Periodontitis as a risk factor in patients with ischemic heart disease

LUIS-DELGADO O, ECHEVARRÍA-GARCÍA JJ, BERINI-AYTÉS L, GAY-ESCODA C. PERIODONTITIS AS A RISK FACTOR IN PATIENTS WITH ISCHEMIC HEART DISEASE. MED ORAL 2004;9:125-37.

SUMMARY

Cardiovascular disease, and particularly ischemic heart disease (IHD), constitutes one of the principal causes of mortality in the western world. Interest has recently increased in the relationship between IHD and different infectious processes as triggering factors of the former, such as Chlamydia pneumoniae and Helicobacter pylori infection. Periodontitis has also been related to an increased risk of coronary disease, since both disorders share common characteristics such as patient age and sex, and a smoking habit, among other aspects. There are many similarities between vascular pathology induced by bacteria and the natural history of atherogenesis. The principal mechanism of action underlying periodontitis and IHD centers on the effect of bacteria and their endotoxins upon inflammatory reaction, hemostasia and lipid metabolic alterations. However, some authors are of the opinion that periodontitis constitutes an epiphenomenon, and that further studies are needed to clarify the cause-effect relation between these two multifactor pathologies.

Key words: Periodontitis, ischemic heart disease, coronary disease, atherosclerosis.

INTRODUCTION

Cardiovascular disease is highly prevalent among the adult population and constitutes one of the first causes of death in the western world. The term encompasses a broad range of cardiac and vascular disorders affecting both the arterial and venous systems, e.g., cardiac arrhythmias, valve lesions, ischemic disease and heart failure, among other problems. Of all these disorders, ischemic heart disease (IHD) is the most interesting in terms of its possible relation to periodontal disease.

Ischemic heart disease is defined as a reduction in myocardial perfusion, resulting in a diminished oxygen supply to the tissues of the heart and an increased accumulation of metabolites which normally would be eliminated (1). It is common practice to use synonymous terms such as myocardial ischemia, coronary insufficiency or coronary disease to describe these situations. The most common cause of IHD is coronary arterial obstruction, in most cases secondary to atherosclerosis. The latter constitutes a chronic disease affecting the elastic and muscle layers of the medium and large caliber arteries (2). Atherosclerosis of the coronary arteries produces narrowing or occlusion of the vascular lumen, which in turn leads to deficient cardiac irrigation and an increased risk of anginal chest pain and/or acute myocardial infarction (3).

Interest has recently increased in the relationship between IHD and different infectious processes as triggering factors of the former. Such processes include periodontitis, which has also been related to an increased risk of coronary disease (3). Many studies (3-10) refer to the possibility of an association between periodontitis and the risk of cardiovascular disease - including IHD and myocardial infarction. Both disorders share common characteristics such as patient age, sex and educational level, a smoking habit, and arterial hypertension, among other aspects. However, a number of authors such as Kinane (11), Seymour (12), Seymour and Steele (13), or Armitage (14), consider that insufficient evidence is available to confirm that systemic disorders - with the exception of bacterial endocarditis - are related to periodontitis.

The present study evaluates the factors associated with periodontitis which may increase the risk of IHD.

EPIDEMIOLOGY

According to the World Health Organization (WHO), cardiovascular disease is responsible for 20% of the world population mortality rate (15). In turn, IHD is one of the first causes of death after age 40 and 64 years in males and females, respectively (16). The condition is recorded in 4 out of every 1000 males between 35-44 years of age, in 10 out of every 1000 in the 45-54 years age interval, and in 20 out of every 1000 individuals between 55 and 64 years of age (3). The disease in turn causes 70% of all deaths after age 75 (16). In the United States, coronary thrombosis and myocardial infarction are responsible for 56.5% of all deaths, and are generally attributed to some complication of atherosclerosis (11,15-17).

