α, IL-1β, MMP-8 Crevicular Profile in Patients with Chronic Kidney Disease and Periodontitis
 
 
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Review

Acute Myocardial Infarction and Periodontitis: Importance of Awareness and Prevention in Latin America

by
Javier González-Ramírez
1,
Gustavo Martínez-Coronilla
2,
Laura Dayanara López-Rocha
2,
Ana Gabriela Leija-Montoya
2,
Adrián Hernández-Díazcouder
3,
Zureya Fontes-Garcia
4,
Marina Silva-Mancilla
4 and
Fausto Sánchez-Muñoz
3,*
1
Facultad de Enfermería, Universidad Autónoma de Baja California, Av. Álvaro Obregón y Calle “G” S/N, Col. Nueva, Mexicali 21100, BC, Mexico
2
Facultad de Medicina Mexicali, Universidad Autónoma de Baja California, Centro Cívico, Mexicali 21000, BC, Mexico
3
Departamento de Inmunología, Instituto Nacional de Cardiología, Juan Badiano No. 1, Col. Sección XVI, Tlalpan 140080, DF, Mexico
4
Facultad de Odontología, Universidad Autónoma de Baja California, Zotoluca s/n, Fracc. Calafia, Mexicali 21040, BC, Mexico
*
Author to whom correspondence should be addressed.
Submission received: 30 December 2021 / Revised: 14 February 2022 / Accepted: 22 February 2022 / Published: 18 March 2022

Abstract

:
By 2030, non-communicable diseases will have accounted for more than three-quarters of deaths worldwide. Cardiovascular diseases (CVDs) have been the leading cause of death worldwide for several years. Acute myocardial infarction (AMI) is a CVD characterized by necrosis of the heart at the myocardial level due to prolonged ischemia caused by the reduction or sudden absence of coronary blood supply. The prevalence of AMI is higher in men at all ages. The incidence of AMI has decreased in industrialized nations; however, it has been on the rise in Latin America (LATAM) due to lifestyle changes. These changes have caused the combined incidence of CVDs and unresolved health concerns in LATAM, such as infections and malnutrition. It is well known that periodontitis, a highly prevalent chronic infectious inflammatory disease, has been associated with systemic diseases, such as diabetes, kidney diseases, and AMI. This review addresses proposed aspects of the correlation between periodontitis and AMI, explains the importance of preventing periodontitis and CVDs, and analyzes the preventative measures being implemented in LATAM, particularly in Mexico.

1. Introduction

Cardiovascular diseases (CVDs) are among the leading causes of death worldwide [1], with ischemic heart disease (IHD) being the main cause. Ischemic refers to the lack of blood and oxygen supply, in this case, to the heart. It is also known as coronary artery disease (CAD) or coronary heart disease and defined as a disorder caused by narrowed coronary arteries that decrease the blood supply to the myocardium. Acute myocardial infarction (AMI) occurs when the heart’s blood supply is disrupted [2]. Since 2000, IHD-related deaths have increased dramatically, from 2 million to 8.9 million annually [1]. The leading cause of mortality is CAD, with 7.4 million deaths annually [3]. More than 80% of deaths occur in low- and middle-income countries [4,5]. In Latin America (LATAM), particularly Mexico, IHD is the leading cause of CVD-related death [6].
Non-communicable diseases are expected to account for more than three-quarters of deaths worldwide by 2030, with CVD alone being responsible for more deaths in low-income countries than infectious diseases, maternal and perinatal conditions, and nutritional disorders combined [4].
Periodontitis is a common disorder that leads to tooth loss and reduced quality of life in advanced cases. The etiology of periodontitis is multifactorial, including local, systemic, environmental, and genetic factors [7]. To achieve a successful outcome when controlling periodontitis, dental professionals must understand the pathogenesis, including the primary etiology, risk factors, contributing factors, and treatment protocols [8]. A careful diagnosis should consider eliminating the causes and encouraging the patient to initiate changes in their habits to help reduce the modifiable risk factors. These aspects are important for patient-led prevention and can support its successful treatment [9]. Subsequently, periodontal maintenance therapy at regular intervals and long-term follow-up are essential [10]. A 99.6% prevalence of inflammatory periodontal diseases in LATAM was recently reported in Mexico, Colombia, and Costa Rica [11].
For the development of periodontitis, a patient must present with an increase in the population and activity of a specific group of periodontal pathogens, predominantly gram-negative anaerobic bacteria. These bacteria are responsible for altering the normal symbiotic relationship between the host and its resident microbiota, leading to an alteration in the immune response and provision of a proinflammatory environment [12]. The immune response triggered can be a “double-edged sword”, since it is also responsible for degrading periodontal tissue [13]. Moreover, periodontitis has been associated with other systemic conditions, such as adverse pregnancy outcomes, CVDs, diabetes, respiratory disorders, chronic renal disease, lupus, cancer, neurodegenerative diseases, and metabolic syndrome [14,15]. These associations are mainly related to the systemic inflammatory burden associated with periodontitis [14,16]
This review addresses the proposed mechanisms of the correlation between periodontitis and AMI, explains the importance of curbing the development of periodontitis as well as AMI in LATAM (specifically Mexico), and highlights the importance of applying preventive measures, since both pathologies are highly prevalent.

2. Acute Myocardial Infarction

AMI is defined as cardiomyocyte necrosis in a clinical setting, consistent with acute myocardial ischemia [17], as a consequence of a prolonged reduction or sudden absence of the coronary blood supply that compromises one or more myocardial areas [18]. In most cases, this results from the rupture or erosion of a vulnerable atherosclerotic plaque [19]. The above results in an intraluminal thrombus which leads to the partial (at least 70%) or complete occlusion of one or more of the coronary arteries [17,18]. Five types of AMI have been defined (Table 1).
IHD manifests as acute coronary syndrome (ACS) [20] with symptoms consistent with myocardial ischemia, such as recurrent or persistent chest pain and the radiation of pain to the left arm, lower jaw, or neck [21]. Other chest pain-equivalent symptoms include dyspnea and epigastric pain [17]. Less typical presentations include nausea, vomiting, fatigue, syncope, or palpitations [21]. AMI is the most severe manifestation of CAD [22].

2.1. Epidemiology

AMI accounts for more than one-third of all deaths in developed countries [22]. Its incidence is lower in industrialized nations and tends to increase in developing countries, such as South Asia, LATAM, and Eastern Europe [23].
Premenopausal women are at a lower risk of AMI than age-matched men [24,25]. It is assumed that exposure to endogenous estrogens during the reproductive years delays the manifestation of atherosclerotic disease in women [24,26]. Moreover, estrogens play a role in several metabolic factors by regulating lipids, inflammatory markers, and coagulation [26] as well as promoting a direct vasodilator effect through alpha and beta receptor activation in the vessel wall, which stimulates angiogenesis and decreases oxidative stress [25]. The average risk of AMI is three times higher in men than in premenopausal women. However, premenopausal women tend to have an equal risk of AMI to that of men when certain cardiovascular risk factors are present, such as hypertension, smoking, and diabetes [26,27].
Certain risk factors are strongly associated with the development of AMI, such as smoking, hypertension, diabetes, dyslipidemia, psychosocial stressors, obesity, alcohol consumption, physical inactivity, and a diet low in fruits and vegetables [23,27]. According to the INTERHEART study, these risk factors account for more than 90% of an individual’s overall risk [28].

2.2. Epidemiology of AMI in LATAM

Since 2000, CVDs including AMI in LATAM have shown an upward trend due to lifestyle changes, economic evolution, urbanization, industrialization, globalization, and a demographic transition from a young population toward an aging population [29]. In 2001, 31% of the overall deaths in LATAM were attributed to CVD [30]; this figure has only increased since. The population of LATAM has a high prevalence of cardiovascular risk factors, primarily overweight/obesity, smoking, physical inactivity, and alcohol consumption [31].
The INTERHEART study is an international case-control study that determined the impact of conventional and emerging cardiovascular risk factors on AMI [31,32]. Between 1999 and 2003, the INTERHEART was conducted in LATAM; to date, it is the most representative study of the risk factors for AMI in this region [28,32]. It was performed specifically in Argentina, Brazil, Colombia, Chile, Guatemala, and Mexico, where 1237 cases of AMI and 1888 controls were registered. Obesity, smoking, and dyslipidemia reportedly represent an 88% risk of AMI [32].

2.3. Epidemiology of AMI in Mexico

Of the countries that are part of the Organization for Economic Cooperation and Development (OECD), Mexico has had the highest AMI-related mortality rate in patients over 45 years of age since 2013 [33,34]. In 2019, Mexico was the only country that showed an increase in deaths due to AMI and other IHD, as the rest of the OECD countries presented decreases (Figure 1) [35].
In 2015, the National Institute of Statistics and Geography recorded 116,002 deaths due to CVD, 70% of which were AMI-related [36]. Every 4.3 min, an estimated one person dies of IHD, making it the leading cause of years of healthy life lost due to premature death and disability [37]. Mexico has a high prevalence of CVD risk factors, such as obesity, diabetes, systemic arterial hypertension, smoking, sedentary lifestyle, and a high-carbohydrate, high-fat diet, among others [38].
The RENASCA (Real-World Study in Mexico), performed at the Mexican Social Security Institute (IMSS), represents the largest study on ACS to date in Mexico [33]. In 2010, this study documented that up to 68% of the Mexican population had at least three associated risk factors for ACS [33]. The most recent RENASCA-IMSS study included 21,827 patients enrolled between 1 March 2014 and 25 December 2017. It reported that, of the enrolled patients, 73.2% suffered ACS due to AMI with ST segment elevation; for the rest, it was due to AMI with non-ST segment elevation. The predominant risk factors for the development of these conditions were high blood pressure, smoking, diabetes, dyslipidemia, and metabolic syndrome [33].

2.4. Predisposition to the Development of CVDs in LATAM

In recent years, socioeconomic status, education level, and ethnic origin have been demonstrated as the independent predictors of an increased risk of CVD-related death. Furthermore, risk factors such as smoking, age, blood pressure, sex, and cholesterol remain important predictors [39]. For example, an association between education and the development of certain diseases has been observed. In this sense, a study found that in Eastern European countries, women aged 15–44 years with a lower education level showed a 2.3 times higher risk of AMI than those with a higher education level. However, among non-European women, the risk of AMI was 33% higher in those with a higher education level. This suggests that a low education level is associated with an increased risk of AMI in Eastern Europe but not in the other three regions. Thus, factors are differentially involved in the interplay of population-specific characteristics affecting educational differences in the risk of AMI and stroke [40]. In another study, individuals in high-income countries that have large seasonal oscillations in temperature could be influenced by cold weather and develop CVDs. In these countries, winter can produce biological mechanisms, such as higher sympathetic nervous system activation, uncontrolled hypertension, and an increased incidence of respiratory diseases. Other conditions such as shorter days, reduced physical activity, depression, and higher pollution levels were involved. Moreover, in low- and middle-income regions with tropical and subtropical climates (Brazil), the numbers of heart failure and AMI hospitalizations also increase in winter. This is not related to the temperature oscillations. However, other factors, such as precarious housing conditions, lack of thermal insulation, and greater pollution might increase the seasonal effect of winter on risk [41].
Regarding ethnicity, some authors reported marked racial and ethnic disparities with respect to access to a diagnosis and adequate treatment of valvular heart disease. In addition to the scarcity of research on the causes of heart disease, some authors reported that, during patient recruitment for determining the in-depth causes of AF, most observational studies and clinical trials have included predominantly white populations with an underrepresentation of minorities’ racial and ethnic differences, highlighting the need for an inclusive participation in research [42].
Thus, CVDs show an increased prevalence in LATAM countries (specifically Mexico), given that LATAM probably has the greatest economic disparities that cause high poverty, malnutrition, disease, and limited opportunities [43]. Unique features have allowed the development of health problems specific to this region [40]. Regardless, health infrastructure and research are lacking.
On the other hand, additional AMI-associated factors have demonstrated an upward trend due to the particular characteristics of LATAM populations. For example, the rate of increase of obesity appears to be slowing in most high-income countries; however, it continues to rise in many low- and middle-income countries [44]. The possible causes for this vary, but some authors cited that the prevalence of excess weight and obesity has increased since the signing of the North American Free Trade Agreement in Mexico. This was caused by the new economic model that allowed rural populations to move from rural to urban centers, resulting in a food transition [45]. This transition increased food security, augmented the availability of cheap sources of vegetable oils, resulted in more meals away from home, decreased the arduous nature of working, and increased passive recreation (especially television). These pathways have transformed the dietary and physical activity patterns and consequently tipped the scales in favor of obesity [46].

3. Periodontitis

Periodontitis is a chronic and infectious inflammatory disease with a variety of related factors [47,48]. When periodontitis is detected in the initial stage, the dentist may be able to provide appropriate treatment that restores the patient’s oral health [49]. However, if it is not detected and treated in time, continuous bleeding, pain while brushing, and bad breath often occur. Periodontal pockets can also form, leading to the loss of one or more teeth in severe cases [49] (Figure 2).

3.1. Epidemiology of Periodontitis

Periodontitis also has a high prevalence; in 2017, it was the eleventh most prevalent condition worldwide [51]. It is estimated that periodontitis, in its various stages, affects 45–50% of the world’s population. Its most severe form affects 11.2% of the world’s population [52]. In addition, severe periodontal disease has a sustained prevalence, with no data currently indicating a decrease [53]. Moreover, the prevalence of periodontal disease is expected to increase owing to the aging population [54].

3.2. Epidemiology of Periodontitis in LATAM

Developing countries generally have a higher prevalence of periodontal disease signs, which is clearly reflected in comparisons of adult populations [47]. Overall, periodontal disease affects approximately 20–50% of the world’s population [47]. However, the epidemiological data on gingivitis and periodontitis in LATAM are scarce. The reported data show significant variations in the results between different LATAM countries. Generally, the data revealed that the prevalence of the periodontal disease is higher in LATAM populations than those in the United States or Europe [55]. It was recently reported that, on average, the prevalence of severe forms of periodontal disease in North and South America in adults 35–44 years is 20%, or 40% for less severe presentations [56].

3.3. Predisposition to the Development of Dental Diseases in LATAM

Regarding dental diseases, the behavior is similar to the panorama summarized in CVDs, since both are important health problems to which socioeconomic factors predispose residents of low-income regions. For example, dental health resources comprise 5–10% of health care spending costs per year in developed countries, and oral disease is the fourth most expensive disease to treat [57]. Treating dental caries in children alone often exceeds the total budget for children’s health care [58]. This is aggravated by a recent unprecedented migration crisis in Venezuela and Central America that creates a complex and inhospitable scenario that complicates the management of dental diseases [59].
On the other hand, education can also have an influence, and health education is the most cost-effective method of disease prevention. It is well documented in dentistry that knowledge can empower populations, allowing them to take action to protect their health [60].
Ethnic influence has also been explored with discrepant results. One study explored whether there were ethnic differences in oral health that could be explained by differences in sociodemographic or lifestyle factors or the use of dental services in the UK and reported that, despite generally lower use of dental hygiene and preventive dental services, Black and South Asian participants were less likely to report tooth extractions and tooth loss. The above may reflect genuinely better oral health, especially as some of these differences could be explained by a lower consumption of cakes and sweets. However, the study did not provide detailed information about sugar consumption amount and frequency. The authors suggest that dietary sugar may be the main driver of overall and ethnicity-specific oral health [61].
LATAM presents its peculiarities; dental care in Mexico is generally provided in private, public, or social security services. However, the public health services offer basic care and do not include orthodontic treatment or aesthetic rehabilitation. Thus, they use private services to complete their treatment. Because these low-income populations lack access to dental care due to its high cost, notably, these inequities reflect social problems since citizens who can pay do have access [62]. In addition, it must be considered that the population presents several risk factors in dietary practices, such as a high intake of total and added sugars [63].

4. Interaction between Periodontitis and AMI

Periodontitis is associated with AMI in several populations [52]. Moreover, periodontitis and AMI share common risk factors, such as smoking and diabetes [14]. This is especially important because of the close link between diabetes and AMI, since the latter is the most frequent cause of mortality and morbidity in diabetic populations [15]. Patients with periodontitis tend to have an increased frequency of being overweight and experiencing endothelial dysfunction, hypertension, platelet hyperreactivity, dyslipidemia, and a prothrombotic state [16], which are known risk factors for AMI [64].
Local/systemic inflammation caused by periodontitis also contributes to the risk of CVD [65,66]. This is supported by a large number of studies that show an increase in the circulation of inflammatory mediators in patients with periodontal diseases [66], such as C-reactive protein (CRP), interleukin-6, fibrinogen, and platelet-activating factor, among others, compared to healthy controls [66,67]. Moreover, an increased serum leptin concentration has been reported due to periodontal disease, which promotes atherosclerosis by enhancing platelet aggregation, the production of proinflammatory cytokines such as interleukin-2 and interleukin-6, and arterial wall calcification [65,68]. In addition, the translocation of periodontitis-causing microorganisms into the bloodstream and their accumulation in atheroma plaques may contribute to plaque instability and reduce the risk of AMI development [16].
Evidence has confirmed the presence of bacterial DNA in atheromatous plaques [69]. The bacterial species most commonly found were Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Tannerella forsythia, Prevotella intermedia [70], Fusobacterium nucleatum, and Campylobacter rectus [71], suggesting the migration of these oral pathogens to distant body sites [69].
The mechanisms by which periodontitis can participate in AMI development include bacteremia and associated systemic inflammatory sequelae, including elevations in CRP and oxidative stress [52]. These mechanisms favor atherosclerotic plaque formation and instability [65,66]. Several authors have proposed that periodontitis may be a non-traditional modifiable risk factor for AMI [52].

4.1. Pathophysiology and Effect of Periodontitis on AMI

It is well known that periodontitis raises inflammatory markers such as CRP and fibrinogen. These proteins lead to the release of cytokines, such as tumor necrosis factor-α and inerleukin-6, through certain processes [72]. Moreover, bacteria in the oral cavity that induce periodontitis can cause local and systemic inflammation, causing the liver to respond and enter an acute phase [66,72].
Stein et al. showed a strong relationship between periodontitis patients and pathogens from AMI patients. They found a high association between periodontitis and heart disease and concluded that pathogens such as P. gingivalis could be considered risk factors for AMI [73]. Furthermore, P. gingivalis can reportedly evade innate immune detection by toll-like receptor 4, favoring chronic vascular inflammation [69,74]. According to Pussinen et al., the levels of immunoglobulin A against P. gingivalis were risk factors for AMI [75]. Likewise, Holmlund et al. reported that the levels of immunoglobulin G against P. gingivalis increased upon deterioration in patients with AMI [76].
The search for bacteria associated with periodontitis continues. Through immunofluorescence microscopy, pathogens such as Tannerella forsythensis and P. intermedia have been demonstrated to be associated with a greater risk of AMI [77]. Moreover, a more recent study of P. intermedia placed its relationship with periodontitis and AMI closer to the spotlight [78]. A meta-analysis by Bahekar et al. of five cohort studies showed that people with periodontal disease had a 1.14 times higher risk of developing CAD compared to controls independent of confounding factors [79]. Some relevant sample studies are shown in Table 2.
Other studies reported that a small dental intervention such as the removal of tartar (a form of hardened dental plaque) could increase the risk of periodontitis in patients presenting with bacteremia. This would cause pro-inflammatory mediator activation by these microorganisms within the bloodstream, increasing the inflammation of atheroma plaques and the risk of their detachment or fragmentation [87]. Figure 3 shows a diagram of the microbial components of atherogenesis.