Periodontitis is a chronic infection of the tooth-supporting tissues which is found in 15% of all adults in the 21-50 years age range, and in over 30% of those over 50 years of age (18). In the United States, 40% of all adults over age 50 are partially or totally edentulous as a consequence of periodontitis (19).

PATHOGENESIS OF ISCHEMIC HEART DISEASE

Atherosclerosis is present in 90% of all cases of IHD (1). It may therefore be regarded as the main etiological factor underlying IHD, though the latter can also be seen in patients with completely normal coronary arteries or in situations of obstruction of non-atheromatous origin.

Moderate or severe coronary luminal narrowing, without total occlusion, maintains insufficient myocardial perfusion, which can give rise to chest pain (ischemia-induced angina) or acute myocardial infarction (necrosis). Important coronary obstruction causes ischemia and/or necrosis as a result of a 75% reduction in the coronary vascular lumen (2).

Atherosclerosis is a form of arteriosclerosis (hardening and thickening of the vascular wall) that mainly affects the intimal layer of the thoracic or abdominal aorta and its branches - including the coronary arteries - together with the renal, cerebral and peripheral arteries of the lower limbs (2,17,20). The most vulnerable zones correspond to those vascular areas where flow turbulence is greatest, such as at the arterial bifurcations (4,21). According to the WHO, atherosclerosis contributes to the local accumulation of lipids, complex carbohydrates, blood and related products, fibrous tissue and calcium deposits - thereby giving rise to the formation of platelet thrombi (2,4,20-22).

The early atherosclerotic lesion consists of a yellowish and slightly elevated lipid striation composed of subendothelial accumulations of foam cells (macrophages filled mainly with cholesterol). These striations may either disappear spontaneously or evolve towards elevated fibrous plaques composed of a dense layer of hypertrophic smooth muscle cells and connective tissue surrounding a necrotic center or core of cell remains, cholesterol crystals and foam cells, macrophages and lymphocytes (2,21). These atheroma plaques in turn can give rise to a number of complications in the form of fissures or cracks, vascular thrombosis, calcification, hemorrhage and/or aneurysms.

IHD can also be a result of arterial thrombosis, thromboembolia and/or increased blood viscosity. Arterial thrombosis occurs following atheroma plaque rupture, which exposes the vascular subendothelial layer to the bloodstream, thereby activating the coagulation cascade. These thrombi in turn can either enhance the atheromatous lesions or may totally or partially occlude the vascular lumen - giving rise to myocardial infarction, unstable angina or cerebrovascular events. The term thromboembolism is used in reference to the latter situation. On the other hand, increased blood viscosity elevates blood flow resistance. This condition is commonly observed in polycythemias (increased erythrocyte counts), paraproteinemias (increased presence of immunoglobulins or other blood complexes), and in hyperleukocytic leukemias (increased white blood cell counts) (4).

The factors which favor the development of atherosclerosis include patient age and sex, hypercholesterolemia, smoking, diabetes mellitus, a sedentary lifestyle (3-7,16,20,22) and chronic infection (6,7,20) - though in many cases the presence of such factors does not allow the prediction of coronary disease (8).

However, some patients develop no coronary complications despite the presence of such risk factors. This may be attributable to environmental or genetic factors which induce interindividual variations in susceptibility to ischemic pathology. Some authors have pointed to infection-inflammation as a factor predisposing to IHD (5, 20).

FACTORS ASSOCIATED TO ISCHEMIC HEART DISEASE AND PERIODONTITIS

A series of physiological or pathological conditions can be associated with the presence of periodontitis and coronary disease. A description is provided below of the factors which may variably influence the development of both disorders.

1.- Sex. Males are more affected by IHD than females. Men under the age of 75 years show an increased frequency of cerebrovascular events compared with women of the same age (16). Among the latter the incidence is delayed 10 years with respect to males for IHD, and 20 years for acute myocardial infarction. After age 65, women become as vulnerable to cardiovascular mortality as males.