4.2. Biomarkers for the Detection of Periodontitis and CVDs

For several years in dental care, clinical methods such as periodontal probing and radiographic techniques have been used to diagnose periodontal disease [89]. Recent attempts have been made to use markers associated with this and other diseases, including CVD, to identify periodontal disease [90]. These procedures are useful. The dentist can offer the patient a diagnosis specific to the patient’s condition and assess whether the delivered treatment is the most appropriate [90].
Oral fluids play an important role in the diagnosis of periodontitis. Saliva and crevicular fluid have been used, as they are the two elements through which inflammatory molecules can be collected in places where there are alterations in the periodontal tissues [91]. Additionally, serum and peripheral blood have been used to search for periodontal and CVD markers [92].
The following table summarizes the main conclusions of studies on periodontitis and heart diseases in which biomarkers have been used to correlate them (Table 3). Notable reviews addressing this point were published previously [93].

5. Association between Periodontal Disease, AMI, and Other Health Conditions

Periodontitis, a chronic inflammatory disease, is one of the most common human diseases and associated with systemic inflammation [52]. Inflammation has been hypothesized to promote the initiation and evolution of atherosclerosis. Accordingly, systemic inflammation induced by periodontitis stimulates the development of atherosclerotic cardiovascular disease and contributes to acute atherothrombotic complications in AMI [52,99]. The immune response plays an important role in the development and clinical manifestations of atherosclerotic plaques. Moreover, some clinical studies suggested a correlation between inflammatory circulating markers such as CRP and homocysteine and a susceptibility to AMI [99].
Chronic inflammation is also related to insulin resistance and worsening glycemic control, and in patients with diabetes, the aggressive treatment of periodontitis is associated with improved glycemic control and vascular function [100,101]. An association has been found between dyslipidemia and periodontal disease in which low-density lipoproteins are reportedly smaller and denser, which promotes atherogenesis [101,102]. Obesity and periodontitis share common risk factors, such as dietary components, diabetes, and suboptimal lifestyle behaviors. Adipocytes contain activated macrophages, and as the number of adipocytes increases, these activated macrophages induce the production of cytokines such as pro-inflammatory interleukins and tumor necrosis factors [101]. Dental plaque could possibly serve as a reservoir for respiratory pathogens, causing respiratory tract infections and pneumonia [69]. Recent studies reported a relationship between periodontitis and oral, pancreatic, head, neck, and lung cancer [69,103]. Inflammation is the suggested link between periodontal disease and Alzheimer’s disease, as the brain undergoes diverse inflammatory processes, such as complement activation and cytokine production, that favor its development [69]. Periodontal disease is also associated with adverse pregnancy outcomes; due to hormonal changes, pregnant women are more susceptible to gingivitis and periodontitis than non-pregnant women [104]. The mechanisms proposed are bacterial translocation from the oral cavity and across the placental barrier, thereby reaching the amniotic fluid and the entering fetal circulation, and the systemic dissemination of endotoxins and inflammatory mediators derived from oral pathogens which could affect fetal development or trigger a spontaneous abortion [69].

6. Importance of Prevention in Periodontitis and AMI

6.1. Lack of Effectiveness of Periodontitis Preventative Measures in LATAM

In analyzing why periodontitis is a larger problem in LATAM than in more economically powerful countries, we must consider certain fundamental aspects. For instance, there is insufficient knowledge among LATAM populations of risk factors, possible systemic effects, prevention, diagnosis, and treatment. For example, several patients in LATAM do not consider the clinical signs of periodontal disease a health problem. Habits such as flossing are rarely practiced in LATAM populations [105]. Moreover, focusing on individuals is important in prevention. However, there has been little governmental intervention, such as public strategies related to oral health prevention in LATAM (91). Another aspect recently highlighted is the average income of the population, which is significantly lower than that of people in developed countries. Their lack of purchasing power means that the bulk of people in developing countries do not have access to adequate dental care [106]. Furthermore, oral care centers are often located far away, and it is difficult to find locations where people in need can be seen by experts [107]. This is caused by low investments in oral care [108]. Moreover, although public oral care centers are cheaper than private ones, they continue to present high costs because dental materials are expensive [109]. Another aspect to consider is the difficulty of performing high-quality epidemiological studies in the region [110], which leads to a lack of precise data about oral care on which ideal therapy for LATAM people may be planned [111]. Several studies to date have not followed a methodology that increases our understanding of which risk factors are related to periodontal diseases, or the information is incomplete. Since the completion of some studies, the results have been cast into doubt [110].
Considering the above information, well-conducted cross-sectional and longitudinal studies with clear objectives and sound methodologies are required [110] to enable the planning of regional interventions with adequate follow-up periods that facilitate rehabilitation [112].

6.2. Lack of Efficacy of AMI Prevention Measures in Mexico

Attempts have been made to reduce the frequency of AMI cases along with proposals to analyze the current situation in Mexico. Some authors consider that the existing problem is mainly caused by delays before, during, and after the detection of AMI. The first delay is that the patient does not know the symptoms of an AMI; therefore, they do not request timely medical attention, commonly taking up to 5 h to decide to go to the hospital. As a result, 50% of patients die in their homes. The second delay occurs when doctors who receive a patient with symptoms associated with AMI fail to diagnose it, as occurs in approximately 80% of cases due to a lack of knowledge or diagnostic studies. The ideal situation would be that no more than 10 min pass from the first contact with the doctor until the point of diagnosis. The third and last delay is the one that occurs between diagnosis and start of treatment [113].
Some risk factors for AMI development have already been mentioned, among which it is important to consider that the majority of the Mexican population is diabetic and has high blood pressure. In addition, there is a high prevalence of overweight or obese, as an estimated 80% of the population over 20 years of age is above their ideal weight [114].
Although the high prevalence of diabetes and hypertension in Mexico is almost equivalent to that in high-income countries, as in many developing countries, there are insufficient resources and infrastructure in Mexico to supply the demand for treatment of these conditions, which presents a challenge for the healthcare system [20].

6.3. Importance of Prevention to Avoid the Development of Periodontitis in Mexico

Mexico currently has an aging population whose number of elderly people is increasing. Notably, a large part of this population has lost one or more teeth due to cavities and periodontal disease. Accordingly, there is a need for dentists to educate these patients about their oral health to improve their quality of life [115]. Substantial evidence from observational studies highlights how certain oral health interventions, such as proper oral hygiene habits, increased dental visits, dental prophylaxis, and periodontal treatment, reduce the incidence of CVD-related events [52].
Notably, Mexico is a nation with very restricted oral care, and a high portion of the population has insufficient resources to cover dental expenses. Therefore, it is challenging to restore the oral health of these patients and help them to improve their quality of life [116].
Furthermore, there is little awareness of oral care in the young population. They are not aware that with good oral brushing, the development of diseases such as gingivitis can be avoided. In addition, when they go to the dentist, the advice they are given is not usually followed, meaning that they often contract diseases that could progress to periodontitis [117].

6.4. Importance of Prevention to Avoiding AMI Development

Due to the limited possibility of applying the most advanced and efficient treatments to the population with AMI, it is vitally important to reinforce primary prevention programs that focus on diseases and lifestyles that facilitate the progression of CVDs. However, the prevention of mortality must also be stressed, and once the AMI has already manifested, we must establish and promote a methodology that allows patients to access definitive treatments. Preventive measures are closely related to time, since the less time wasted, the greater the possibility of saving lives [20].
Health promotion and continuing medical education are considered preventive measures [20]. The first refers to offering campaigns to the general population to raise awareness about AMI, emphasizing lifestyle changes (not smoking, engaging in physical activity, and eating healthily, among others) [34] and the identification of symptoms suggestive of AMI so they can seek medical attention as soon as possible [20].
When first- and second-level doctors manage to treat a patient with AMI in a timely manner, the patient can remain stable until they are treated in a third-level medical unit, where they will be operated on for final treatment (coronary reperfusion), a process that decreases their risk of mortality from 20% to less than 10%. This can reduce the likelihood of or prevent heart failure due to the loss of heart muscle secondary to necrosis caused by an AMI [20].

7. Discussion

CVDs are the leading cause of global mortality and major contributors to disability [118]. Thus, it is important to understand the pathophysiology of these diseases to identify timely treatment solutions [119]. However, it is also important to determine the main associated risk factors to enable the establishment of preventive measures [120]. In this sense, different studies have associated periodontitis with a higher risk of AMI. Although the involved molecular mechanisms are not completely clear, inflammatory and bacterial factors play a part in the most studied underlying mechanism [121].
Periodontal disease is a highly prevalent disease associated with comorbidities that are quite common, such as diabetes and obesity [122,123]. Notably, these same comorbidities are intricately linked to the development of CVDs, and the alteration of inflammatory factors seems to be the common denominator. Accordingly, inflammatory factors have been considered possible biomarkers, mainly for monitoring or diagnosing CVDs in relation to periodontal disease.
Understanding the relationship between these two diseases could aid in the development of preventive strategies that benefit those populations that are highly affected by both diseases, such as the Mexican population. Thus, studies that determine the causal relationships and molecular mechanisms involved should be conducted to establish schemes for the prevention or treatment of these diseases.