Another influencing condition in relation to patient sex is represented by endocrine changes. Thus, in postmenopausal women the incidence of coronary disease is 2- to 3-fold greater than in women of the same age who have not yet experienced menopause (16) - thus suggesting a possible protective effect on the part of the females sex hormones (23).

2.- Age. Advanced age is a risk factor for both cardiovascular disease and periodontitis, since as has been commented above, over 30% of all adults over age 50 present periodontitis. IHD in turn accounts for almost 75% of all cardiovascular disorders in males and females over age 75 years. Cardiovascular events secondary to coronary disease decrease with age, while cerebrovascular stroke and heart failure tend to increase with advancing age (16). The incidence and severity of IHD has been shown to increase with age in both sexes.

3.- Arterial hypertension. It is well known that arterial hypertension is a risk factor for IHD (23). However, no direct relationship has been described between periodontitis and arterial hypertension.

4.- Smoking. Tobacco smoking is one of the principal risk factors of IHD, particularly among those who smoke cigarettes rather than cigars or pipes (23). Tobacco smoking has been shown to be closely related to plasma fibrinogen elevations, and the latter is in turn very directly related to the possible appearance of coronary disease. An increase in plasma fibrinogen could accelerate the development of atherosclerotic lesions, or could increase the risk of occlusive thrombosis arising from an atheroma plaque (23). Smoking has also been associated with an increase in leukocyte count, hematocrit and blood viscosity - all these conditions in turn being related to IHD risk (4,24).

On the other hand, cigarette smoking aggravates periodontal disease and is considered to be a predictive factor for gingival attachment loss, a reduction in bone level, and deficient response to conventional management strategies (24).

Smoking induces a series of hematological changes, including the formation of free radicals from peripheral neutrophils, an increased presence of lipid peroxidation products, and chemotactic alterations. On the other hand, smoking reduces the inhibitory action of a-1 antitrypsin upon trypsin, with a worsening of the severity of periodontitis (24). Emingil et al. (7) found 73% of all patients with a history of myocardial infarction to be smokers.

Fredriksson et al. (24) showed tobacco smoking to increase leukocyte counts and reduce immunoglobulin G (IgG) synthesis, the latter being significantly lower than in non-smokers - regardless of whether they presented periodontitis or not. This is explained by the fact that smoking may affect lymphocyte function, and therefore also immunoglobulin production.

5.- Diabetes. It is generally agreed that infectious processes must be adequately controlled in diabetic patients, since they can decompensate the background disease. Periodontitis, as an infectious disease, worsens diabetes, and the latter in turn exerts a negative influence upon both periodontal disease and IHD (25). Katz et al. (22) found individuals with diabetes and IHD to present increased periodontal pocket depths compared with the healthy controls.

According to a model proposed by Beck et al. (7) for determining the possible mechanism whereby periodontitis may lead to IHD, patients with periodontitis and insulin-dependent diabetes mellitus may present abnormal cytokine secretion, thereby conditioning an important risk of IHD.

On the other hand, poorly controlled diabetes mellitus can produce prolonged hyperlipidemia which would affect myeloid cell function (26,27). Patients with poorly controlled type II diabetes and hyperlipidemia present severe gingival inflammation and tend to present increased interleukin IL-1 concentrations in crevicular fluid. Lipid metabolism is influenced by IL-1, IL-6, IL-8 and tumor necrosis factor (TNF-), which increase lipoprotein synthesis in the liver (29).

6.- Diet. A close relation is known to exist between average lipid and cholesterol consumption, serum cholesterol concentration, the severity of atherosclerosis and the associated morbidity and mortality rates. However, some authors consider that lipid consumption in the diet is not directly related to high blood cholesterol. This is in part due to genetic differences among individuals and the way in which dietary fat is metabolized. It is clear, however, that high blood cholesterol is related to IHD risk (9,23,27,28).

It should be pointed out that total cholesterol in serum is neither homogeneous nor water-soluble, and must therefore bind to plasma proteins to remain in soluble form as lipoprotein complexes (high- and low- density lipoproteins, HDL and LDL). In this context, LDL possesses an important atherogenic potential, particularly the small particles which can be filtered through the arterial wall, thereby favoring atherogenesis (23).

Authors such as Katz et al. (22), Wu et al. (9), Seymour (12) and Saito et al. (27) have confirmed a relation between periodontitis and hypercholesterolemia. As to triglycerides, high concentrations can be found in patients with periodontitis, though Katz et al. (22) observed no relation between triglyceride levels and periodontitis. Chronic hyperlipidemia can adversely affect host resistance to bacterial infections. A lipid-rich diet reduces polymorphonuclear cell (PMN) function while increasing the release of superoxide anions (13) or reactive oxidants (29), cytokines and growth factors from stimulated PMNs (4,9,18,24,26). Activated PMNs are related both to periodontal tissue lesions and to cardiac valve damage.

The relation between hyperlipidemia and periodontitis is fundamented on the inflammatory response of the individual to the lipopolysaccharides (LPS) of pathogens such as Porphyromonas gingivalis (12,13,27). LPS activate a cytokine-mediated inflammatory response and generate problems associated with atherosclerosis (9). Cutler et al. (26) found the factors most associated with periodontitis to be triglycerides and antibodies against Porphyromonas gingivalis. This in vitro study found increasing triglyceride levels to enhance IL-1 production by PMNs.

INFECTION AS A TRIGGERING FACTOR OF ISCHEMIC HEART DISEASE

Infection is an acknowledged risk factor for both atherosclerosis and thromboembolic disease. Many similarities exist between vascular pathology induced by bacteria and the natural history of atherosclerosis - a fact that has led many authors to suggest that in addition to genetic factors, diet and sedentarism, infections of unknown origin could contribute to the development of cardiovascular disease (4,6,10,20,30-32). Patel et al. (32) postulate that chronic infections accompanied by a persistent inflammatory response could increase the risk of IHD as a result of increased fibrinogen and sialic acid concentrations the latter in turn being predictors of coronary disease.

Among the chronic infections which have been related to such risk, mention should be made of processes caused by cytomegalovirus (CMV), Helicobacter pylori and Chlamydia pneumoniae (4,6,10,14,20,30-33). Periodontitis is a chronic infection often produced by gramnegative bacteria such as Porphyromonas gingivalis, Bacteroides forsythus and/or Actinobacillus actinomycetemcomitans, which interact with neutrophils and monocytes to facilitate inflammatory reaction and thrombus formation via platelet aggregation (6). It has been shown that Porphyromonas gingivalis can invade endothelial cells and thus colonize the subendothelial space, and this microorganism has been identified in atheroma plaques of patients with IHD (25).

Herzberg and Meyer (28) conducted an in vivo study where the inoculation of Streptococcus sanguis in rabbits was seen to induce rapid platelet aggregation with electrocardiographic, blood pressure and cardiac contractility alterations in direct proportion to the dose administered.

Mattila et al. (29) suggested that the association between periodontitis and IHD could be due to the effect of bacteria upon the cells which participate in the pathogenesis of atherosclerosis and arterial thrombosis.

These bacteria or their endotoxins such as LPS may alter vascular endothelial integrity, cause smooth muscle hyperplasia of the large arteries, with possible fatty degeneration of the latter, and increase the release of cytokines such as IL-1, TNF- and C-reactive protein (CRP) (26). These factors can favor the development and course of atherosclerosis (34), and may lead to intravascular coagulation as a result of altered platelet function, blood coagulation and lipid metabolism thereby facilitating the appearance of hyperlipidemia (9,26).

PERIODONTITIS AND ISCHEMIC HEART DISEASE

Periodontitis is believed to play an important role in different systemic disorders (35), and many authors consider it to be related to certain cardiovascular problems (4-10). It has been reported that the severity of periodontal pathology may be directly associated to the risk of coronary disease (12). The relation between deficient oral hygiene and the risk of coronary disease is independent of arterial hypertension, patient age or sex, smoking or the presence of diabetes (13). This affirmation is based on the capacity of periodontal infection to alter the inflammatory response of the individual (20). However, Mattila et al. (36) reported that a close relation exists between IHD, patient age and chronic dental infections such as periodontitis. Thus, patients who develop IHD at an early age may correspond to those subjects who have suffered chronic periodontal disease since youth.