8. Conclusions

Periodontitis and AMI share risk factors, and several studies have reported an association between them, even indicating that periodontal disease may be a modifiable risk factor for AMI and other CVDs. However, uncertainties remain; therefore, we must continue this research to determine the details of their causal relationship. Further interdisciplinary studies are required in LATAM to support efforts to establish preventative measures for periodontitis and AMI, since both diseases are prevalent in this population.

Author Contributions

J.G.-R., G.M.-C., L.D.L.-R., A.G.L.-M., A.H.-D., Z.F.-G., M.S.-M., and F.S.-M. All those mentioned contributed equally to the design and implementation of the review and the analysis and writing of the manuscript. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Not applicable.

Acknowledgments

We thank Damiana De Jesus Oviedo Mandujano and Ely Sanchez Felix for their critical review of the document.

Conflicts of Interest

The authors declare no conflict of interest.

References

  1. World Health Organization. The Top 10 Causes of Death. Available online: https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death (accessed on 13 October 2021).
  2. Institute of Medicine (US) Committee on Social Security Cardiovascular Disability Criteria. Ischemic Heart Disease. In Cardiovascular Disability: Updating the Social Security Listings; National Academies Press (US): Washington, DC, USA, 2010. Available online: https://0-www-ncbi-nlm-nih-gov.brum.beds.ac.uk/books/NBK209964/ (accessed on 17 January 2022).
  3. Tibaut, M.; Mekis, D.; Petrovic, D. Pathophysiology of Myocardial Infarction and Acute Management Strategies. Cardiovasc. Hematol. Agents Med. Chem. 2017, 14, 150–159. [Google Scholar] [CrossRef]
  4. Institute of Medicine (US) Committee on Preventing the Global Epidemic of Cardiovascular Disease: Meeting the Challenges in Developing Countries. Promoting Cardiovascular Health in the Developing World: A Critical Challenge to Achieve Global Health; Fuster, V.; Kelly, B.B. (Eds.) The National Academies Collection: Reports funded by National Institutes of Health; National Academies Press (US): Washington, DC, USA, 2010. Available online: http://0-www-ncbi-nlm-nih-gov.brum.beds.ac.uk/books/NBK45693/ (accessed on 1 October 2020).
  5. Martínez, M.L.-P.; Luna, M.J.E. Enfermedad cardiovascular y riesgo metabólico. Rev. Enferm. Vasc. 2018, 1, 4–10. [Google Scholar] [CrossRef]
  6. Berrocal, I.; Peix, A.; Mut, F.; Shaw, L.J.; Karthikeyan, G.; Estrada Lobato, E.; Paez, D. Uso adecuado de las pruebas no invasivas de isquemia para guiar la toma de decisión sobre revascularización tras un infarto agudo de miocardio con elevación del segmento ST en países iberoamericanos: Resultados de la reunión de un panel de expertos de la International Atomic Energy Agency. Rev. Esp. Med. Nucl. Imagen Mol. 2018, 37, 237–243. [Google Scholar] [PubMed]
  7. Könönen, E.; Gursoy, M.; Gursoy, U.K. Periodontitis: A Multifaceted Disease of Tooth-Supporting Tissues. J. Clin. Med. 2019, 8, 1135. [Google Scholar] [CrossRef] [Green Version]
  8. Kwon, T.; Lamster, I.B.; Levin, L. Current Concepts in the Management of Periodontitis. Int. Dent. J. 2021, 71, 462–476. [Google Scholar] [CrossRef]
  9. Pihlstrom, B.L. Periodontal Risk Assessment, Diagnosis and Treatment Planning. Periodontology 2000 2001, 25, 37–58. [Google Scholar] [CrossRef] [PubMed]
  10. Manresa, C.; Sanz-Miralles, E.C.; Twigg, J.; Bravo, M. Supportive Periodontal Therapy (SPT) for Maintaining the Dentition in Adults Treated for Periodontitis. Cochrane Database Syst. Rev. 2018, 1, 8–10. [Google Scholar] [CrossRef] [PubMed]
  11. Carvajal, P.; Vernal, R.; Reinero, D.; Malheiros, Z.; Stewart, B.; Pannuti, C.M.; Romito, G.A. Periodontal Disease and Its Impact on General Health in Latin America. Section II: Introduction Part II. Braz. Oral Res. 2020, 34, e023. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  12. Bartold, P.M.; Van Dyke, T.E. Periodontitis: A Host-Mediated Disruption of Microbial Homeostasis. Unlearning Learned Concepts. Periodontology 2000 2013, 62, 203–217. [Google Scholar] [CrossRef] [Green Version]
  13. Di Benedetto, A.; Gigante, I.; Colucci, S.; Grano, M. Periodontal Disease: Linking the Primary Inflammation to Bone Loss. Clin. Dev. Immunol. 2013, 2013, 503754. [Google Scholar] [CrossRef] [Green Version]
  14. Kodovazenitis, G.; Pitsavos, C.; Papadimitriou, L.; Deliargyris, E.N.; Vrotsos, I.; Stefanadis, C.; Madianos, P.N. Periodontal Disease Is Associated with Higher Levels of C-Reactive Protein in Non-Diabetic, Non-Smoking Acute Myocardial Infarction Patients. J. Dent. 2011, 39, 849–854. [Google Scholar] [CrossRef]
  15. Leon, B.M.; Maddox, T.M. Diabetes and Cardiovascular Disease: Epidemiology, Biological Mechanisms, Treatment Recommendations and Future Research. World J. Diabetes 2015, 6, 1246–1258. [Google Scholar] [CrossRef]
  16. Nocini, R.; Favaloro, E.J.; Sanchis-Gomar, F.; Lippi, G. Periodontitis, Coronary Heart Disease and Myocardial Infarction: Treat One, Benefit All. Blood Coagul. Fibrinolysis 2020, 31, 339–345. [Google Scholar] [CrossRef] [PubMed]
  17. Collet, J.-P.; Thiele, H.; Barbato, E.; Barthélémy, O.; Bauersachs, J.; Bhatt, D.L.; Dendale, P.; Dorobantu, M.; Edvardsen, T.; Folliguet, T.; et al. 2020 ESC Guidelines for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation. Eur. Heart J. 2021, 42, 1289–1367. [Google Scholar] [CrossRef] [PubMed]
  18. Coll-Muñoz, Y.; Valladares-Carvajal, F.; González-Rodríguez, C. Infarto Agudo de Miocardio. Actualización de La Guía de Práctica Clínica. Rev. Finlay 2016, 6, 170–190. [Google Scholar]
  19. Anderson, J.L.; Morrow, D.A. Acute Myocardial Infarction. N. Engl. J. Med. 2017, 376, 2053–2064. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  20. Ríos, M.A.M. Infarto Agudo al Miocardio, 1st ed.; Intersistemas: Mexico City, Mexico, 2014. [Google Scholar]
  21. Ibanez, B.; James, S.; Agewall, S.; Antunes, M.J.; Bucciarelli-Ducci, C.; Bueno, H.; Caforio, A.L.P.; Crea, F.; Goudevenos, J.A.; Halvorsen, S.; et al. 2017 ESC Guidelines for the Management of Acute Myocardial Infarction in Patients Presenting with ST-Segment Elevation: The Task Force for the Management of Acute Myocardial Infarction in Patients Presenting with ST-Segment Elevation of the European Society of Cardiology (ESC). Eur. Heart J. 2018, 39, 119–177. [Google Scholar] [CrossRef] [Green Version]
  22. Reed, G.W.; Rossi, J.E.; Cannon, C.P. Acute Myocardial Infarction. Lancet 2017, 389, 197–210. [Google Scholar] [CrossRef]
  23. Jayaraj, J.C.; Davatyan, K.; Subramanian, S.S.; Priya, J. Epidemiology of Myocardial Infarction; IntechOpen: London, UK, 2018. [Google Scholar] [CrossRef]
  24. Arnold, A.P.; Cassis, L.A.; Eghbali, M.; Reue, K.; Sandberg, K. Sex Hormones and Sex Chromosomes Cause Sex Differences in the Development of Cardiovascular Diseases. Arterioscler. Thromb. Vasc. Biol. 2017, 37, 746–756. [Google Scholar] [CrossRef] [Green Version]
  25. Iorga, A.; Cunningham, C.M.; Moazeni, S.; Ruffenach, G.; Umar, S.; Eghbali, M. The Protective Role of Estrogen and Estrogen Receptors in Cardiovascular Disease and the Controversial Use of Estrogen Therapy. Biol. Sex. Differ. 2017, 8, 33. [Google Scholar] [CrossRef]
  26. Maas, A.H.E.M.; Appelman, Y.E.A. Gender Differences in Coronary Heart Disease. Neth. Heart J. 2010, 18, 598–602. [Google Scholar] [CrossRef] [PubMed]
  27. Millett, E.R.C.; Peters, S.A.E.; Woodward, M. Sex Differences in Risk Factors for Myocardial Infarction: Cohort Study of UK Biobank Participants. BMJ 2018, 363, k4247. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  28. Yusuf, S.; Hawken, S.; Ounpuu, S.; Dans, T.; Avezum, A.; Lanas, F.; McQueen, M.; Budaj, A.; Pais, P.; Varigos, J.; et al. Effect of Potentially Modifiable Risk Factors Associated with Myocardial Infarction in 52 Countries (the INTERHEART Study): Case-Control Study. Lancet 2004, 364, 937–952. [Google Scholar] [CrossRef]
  29. Lanas, F.; Serón, P.; Lanas, A. Coronary Heart Disease and Risk Factors in Latin America. Glob. Heart 2013, 8, 341–348. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  30. Hernández-Leiva, E. Epidemiology of acute coronary syndrome and heart failure in Latin America. Rev. Esp. Cardiol. 2011, 64, 34–43. [Google Scholar] [CrossRef]
  31. Pereira-Rodríguez, J.; Peñaranda-Florez, D.; Reyes-Saenz, A.; Caceres-Arevalo, K.; Cañizarez-Pérez, Y. Prevalence of Cardiovascular Risk Factors in Latin America: A Review of the Published Evidence 2010–2015. Rev. Mex. Cardiol. 2015, 26, 125–139. [Google Scholar]
  32. Lanas, F.; Avezum, A.; Bautista, L.E.; Diaz, R.; Luna, M.; Islam, S.; Yusuf, S.; INTERHEART Investigators in Latin America. Risk Factors for Acute Myocardial Infarction in Latin America: The INTERHEART Latin American Study. Circulation 2007, 115, 1067–1074. [Google Scholar] [CrossRef]
  33. Borrayo-Sánchez, G.; Rosas-Peralta, M.; Pérez-Rodríguez, G.; Ramírez-Árias, E.; Almeida-Gutiérrez, E.; de Jesús Arriaga-Dávila, J. Acute myocardial infarction with ST-segment elevation: Code I. Rev. Med. Inst. Mex. Seguro Soc. 2018, 56, 26–37. [Google Scholar]
  34. Narro-Robles, J.R. Enfermedades no Transmisibles: Situación y Propuesta de Acción una Perspectiva desde la Experiencia de México, 1st ed.; Secretaria de Salud: Mexico City, Mexico, 2018. [Google Scholar]
  35. OECD. Health at a Glance 2019: OECD Indicators; Health at Glance; OECD: Paris, France, 2019. [Google Scholar] [CrossRef]
  36. de Jesús Arriaga-Dávila, J.; Pérez-Rodríguez, G.; Borrayo-Sánchez, G. Dimensiones de calidad enfocadas en el protocolo de atención Código infarto. Rev. Med. Inst. Mex. Seguro Soc. 2017, 55, 382–387. [Google Scholar]