Both disorders are chronic multifactor diseases that possibly share a series of etiological characteristics and factors, as a result of which both might coexist as a complex or syndrome (25). Frequent features common to both diseases include male status, a low cultural level, a smoking habit, and diabetes - though other clinical situations cannot be excluded.

The factors that favor the development of atherosclerosis and myocardial infarction include periodontitis, diabetes and obesity (13, 27). Katz et al. (22) reported that individuals with periodontal disease present twice the risk of suffering cardiovascular pathology compared with healthy subjects. In an individual with heart disease, the presence of periodontitis has been considered to be as important as arterial hypertension, dyslipidemia or body mass alterations. In the case of myocardial infarction, periodontitis would appear to be as determinant as smoking or arterial hypertension (15).

1.- Characteristics of periodontitis in patients with ischemic heart disease

Different studies have been made to determine the relation between periodontitis and IHD. A variety of methods are used to assess buccal health, including the dental index, which quantifies the presence of caries, periodontal pocket probing, the presence of periapical lesions, gingival bleeding, the number of missing teeth, and the presence or absence of pericoronitis.

Beck et al. (17), in 1996, found that a periodontal pocket probe depth of over 3 mm recorded throughout the oral cavity increases the risk of IHD. A strong correlation was observed between the degree of periodontal bone loss and myocardial infarction, with an increased risk of thromboembolic phenomena. Mackenzie and Milard (37) published similar results, bone height loss being more manifest in patients with atherosclerosis than in the control group. Emingil et al. (6) found an association between periodontitis and acute myocardial infarction, with the generalized presence of periodontal pockets measuring ³ 4 mm in depth in 45% of the patients with a history of infarction, versus in 25% of the controls. In a case-control study, Syrjänen (38) found poor oral hygiene to be significantly greater in males with IHD than in the controls. In a series of 50 patients, Kweider et al. (39) found subjects with periodontitis to have significantly higher fibrinogen levels and leukocyte counts than the controls.

Ebersole et al. (5) described the relation between periodontitis and alterations in lipid and lipoprotein profiles, a positive correlation being observed between the severity of periodontitis and the concentrations of total cholesterol, triglycerides and LDL-cholesterol. In contrast, few changes were recorded in the levels of HDL (5,9) and Apo-A1, the latter being an important antiatherogenic component of HDL. For this reason, periodontitis may be considered to favor dyslipoproteinemia.

The most common lipid metabolic alterations related to infection are an increase in very low-density lipoproteins (VLDL) and a reduction in HDL-cholesterol (9).

Seymour and Steele (13) carried out a review of the studies published in the literature, with the aim of evaluating the relation between periodontitis and IHD. They mentioned the study conducted by Mattila et al. (39), who concluded that buccodental health is a predictive index of coronary disease and is indicative of a history of myocardial infarction and diabetes, since patients who had suffered an infarction were seen to have periodontitis and poorer oral health than healthy subjects. Another conclusion was that the severity of dental infections is correlated to the extent of coronary atheromatosis, and moreover those individuals with severe dental infections present higher levels of Von Willebrand antigen factor, leukocytes and fibrinogen.

In the 1993 supplement of the European Heart Journal (37), a number of findings were commented in relation to periodontitis and IHD: (1) coagulation Factor VIII is associated with poor buccodental hygiene; (2) the number of teeth missing as a result of periodontitis is directly proportional to the prevalence of IHD; and (3) individuals with periodontitis present high fibrinogen levels in blood (40).