  37. Gómez, F.C.X.; Díaz, E.A.; Lara, M.L.; Maldonado, A.J.; Rangel, P.F.V.; Vázquez, O.L.M. Infarto agudo del miocardio como causa de muerte: Análisis crítico de casos clínicos. Rev. Fac. Med. UNAM 2021, 64, 49–59. [Google Scholar] [CrossRef]
  38. Dávila, C.C.A. Trend and impact of mortality by cardiovascular diseases in Mexico, 1990–2015. Rev. Cubana Salud Públ. 2019, 45, 1–18. [Google Scholar]
  39. Kist, J.M.; Smit, G.W.G.; Mairuhu, A.T.A.; Struijs, J.N.; Vos, R.C.; van Peet, P.G.; Vos, H.M.M.; Beishuizen, E.D.; Sijpkens, Y.W.J.; Groenwold, R.H.H.; et al. Large Health Disparities in Cardiovascular Death in Men and Women, by Ethnicity and Socioeconomic Status in an Urban Based Population Cohort. EClinicalMedicine 2021, 40, 101120. [Google Scholar] [CrossRef] [PubMed]
  40. Chang, C.-L.; Marmot, M.G.; Farley, T.M.M.; Poulter, N.R. The Influence of Economic Development on the Association between Education and the Risk of Acute Myocardial Infarction and Stroke. J. Clin. Epidemiol. 2002, 55, 741–747. [Google Scholar] [CrossRef]
  41. Levin, R.K.; Katz, M.; Saldiva, P.H.N.; Caixeta, A.; Franken, M.; Pereira, C.; Coslovsky, S.V.; Pesaro, A.E. Increased Hospitalizations for Decompensated Heart Failure and Acute Myocardial Infarction during Mild Winters: A Seven-Year Experience in the Public Health System of the Largest City in Latin America. PLoS ONE 2018, 13, e0190733. [Google Scholar] [CrossRef] [Green Version]
  42. Mensah, G.A.; Fuster, V. Race, Ethnicity, and Cardiovascular Disease: JACC Focus Seminar Series. J. Am. Coll. Cardiol. 2021, 78, 2457–2459. [Google Scholar] [CrossRef] [PubMed]
  43. Legetic, B.; Medici, A.M.A.; Hernández-Avila, M.; Alleyne, G.; Hennis, A. Economic Dimensions of Non-Communicable Disease in Latin America and the Caribbean, 3rd ed.; Pan American Health Organization: Washington, DC, USA, 2016; Available online: https://iris.paho.org/handle/10665.2/28501 (accessed on 12 January 2022).
  44. Loos, R.J.; Yeo, G.S.H. The Genetics of Obesity: From Discovery to Biology. Nat. Rev. Genet. 2022, 23, 120–133. [Google Scholar] [CrossRef] [PubMed]
  45. Jacobs, A.; Richtel, M. The New York Times—El TLCAN y su Papel en la Obesidad en México. Available online: https://www.nytimes.com/es/2017/12/11/espanol/america-latina/tlcan-obesidad-mexico-estados-unidos-oxxo-sams-femsa.html (accessed on 28 January 2022).
  46. Popkin, B.M. Global Nutrition Dynamics: The World Is Shifting Rapidly toward a Diet Linked with Noncommunicable Diseases. Am. J. Clin. Nutr. 2006, 84, 289–298. [Google Scholar] [CrossRef]
  47. Nazir, M.A. Prevalence of Periodontal Disease, Its Association with Systemic Diseases and Prevention. Int. J. Health Sci. 2017, 11, 72–80. [Google Scholar]
  48. Winning, L.; Linden, G.J. Periodontitis and Systemic Disease. BDJ Team 2015, 2, 1–4. [Google Scholar] [CrossRef]
  49. Gasner, N.S.; Schure, R.S. Periodontal Disease. In StatPearls; StatPearls Publishing: Treasure Island, FL, USA, 2021. Available online: http://0-www-ncbi-nlm-nih-gov.brum.beds.ac.uk/books/NBK554590/ (accessed on 20 December 2021).
  50. Hajishengallis, G. Periodontitis: From Microbial Immune Subversion to Systemic Inflammation. Nat. Rev. Immunol. 2015, 15, 30–44. [Google Scholar] [CrossRef]
  51. GBD 2016 Disease and Injury Incidence and Prevalence Collaborators. Global, Regional, and National Incidence, Prevalence, and Years Lived with Disability for 328 Diseases and Injuries for 195 Countries, 1990–2016: A Systematic Analysis for the Global Burden of Disease Study 2016. Lancet 2017, 390, 1211–1259. [Google Scholar] [CrossRef] [Green Version]
  52. Sanz, M.; Marco Del Castillo, A.; Jepsen, S.; Gonzalez-Juanatey, J.R.; D’Aiuto, F.; Bouchard, P.; Chapple, I.; Dietrich, T.; Gotsman, I.; Graziani, F.; et al. Periodontitis and Cardiovascular Diseases: Consensus Report. J. Clin. Periodontol. 2020, 47, 268–288. [Google Scholar] [CrossRef] [PubMed]
  53. Frencken, J.E.; Sharma, P.; Stenhouse, L.; Green, D.; Laverty, D.; Dietrich, T. Global Epidemiology of Dental Caries and Severe Periodontitis—A Comprehensive Review. J. Clin. Periodontol. 2017, 44, S94–S105. [Google Scholar] [CrossRef] [PubMed]
  54. Tonetti, M.S.; Bottenberg, P.; Conrads, G.; Eickholz, P.; Heasman, P.; Huysmans, M.-C.; López, R.; Madianos, P.; Müller, F.; Needleman, I.; et al. Dental Caries and Periodontal Diseases in the Ageing Population: Call to Action to Protect and Enhance Oral Health and Well-Being as an Essential Component of Healthy Ageing—Consensus Report of Group 4 of the Joint EFP/ORCA Workshop on the Boundaries between Caries and Periodontal Diseases. J. Clin. Periodontol. 2017, 44, S135–S144. [Google Scholar] [CrossRef] [Green Version]
  55. Gamonal, J.; Bravo, J.; Malheiros, Z.; Stewart, B.; Morales, A.; Cavalla, F.; Gomez, M. Periodontal Disease and Its Impact on General Health in Latin America. Section I: Introduction Part I. Braz. Oral Res. 2020, 34, e024. [Google Scholar] [CrossRef]
  56. Carrizales-Sepúlveda, E.F.; Ordaz-Farías, A.; Vera-Pineda, R.; Flores-Ramírez, R. Periodontal Disease, Systemic Inflammation and the Risk of Cardiovascular Disease. Heart Lung Circ. 2018, 27, 1327–1334. [Google Scholar] [CrossRef]
  57. León, S.; De Marchi, R.J.; Tôrres, L.H.; Hugo, F.N.; Espinoza, I.; Giacaman, R.A. Oral Health of the Latin American Elders: What We Know and What We Should Do-Position Paper of the Latin American Oral Geriatric Group of the International Association for Dental Research. Gerodontology 2018, 35, 71–77. [Google Scholar] [CrossRef]
  58. Amin, T.T.; Al-Abad, B.M. Oral Hygiene Practices, Dental Knowledge, Dietary Habits and Their Relation to Caries among Male Primary School Children in Al Hassa, Saudi Arabia. Int. J. Dent. Hyg. 2008, 6, 361–370. [Google Scholar] [CrossRef]
  59. Sampaio, F.C.; Bönecker, M.; Paiva, S.M.; Martignon, S.; Ricomini Filho, A.P.; Pozos-Guillen, A.; Oliveira, B.H.; Bullen, M.; Naidu, R.; Guarnizo-Herreño, C.; et al. Dental Caries Prevalence, Prospects, and Challenges for Latin America and Caribbean Countries: A Summary and Final Recommendations from a Regional Consensus. Braz. Oral Res. 2021, 35, e056. [Google Scholar] [CrossRef]
  60. Nakre, P.D.; Harikiran, A.G. Effectiveness of Oral Health Education Programs: A Systematic Review. J. Int. Soc. Prev. Commun. Dent. 2013, 3, 103–115. [Google Scholar] [CrossRef] [Green Version]
  61. Arora, G.; Mackay, D.F.; Conway, D.I.; Pell, J.P. Ethnic Differences in Oral Health and Use of Dental Services: Cross-Sectional Study Using the 2009 Adult Dental Health Survey. BMC Oral Health 2016, 17, 17. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  62. Cruz, G.; Picazzo, E. The paradigm of oral health in Mexico. J. Oral Res. 2017, 6, 8–9. [Google Scholar] [CrossRef] [Green Version]
  63. Fisberg, M.; Kovalskys, I.; Gómez, G.; Rigotti, A.; Sanabria, L.Y.C.; García, M.C.Y.; Torres, R.G.P.; Herrera-Cuenca, M.; Zimberg, I.Z.; Koletzko, B.; et al. Total and Added Sugar Intake: Assessment in Eight Latin American Countries. Nutrients 2018, 10, 389. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  64. González, G.R.; Alcalá, R.J. Enfermedad isquémica del corazón, epidemiología y prevención. Rev. Fac. Med. UNAM 2010, 53, 35–432. [Google Scholar]
  65. Gundala, R.; Chava, V.K.; Ramalingam, K. Association of Leptin in Periodontitis and Acute Myocardial Infarction. J. Periodontol. 2014, 85, 917–924. [Google Scholar] [CrossRef]
  66. Schenkein, H.A.; Loos, B.G. Inflammatory Mechanisms Linking Periodontal Diseases to Cardiovascular Diseases. J. Clin. Periodontol. 2013, 40 (Suppl. 14), S51–S69. [Google Scholar] [CrossRef]
  67. Ridker, P.M.; Silvertown, J.D. Inflammation, C-Reactive Protein, and Atherothrombosis. J. Periodontol. 2008, 79 (Suppl. 8), 1544–1551. [Google Scholar] [CrossRef] [Green Version]
  68. Karthikeyan, B.V.; Pradeep, A.R. Gingival Crevicular Fluid and Serum Leptin: Their Relationship to Periodontal Health and Disease. J. Clin. Periodontol. 2007, 34, 467–472. [Google Scholar] [CrossRef]
  69. Bui, F.Q.; Almeida-da-Silva, C.L.C.; Huynh, B.; Trinh, A.; Liu, J.; Woodward, J.; Asadi, H.; Ojcius, D.M. Association between Periodontal Pathogens and Systemic Disease. Biomed. J. 2019, 42, 27–35. [Google Scholar] [CrossRef]
  70. Figuero, E.; Sánchez-Beltrán, M.; Cuesta-Frechoso, S.; Tejerina, J.M.; del Castro, J.A.; Gutiérrez, J.M.; Herrera, D.; Sanz, M. Detection of Periodontal Bacteria in Atheromatous Plaque by Nested Polymerase Chain Reaction. J. Periodontol. 2011, 82, 1469–1477. [Google Scholar] [CrossRef] [Green Version]
  71. Haraszthy, V.I.; Zambon, J.J.; Trevisan, M.; Zeid, M.; Genco, R.J. Identification of Periodontal Pathogens in Atheromatous Plaques. J. Periodontol. 2000, 71, 1554–1560. [Google Scholar] [CrossRef] [PubMed]
  72. Bansal, M.; Rastogi, S.; Vineeth, N. Influence of Periodontal Disease on Systemic Disease: Inversion of a Paradigm: A Review. J. Med. Life 2013, 6, 126–130. [Google Scholar]
  73. Stein, J.M.; Kuch, B.; Conrads, G.; Fickl, S.; Chrobot, J.; Schulz, S.; Ocklenburg, C.; Smeets, R. Clinical Periodontal and Microbiologic Parameters in Patients with Acute Myocardial Infarction. J. Periodontol. 2009, 80, 1581–1589. [Google Scholar] [CrossRef] [PubMed]
  74. Slocum, C.; Coats, S.R.; Hua, N.; Kramer, C.; Papadopoulos, G.; Weinberg, E.O.; Gudino, C.V.; Hamilton, J.A.; Darveau, R.P.; Genco, C.A. Distinct Lipid A Moieties Contribute to Pathogen-Induced Site-Specific Vascular Inflammation. PLoS Pathog. 2014, 10, e1004215. [Google Scholar] [CrossRef] [PubMed]
  75. Pussinen, P.J.; Alfthan, G.; Rissanen, H.; Reunanen, A.; Asikainen, S.; Knekt, P. Antibodies to Periodontal Pathogens and Stroke Risk. Stroke 2004, 35, 2020–2023. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  76. Holmlund, A.; Hedin, M.; Pussinen, P.J.; Lerner, U.H.; Lind, L. Porphyromonas Gingivalis (Pg) a Possible Link between Impaired Oral Health and Acute Myocardial Infarction. Int. J. Cardiol. 2011, 148, 148–153. [Google Scholar] [CrossRef] [PubMed]