DeStefano et al. (41) found patients with periodontitis to present a 25% greater risk of developing IHD than the controls, while in the case of patients with periodontitis over age 50 this risk increment reached 70%. Likewise, individuals with important bone loss showed a 50% increase in the incidence of IHD.

Joshipura et al. (19,42) described that edentulous patients consume comparatively more saturated fats and cholesterol, with less fruit, vegetables, carotenes and fiber. They found the incidence of IHD to increase in patients with 10 or fewer teeth remaining in the mouth, in those situations where edentulism was attributable to periodontitis. Loesche et al. (8) reported similar results, with an association between coronary disease and the number of missing teeth. In effect, 53% of their edentulous patients were seen to present coronary disease. Takata et al. (43) described a predictive relation between the number of missing teeth and the risk of IHD in octogenarians. Subjects with 20 or more teeth present in the mouth showed a lesser risk of IHD. However, no linear relation was observed between the number of missing teeth and electrocardiographic alterations.

In the studies of Mercado et al. (44,45), a 14.2% prevalence of cardiovascular pathology was recorded in patients with moderate to severe periodontitis, compared with a 4% prevalence among the population without periodontitis.

2.- Association between periodontitis and ischemic heart disease

The principal mechanism of action in common between periodontitis and IHD implies the effect of bacteria and their endotoxins upon host inflammatory response, hemostasia and lipid metabolic alterations (9).

Periodontal pockets contain abundant gramnegative bacteria which come into contact with the underlying connective tissue and the periodontal blood vessels. This periodontal infection in turn leads to subclinical chronic bacteremia, as a result of which cytokines are periodically released into the bloodstream, e.g., C-reactive protein, la -1-antitrypsin, haptoglobin, fibrinogen, thromboxanes, IL-1, IL-6, IL-8 and TNF-(5,7,13,18,25,33,39,44). All these factors can in turn initiate platelet adhesion and aggregation, with the formation of foam cells and the accumulation of cholesterol in the intimal layer of the arteries - thereby favoring the development of atherosclerosis and thrombosis, and thus ultimately also coronary disease (13).

According to Ebersole et al. (5), the C-reactive protein levels decrease in the presence of gingivitis and increase in the case of periodontitis. In contrast, fibrinogen levels increase with both gingivitis and periodontitis. However, Wu et al. (9) found C-reactive protein to be more related to gingivitis with little bleeding than to mild or moderate periodontitis.

Periodontitis has also been related to von Willebrand factor, which is found to be elevated in diabetics with infections caused by gramnegative bacteria the latter facilitating the release of this factor by the endothelial cells (13).

Another mechanism which has also received attention is the host immune response, since the reaction to periodontitis varies from one individual to another as a result of genetic differences particularly monocyte secretory capacity. In this context, a hyperinflammatory phenotype (MØ+) has been identified for monocytes which can release 3- to 10-fold more proin-flammatory mediators such as PGE2, IL-1 and TNF-than monocytes which lack this phenotype (MØN)(12-14,17,30,46). The presence of this phenotype has been documented in patients with aggressive forms of periodontitis, and moreover the (MØ+) phenotype may can be exacerbated by certain factors such as diet. These monocytes play a very important role in atheroma formation and in determining the risk of thromboembolism, and this in turn may relate periodontitis to IHD (46).

3.- Hematological findings in patients with ischemic heart disease and periodontitis

Many systemic markers have been identified in different cardiac disorders, including C-reactive protein, which is considered to be an independent risk factor for cardiac events (9,10). Loos et al. (10) evaluated the presence of certain inflammatory markers in peripheral blood among patients with periodontitis and IHD, including C-reactive protein, fibrinogen, IL-1, IL-6 and TNF-Their proinflammatory properties could increment the inflammatory activity present in coronary lesions, and thus predispose patients to cardiovascular pathology (4). Both C-reactive protein and IL-6 may be increased in smokers versus non-smokers, and although Loos et al. (10) detected no differences between these groups, they did find IL-6 to induce the liver production of C-reactive protein.