  77. Andriankaja, O.; Trevisan, M.; Falkner, K.; Dorn, J.; Hovey, K.; Sarikonda, S.; Mendoza, T.; Genco, R. Association between Periodontal Pathogens and Risk of Nonfatal Myocardial Infarction. Commun. Dent. Oral Epidemiol. 2011, 39, 177–185. [Google Scholar] [CrossRef]
  78. Anumala, D.; Pasupuleti, M.K.; Nagireddy, R.R. Detection and Characterization of Prevotella Intermedia and Its In Vitro Susceptibility to Selected Antimicrobial Agents in Chronic Periodontitis and Acute Myocardial Infarction. Perio J. 2019, 3, 1–6. [Google Scholar] [CrossRef]
  79. Bahekar, A.A.; Singh, S.; Saha, S.; Molnar, J.; Arora, R. The Prevalence and Incidence of Coronary Heart Disease Is Significantly Increased in Periodontitis: A Meta-Analysis. Am. Heart J. 2007, 154, 830–837. [Google Scholar] [CrossRef]
  80. Zhang, J.; Xie, M.; Huang, X.; Chen, G.; Yin, Y.; Lu, X.; Feng, G.; Yu, R.; Chen, L. The Effects of Porphyromonas Gingivalis on Atherosclerosis-Related Cells. Front. Immunol. 2021, 12, 1–20. [Google Scholar] [CrossRef]
  81. Gaetti-Jardim, E.; Marcelino, S.L.; Feitosa, A.C.R.; Romito, G.A.; Avila-Campos, M.J. Quantitative Detection of Periodontopathic Bacteria in Atherosclerotic Plaques from Coronary Arteries. J. Med. Microbiol. 2009, 58, 1568–1575. [Google Scholar] [CrossRef] [PubMed]
  82. Nikolaeva, E.N.; Tsarev, V.N.; Tsareva, T.V.; Ippolitov, E.V.; Arutyunov, S.D. Interrelation of Cardiovascular Diseases with Anaerobic Bacteria of Subgingival Biofilm. Contemp. Clin. Dent. 2019, 10, 637–642. [Google Scholar] [CrossRef] [PubMed]
  83. Mahendra, J.; Mahendra, L.; Nagarajan, A.; Mathew, K. Prevalence of Eight Putative Periodontal Pathogens in Atherosclerotic Plaque of Coronary Artery Disease Patients and Comparing Them with Noncardiac Subjects: A Case-Control Study. Indian J. Dent. Res. 2015, 26, 189–195. [Google Scholar] [CrossRef] [PubMed]
  84. Mahendra, J.; Mahendra, L.; Felix, J.; Romanos, G.E. Genetic Analysis of Porphyromonas Gingivalis (FimA), Aggregatibacter Actinomycetemcomitans, and Red Complex in Coronary Plaque. J. Investig. Clin. Dent. 2014, 5, 201–207. [Google Scholar] [CrossRef]
  85. 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. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  86. Pavlic, V.; Peric, D.; Kalezic, I.S.; Madi, M.; Bhat, S.G.; Brkic, Z.; Staletovic, D. Identification of Periopathogens in Atheromatous Plaques Obtained from Carotid and Coronary Arteries. Biomed. Res. Int. 2021, 2021, 9986375. [Google Scholar] [CrossRef]
  87. Quesada-Chaves, D. Relación entre la enfermedad Periodontal y enfermedad cardiovascular. La necesidad de un protocolo de manejo. Rev. Costarricense Cardiol. 2018, 20, 37–43. [Google Scholar]
  88. Reyes, L.; Herrera, D.; Kozarov, E.; Roldán, S.; Progulske-Fox, A. Periodontal Bacterial Invasion and Infection: Contribution to Atherosclerotic Pathology. J. Clin. Periodontol. 2013, 40, S30–S50. [Google Scholar] [CrossRef]
  89. Highfield, J. Diagnosis and Classification of Periodontal Disease. Aust. Dent. J. 2009, 54, S11–S26. [Google Scholar] [CrossRef]
  90. Barembaum, S.; Azcurra, A. La saliva: Una potencial herramienta en la Odontología. Rev. Fac. Odontol. 2019, 29, 9–21. [Google Scholar]
  91. González-Quesada, J.; Rivera-Álvarez, S. Biomarkers in Gingival Crevicular Fluid: Review of Literature. ODOVTOS Int. J. Dent. Sci. 2017, 19, 35. [Google Scholar] [CrossRef] [Green Version]
  92. Martínez-Aguilar, V.; Carrillo-Ávila, B.A.; Guzmán-Marín, E.; Puerto Solís, M.; Bermeo-Escalona, J.R.; Pozos-Guillén, A. Proteína C reactiva como marcador inflamatorio en la enfermedad periodontal. Nova Sci. 2017, 9, 51–64. [Google Scholar] [CrossRef] [Green Version]
  93. Bokhari, S.A.H.; Khan, A.A.; Leung, W.K.; Wajid, G. Association of Periodontal and Cardiovascular Diseases: South-Asian Studies 2001–2012. J. Indian Soc. Periodontol. 2015, 19, 495–500. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  94. Górska, R.; Dembowska, E.; Konopka, T.P.; Wysokińska-Miszczuk, J.; Pietruska, M.; Ganowicz, E. Correlation between the State of Periodontal Tissues and Selected Risk Factors for Periodontitis and Myocardial Infarction. Adv. Clin. Exp. Med. 2017, 26, 505–514. [Google Scholar] [CrossRef]
  95. Delange, N.; Lindsay, S.; Lemus, H.; Finlayson, T.L.; Kelley, S.T.; Gottlieb, R.A. Periodontal Disease and Its Connection to Systemic Biomarkers of Cardiovascular Disease in Young American Indian/Alaskan Natives. J. Periodontol. 2018, 89, 219–227. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  96. Turgut-Çankaya, Z.; Bodur, A.; Taçoy, G.; Ergüder, I.; Aktuna, D.; Çengel, A. The Effect of Periodontal Therapy on Neopterin and Vascular Cell Adhesion Molecule-1 Levels in Chronic Periodontitis Patients with and without Acute Myocardial Infarction: A Case-Control Study. J. Appl. Oral Sci. 2018, 26, e20170199. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  97. Ebersole, J.L.; Kryscio, R.J.; Campbell, C.; Kinane, D.F.; McDevitt, J.; Christodoulides, N.; Floriano, P.N.; Miller, C.S. Salivary and Serum Adiponectin and C-Reactive Protein Levels in Acute Myocardial Infarction Related to Body Mass Index and Oral Health. J. Periodontal Res. 2017, 52, 419–427. [Google Scholar] [CrossRef] [PubMed]
  98. Marfil-Álvarez, R.; Mesa, F.; Arrebola-Moreno, A.; Ramírez-Hernández, J.A.; Magán-Fernández, A.; O’Valle, F.; Galindo-Moreno, P.; Catena, A. Acute Myocardial Infarct Size Is Related to Periodontitis Extent and Severity. J. Dent. Res. 2014, 93, 993–998. [Google Scholar] [CrossRef] [Green Version]
  99. Severino, P.; D’Amato, A.; Pucci, M.; Infusino, F.; Adamo, F.; Birtolo, L.I.; Netti, L.; Montefusco, G.; Chimenti, C.; Lavalle, C.; et al. Ischemic Heart Disease Pathophysiology Paradigms Overview: From Plaque Activation to Microvascular Dysfunction. Int. J. Mol. Sci. 2020, 21, 8118. [Google Scholar] [CrossRef]
  100. D’Aiuto, F.; Gkranias, N.; Bhowruth, D.; Khan, T.; Orlandi, M.; Suvan, J.; Masi, S.; Tsakos, G.; Hurel, S.; Hingorani, A.D.; et al. Systemic Effects of Periodontitis Treatment in Patients with Type 2 Diabetes: A 12 Month, Single-Centre, Investigator-Masked, Randomised Trial. Lancet Diabetes Endocrinol. 2018, 6, 954–965. [Google Scholar] [CrossRef]
  101. Gianos, E.; Jackson, E.A.; Tejpal, A.; Aspry, K.; O’Keefe, J.; Aggarwal, M.; Jain, A.; Itchhaporia, D.; Williams, K.; Batts, T.; et al. Oral Health and Atherosclerotic Cardiovascular Disease: A Review. Am. J. Prev. Cardiol. 2021, 7, 100179. [Google Scholar] [CrossRef] [PubMed]
  102. Griffiths, R.; Barbour, S. Lipoproteins and Lipoprotein Metabolism in Periodontal Disease. Clin. Lipidol. 2010, 5, 397–411. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  103. Michaud, D.S.; Fu, Z.; Shi, J.; Chung, M. Periodontal Disease, Tooth Loss, and Cancer Risk. Epidemiol. Rev. 2017, 39, 49–58. [Google Scholar] [CrossRef] [Green Version]
  104. Vamos, C.A.; Thompson, E.L.; Avendano, M.; Daley, E.M.; Quinonez, R.B.; Boggess, K. Oral Health Promotion Interventions during Pregnancy: A Systematic Review. Commun. Dent Oral Epidemiol. 2015, 43, 385–396. [Google Scholar] [CrossRef] [PubMed]
  105. Duque, A.D.; Malheiros, Z.; Stewart, B.; Romanelli, H.J. Strategies for the Prevention of Periodontal Disease and Its Impact on General Health in Latin America. Section III: Prevention. Braz. Oral Res. 2020, 34, e025. [Google Scholar] [CrossRef]
  106. Blas, E.; Sivasankara Kurup, A. Equity, Social Determinants and Public Health Programmes; World Health Organization: Geneva, Switzerland, 2010; p. 291. [Google Scholar]
  107. Sisson, K.L. Theoretical Explanations for Social Inequalities in Oral Health. Commun. Dent Oral. Epidemiol. 2007, 35, 81–88. [Google Scholar] [CrossRef]
  108. Hosseinpoor, A.R.; Itani, L.; Petersen, P.E. Socio-Economic Inequality in Oral Healthcare Coverage: Results from the World Health Survey. J. Dent. Res. 2012, 91, 275–281. [Google Scholar] [CrossRef]
  109. OECD. Health at a Glance 2017: OECD Indicators; Health at Glance; OECD: Paris, France, 2017. [Google Scholar] [CrossRef]
  110. Oppermann, R.V.; Haas, A.N.; Rösing, C.K.; Susin, C. Epidemiology of Periodontal Diseases in Adults from Latin America. Periodontology 2000 2015, 67, 13–33. [Google Scholar] [CrossRef]
  111. Gallardo, W.L.; Rodríguez, H.A. Enfermedad periodontal en Costa Rica 2017. Rev. Odontol. Vital. 2018, 29, 10. [Google Scholar]
  112. Kassebaum, N.J.; Smith, A.G.C.; Bernabé, E.; Fleming, T.D.; Reynolds, A.E.; Vos, T.; Murray, C.J.L.; Marcenes, W.; GBD 2015 Oral Health Collaborators. Global, Regional, and National Prevalence, Incidence, and Disability-Adjusted Life Years for Oral Conditions for 195 Countries, 1990–2015: A Systematic Analysis for the Global Burden of Diseases, Injuries, and Risk Factors. J. Dent. Res. 2017, 96, 380–387. [Google Scholar] [CrossRef]
  113. García-Siasó, S.; Sarabia-González, O.; Pacheco-Estrello, P. La Atención del Infarto Agudo al Miocardio en México; Secretaria de Salud: Mexico. 2017. Available online: http://www.calidad.salud.gob.mx/site/editorial/docs/atencion_infarto_agudo_miocardio_enMexico.pdf (accessed on 7 December 2019).
  114. Córdova Villalobos, J.Á. La obesidad: La verdadera pandemia del siglo XXI. Cirugía Cirujanos 2016, 84, 351–355. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  115. Aranza, O.T.; Coronel, X.C.; Palacios, R.D.H. Perfil de salud bucodental en un grupo de adultos mayores del estado de Hidalgo. Rev. ADM 2014, 71, 77–82. [Google Scholar]
  116. Velázquez-Olmedo, L.B.; Ortíz-Barrios, L.B.; Cervantes-Velazquez, A.; Cárdenas-Bahena, Á.; García-Peña, C.; Sánchez-García, S. Calidad de vida relacionada con la salud oral en adultos mayores. Instrumentos de evaluación. Rev. Med. Inst. Mex. Seguro Soc. 2014, 52, 448–456. [Google Scholar] [PubMed]