Among the hematological findings it is common for patients with heart disease to present leukocytosis, which in many cases may be induced by chronic inflammation or infections that have gone undetected (10).

Wu et al. (9) observed a statistically significant relation between periodontal health, C-reactive protein and fibrinogen. This may be because patients with chronic infectious processes present increased plasma fibrinogen levels (4), as a result of which blood viscosity increases (9).

4.- Periodontitis as an epiphenomenon in patients with ischemic heart disease

In contrast to the above, many authors have reported no relation between periodontitis and IHD, including Hujoel et al. (47), who argued that while periodontitis may coincide with the presence of IHD, it does not necessarily imply an increased risk of ischemic heart problems. If such an association were indeed identified, it should be reversible, since periodontitis treatment would remove the risk of inducing coronary disease.

In totally edentulous patients the risk of IHD should be reduced. However, these patients are generally over age 60, and tend to present other background disorders such as arterial hypertension, hypercholesterolemia or diabetes, which predispose to IHD without any implication on the part of dental infections such as periodontitis.

Hujoel et al. (47) found edentulous patients to have no comparatively lesser risk of developing coronary disease. They therefore do not advocate dental treatment for preventing IHD, particularly considering that the extraction of teeth affected by periodontal disease can cause increased anxiety among such patients thereby contributing to increase the risk of anginal episodes or even acute myocardial infarction.

Chong and Kezele (33), and Armitage (14), carried out a statistical analysis of the studies published by Mattila et al. (29,40), Joshiopura et al. (19,42) and Beck et al. (17,46). They concluded that no association exists between periodontitis and IHD, and that any such relation would be weak, since the risk factors for both disorders overlap as a result of which perio-dontitis could constitute a phenomenon paralleling cardiovascular ischemic disease. On the other hand, the studies which include periodontitis as chronic infection generally do not take into account the possible existence of other infectious processes or chronic inflammation in the enrolled patients a fact that could introduce important bias (14,33).

Seymour (12) and Beck et al. (46) concluded that while many studies indicate a relation between these two multifactorial disorders, a cause-effect relation has not been demonstrated in any of them.

THERAPEUTIC REPERCUSSIONS

It would be very interesting to establish with certainty that periodontitis, as a chronic infectious process, constitutes a risk factor for coronary disease, particularly because IHD is a leading cause of mortality throughout the world. By simply diagnosing periodontitis in an elderly patient who moreover presents other predisposing factors such as hypercholesterolemia, smoking, diabetes or arterial hypertension, it would be possible to more firmly establish the risk of coronary disease.

Periodontitis, tooth loss and cardiovascular diseases can be prevented by modifying behavioral patterns and certain habits (19). It is therefore necessary to improve buccodental health in order to significantly reduce the incidence of coronary pathology (12). Accordingly, periodontal therapy would not only be directed towards the control of periodontitis and the modification of oral hygiene habits but would also constitute preventive management in such patients.

In a number of studies antibiotics have been administered, such as the second-generation macrolides (roxithromycin o azithromycin), for treating chronic infections produced by Chlamydia pneumoniae, with a documented reduction in the incidence of cerebrovascular events or IHD in such patients - though this is probably more a consequence of antiinflammatory action than of the antibiotic effects (14). This response to pharmacological treatment could also be used in patients with periodontitis, where the administration of antibiotics such as penicillins or tetracyclines, antiinflammatory drugs and antiseptics for plaque reduction could reduce the risk of IHD in the event a genuine relationship exists between the two diseases.

CONCLUSIONS

Many hypotheses have been proposed to establish a relation between periodontal disease and ischemic heart disease, though further studies are needed to determine whether such an association truly exists. On the other hand, if the relationship is confirmed, research will be required to determine whether it is of a cause-effect nature.

The association between IHD and infection has been established by a series of clinical studies, though numerous sources of bias may be involved, since risk factors such as patient age, smoking, hypercholesterolemia and socioeconomic level (among others) are common to both periodontitis and IHD, and may thus predispose to both disorders.

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