  117. Romero-Castro, N.S.; Paredes-Solís, S.; Legorreta-Soberanis, J.; Reyes-Fernández, S.; Flores Moreno, M.; Andersson, N. Prevalencia de Gingivitis y Factores Asociados En Estudiantes de La Universidad Autónoma de Guerrero, México. Rev. Cubana Estomatol. 2016, 53, 9–16. [Google Scholar]
  118. Roth, G.A.; Mensah, G.A.; Johnson, C.O.; Addolorato, G.; Ammirati, E.; Baddour, L.M.; Barengo, N.C.; Beaton, A.Z.; Benjamin, E.J.; Benziger, C.P.; et al. Global Burden of Cardiovascular Diseases and Risk Factors, 1990–2019: Update From the GBD 2019 Study. J. Am. Coll. Cardiol. 2020, 76, 2982–3021. [Google Scholar] [CrossRef]
  119. Thompson, S.C.; Nedkoff, L.; Katzenellenbogen, J.; Hussain, M.A.; Sanfilippo, F. Challenges in Managing Acute Cardiovascular Diseases and Follow Up Care in Rural Areas: A Narrative Review. Int. J. Environ. Res. Public Health 2019, 16, 5126. [Google Scholar] [CrossRef] [Green Version]
  120. Brown, J.C.; Gerhardt, T.E.; Kwon, E. Risk factors for Coronary Artery Disease. In StatPearls; StatPearls Publishing: Treasure Island, FL, USA, 2021. Available online: http://0-www-ncbi-nlm-nih-gov.brum.beds.ac.uk/books/NBK554410/ (accessed on 16 November 2021).
  121. Van Dyke, T.E.; Sheilesh, D. Risk Factors for Periodontitis. J. Int. Acad. Periodontol. 2005, 7, 3–7. [Google Scholar]
  122. Jagannathachary, S.; Kamaraj, D. Obesity and Periodontal Disease. J. Indian Soc. Periodontol. 2010, 14, 96–100. [Google Scholar] [CrossRef]
  123. Preshaw, P.M.; Alba, A.L.; Herrera, D.; Jepsen, S.; Konstantinidis, A.; Makrilakis, K.; Taylor, R. Periodontitis and Diabetes: A Two-Way Relationship. Diabetologia 2012, 55, 21–31. [Google Scholar] [CrossRef] [Green Version]
Figure 1. Acute myocardial infarction and other ischemic heart disease mortality change from 2000–2019 (Taken and modified from: Health at a Glance 2019–© OECD 2019) [35].
Figure 1. Acute myocardial infarction and other ischemic heart disease mortality change from 2000–2019 (Taken and modified from: Health at a Glance 2019–© OECD 2019) [35].
Applsci 12 03131 g001
Figure 2. The progression from periodontal health to periodontitis disease. The alveolar bone and connective tissue are covered by the oral epithelium in periodontal health, and the gingival sulcus is 1–3 mm. However, periodontitis is developed when the periodontal pockets are <5 mm deep, and gingival inflammation in sites with apical migration of the epithelial attachment onto the root surfaces is associated with loss of connective tissue and alveolar bone [50].
Figure 2. The progression from periodontal health to periodontitis disease. The alveolar bone and connective tissue are covered by the oral epithelium in periodontal health, and the gingival sulcus is 1–3 mm. However, periodontitis is developed when the periodontal pockets are <5 mm deep, and gingival inflammation in sites with apical migration of the epithelial attachment onto the root surfaces is associated with loss of connective tissue and alveolar bone [50].
Applsci 12 03131 g002
Figure 3. The microbial component of atherogenesis. The bacteria invade the endothelial cells (EC) layer causing apoptosis. The endothelium releases chemokines as monocyte chemoattractant protein 1 (MCP-1) in the lumen, inducing the activation of blood monocytes and macrophages and promoting their adhesion and diapedesis. Moreover, the transmigrating leucocytes can harbor viable bacteria, which allow systemic bacterial dissemination to distant sites. Atheroma can grow due to the proliferation of smooth muscle cells (SMC), which is mediated by macrophages-secreted growth factors [88].
Figure 3. The microbial component of atherogenesis. The bacteria invade the endothelial cells (EC) layer causing apoptosis. The endothelium releases chemokines as monocyte chemoattractant protein 1 (MCP-1) in the lumen, inducing the activation of blood monocytes and macrophages and promoting their adhesion and diapedesis. Moreover, the transmigrating leucocytes can harbor viable bacteria, which allow systemic bacterial dissemination to distant sites. Atheroma can grow due to the proliferation of smooth muscle cells (SMC), which is mediated by macrophages-secreted growth factors [88].
Applsci 12 03131 g003
Table 1. Types of AMI [17,19]. ECG: 12-lead electrocardiogram.
Table 1. Types of AMI [17,19]. ECG: 12-lead electrocardiogram.
Type Description
1 Atherosclerotic plaque disruption with resulting intraluminal thrombus (acute atherothrombosis), leading to decreased myocardial blood flow and/or distal embolization with subsequent necrosis of the myocardium.
2 Due to an imbalance between myocardial oxygen supply and demand, results from hypo/hypertension, arrhythmias, anemia, hypoxemia, coronary artery spasm, dissection or embolism, and so on, not as a consequence of acute atherothrombosis.
3 An infarction that causes sudden death without the opportunity to obtain biomarkers and/or ECG confirmation.
4aAMI is related to percutaneous coronary intervention.
bAMI is related to thrombosis of a coronary stent.
5 AMI is related to coronary-artery bypass grafting.
Table 2. Pathogens involved in the development of periodontitis and CVD.
Table 2. Pathogens involved in the development of periodontitis and CVD.
BacteriaPathologyFindingsReference
Porphyromonas gingivalis (Pg).Oral diseases AtherosclerosisPg can influence the malfunction of the endothelium, it is considered a promoter of foam cells, it stimulates the calcification of the smooth muscle cells of the vessels, it alters the regulatory and auxiliary T lymphocytes.[80]
Aggregatibacter actinomycetemcomitans (Aa)
Porphyromonas Gingivalis (Pg)
Prevotella intermedia (Pi)
Prevotella nigrescens (Pn)
Tannerella forsythiaen (Tf).
Coronary artery diseasePeriodontal bacterial DNA was found in a high percentage in atheromatous plaques.[81]
Aggregatibacter actinomycetemcomitans (Aa)
Porphyromonas gingivalis (Pg)
Tannerella forsythia (Tf)
Prevotella intermedia (Pi)
AMI
Periodontal Disease
Correlation between periodontitis and AMI.
Periodontal destruction correlated with the representation of periodontal pathogens.
Pg as an indicator of potential risk for AMI.
[73]
Porphyromonas Gingivalis (Pg)
Aggregatibacter actinomycetemcomitans (Aa)
Tannerella forsythia (Tf).
AMI
Cardiovascular disease
Periodontal status in patients with AMI is characterized by unsatisfactory and poor hygiene, increased indices of bleeding on probing, and periodontal pocket depth compared to patients without cardiovascular pathology.[82]
Tannerella forsythia (Tf)
Campylobacter rectus (Cr)
Eikenella corrodens (Ec)
Porphyromonas gingivalis (Pg)
Treponema denticola (Td)
Prevotella nigrescens (Pn)
Aggregatibacter actinomycetemcomitans (Aa)
Prevotella intermedia (Pi)
Periodontal disease
Coronary artery disease
Patients with CAD present a mayor growth of periodontal bacteria in dental biofilms surface in comparison of healthy subjects.[83]
Porphyromonas gingivalis (Pg)
Aggregatibacter actinomycetemcomitans (Aa)
Coronary artery diseasePresence of red complex bacteria in samples of coronary plaques, Aa could not be identifies in these samples.[84]
Porphyromonas gingivalis (Pg)Atherosclerosis
Periodontal disease
DNA of the Pg is commonly located in atheromatous plaques of patients with periodontal diseases.[85]
Porphyromonas gingivalis (Pg)
Aggregatibacter actinomycetemcomitans (Aa)
Tannerella forsythia (Tf)
Treponema denticola (Td)
Prevotella intermedia (Pi)
Atherosclerosis
Coronary artery disease
Bacterial presence in carotid and coronary atherosclerotic vessels is correlated with the degree of periodontal inflammation.
Relationship between periodontal pathogenic bacterial and atherogenesis.
[86]
Porphyromonas gingivalis (Pg)
Aggregatibacter actinomycetemcomitans (Aa)
Atherosclerosis
Periodontitis
The presence of bacteria in the atheromatous plaque in the carotid artery recovered by the removal of atheromatous plaques is ratified.
Presence of a possible association between periodontitis and cardiovascular diseases
[70]
Table 3. Biomarkers and their association between periodontitis and CVDs.
Table 3. Biomarkers and their association between periodontitis and CVDs.
BiomarkersFindingsReferences
Plasma cholesterol, glucose, CRP, fibrinogen, and NTproBNPThe prevalence of chronic periodontitis (CP) in patients with AMI was extremely high and associated with a history of previous levels of MI, PAD, smoking, diabetes, TC, LDL, and hsCRP.[94]
Interleukin (IL)
6 and C-reactive Protein
(CRP)
Moderate periodontal disease compared to no or mild periodontal disease was associated with an increase in IL-6 levels. The high levels of CRP found in this population warrant further investigation.[95]
Vascular cell adhesion molecule (VCAM-1)The data suggest that the total amount and concentration of neopterin and VCAM-1 in GCF appear to be strongly associated with the severity of periodontal disease in patients with AMI.[96]
Adiponectin/C-reactive Protein (CRP)The potential that serum and/or salivary biomarkers can help assess CVD risk requires knowledge of how the individual’s oral health would affect the effectiveness of these biological measures.
Serum CRP levels increased in patients with AMI, regardless of their oral health, and both serum and salivary CRP were significantly elevated in patients with ST-segment elevation myocardial infarction.
[97]
Cardiac troponin I and myoglobinThe severity of periodontitis is positively associated with the size of the acute myocardial infarction as measured by the serum levels of troponin I and myoglobin.[98]
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Share and Cite

MDPI and ACS Style

González-Ramírez, J.; Martínez-Coronilla, G.; López-Rocha, L.D.; Leija-Montoya, A.G.; Hernández-Díazcouder, A.; Fontes-Garcia, Z.; Silva-Mancilla, M.; Sánchez-Muñoz, F. Acute Myocardial Infarction and Periodontitis: Importance of Awareness and Prevention in Latin America. Appl. Sci. 2022, 12, 3131. https://0-doi-org.brum.beds.ac.uk/10.3390/app12063131

AMA Style

González-Ramírez J, Martínez-Coronilla G, López-Rocha LD, Leija-Montoya AG, Hernández-Díazcouder A, Fontes-Garcia Z, Silva-Mancilla M, Sánchez-Muñoz F. Acute Myocardial Infarction and Periodontitis: Importance of Awareness and Prevention in Latin America. Applied Sciences. 2022; 12(6):3131. https://0-doi-org.brum.beds.ac.uk/10.3390/app12063131

Chicago/Turabian Style

González-Ramírez, Javier, Gustavo Martínez-Coronilla, Laura Dayanara López-Rocha, Ana Gabriela Leija-Montoya, Adrián Hernández-Díazcouder, Zureya Fontes-Garcia, Marina Silva-Mancilla, and Fausto Sánchez-Muñoz. 2022. "Acute Myocardial Infarction and Periodontitis: Importance of Awareness and Prevention in Latin America" Applied Sciences 12, no. 6: 3131. https://0-doi-org.brum.beds.ac.uk/10.3390/app12063131

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop