Current Literature


Cardiovascular disease and periodontitis were first linked in 1989 by a Finnish case-controlled study involving 202 patients. The researchers found that even after controlling for many potential confounding factors, such as smoking, diabetes, and serum lipid concentrations, heart-attack patients still had significantly worse dental health than control subjects. Many subsequent studies have also shown a connection between heart disease and periodontitis. For example, patients with severe periodontitis have been shown to be twice as likely to have a fatal heart attack and three times as likely to have a stroke as patients without periodontal disease after adjusting for known cardiovascular risk factors such as blood lipids, cholesterol, body mass, diabetes, and smoking (Beck et al. 1996 and Beck et al. 1998).

Current periodontal treatment is aimed at preventing loss of the dentition, as well as restoring periodontal form and function. It is not known whether reducing the oral microbiota and inflammatory burden of periodontitis is sufficient or even appropriate for managing these systemic problems. Optimal treatment may be totally different for the high-risk individual. Current periodontal maintenance programs may prevent further attachment loss, but may not be enough to prevent the inflammatory response leading to a heart attack in the susceptible individual. New data suggests that periodontal infection elicits a mild acute-phase response that changes the systemic blood chemistry. For example, C-reactive protein, an acute-phase reactant currently being labeled as a possible risk indicator for future cardiac events, is elevated in periodontitis patients compared to controls (Ebersole et al. 1997).

More recently, Noak et al. recently reported a positive correlation between increased levels of C-reactive protein and the presence of periodontal pathogens in the oral cavity (2001). Furthermore, the severity of periodontal disease correlated with increased levels of CRP.

Acute phase proteins, such as C-reactive protein and fibrinogen, are elevated in patients with inflammation or infection. Each of these acute phase reactants has been strongly associated with increased risk of cardiovascular disease (Emst, 1990 and Ridker et al. 1997). It has been speculated that this could be an underlying pathway in the association between periodontal disease and the observed higher risk for cardiovascular disease in these patients. Periodontal disease is a gram (-) infection of the supporting structures of the teeth and may cause an infection-related host inflammatory response which has been targeted as a possible mechanism for the periodontitis-cardiovascular disease association. The inflammatory response in the periodontal tissues may become systemic through the transient bacteremias that commonly occur as the result of daily activities such as tooth brushing, flossing, and chewing. Geerts et al. (2002) recently demonstrated that gentle mastication is able to induce the release of bacterial endotoxins from the oral cavity into the bloodstream. This finding suggests that the diseased periodontium can be an underestimated source of chronic bacterial pro-inflammatory components into the circulation. The group also reported that bacteremias occur more frequently in patients with severe periodontal disease. This potentially places them at higher risk for vascular damage due to the aggressive nature of the microbiota present in their gingival tissues. While the bacteremias only last a very short time, they occur several times per day over a period of many years. Moreover, many patients with periodontal disease who are unaware of their condition don’t receive appropriate treatment. The long-term effects of these bacteremias on the patient remain unknown, but it is hypothesized that the circulating bacterial endotoxin may adversely affect the vascular endothelium and induce a cytokine cascade which could account for the elevated acute phase protein levels (Engebretson et al. 1999). The damage to the vascular endothelium may predispose the area to atheroma formation. If this occurs in a coronary artery, the patient may be at increased risk for coronary artery disease or acute myocardial infarction. The initiation of the atheroma is hypothesized to begin with a focal accumulation of lipids and other plasma proteins in the aterial intima at the site of vascular injury (Woolf, 1961). Studies indicate that monocyte-derived macrophages adhere to and penetrate the endothelium during the early stages of atherosclerotic plaque formation (Rosenfeld, 1987). The monocyte adherence is aided by pro-inflammatory cytokines, adhesion molecules, and chemotactic cytokines. These cells become engorged with oxidized low-density lipoproteins and become the characteristic foam cells noted in most atheromas (Klurfeld, 1985). A fibrin cap is produced beneath the endothelium and ischemia occurs (Burke, 1979). Rupture of the fibrin cap is hypothesized to induce thrombus formation within the vessel and subsequent blockage of the vessel thereby causing acute myocardial infarct or stroke.


It is accepted that birth weight is the most important determinant of the chances of a newborn infant to survive, grow, and develop healthily. Preterm delivery is the major cause of neonatal mortality and of nearly one-half of all serious long-term neurological morbidity (McCormick, 1985). Preterm delivery is defined as a gestational age of less than 37 weeks (WHO 1977) and low birth weight as less than 2500g (WHO 1984). In recent studies, it has been demonstrated that women who gave birth to pre-term low birth-weight babies had greater extent and severity of attachment loss associated with periodontal disease than control subjects (Offenbacher, 1997). It is thought that the bacterial burden associated with periodontal disease may represent a challenge to the developing fetus via bacterial endotoxin. Circulating endotoxin has the potential to raise the levels of prostoglandins and arachidonic acid associated with labor. The increased circulating endotoxin levels may raise placental prostaglandin levels, thus contributing to preterm labor. A study by Jeffcoat et al. has demonstrated that pre-existing periodontal disease in the second trimester of pregnancy increases the odds of increased premature birth were increased 4.5- to 7.0-fold (2001).The group is careful not to prematurely apply a causal relationship between periodontitis and premature birth, but does suggest advising women contemplating pregnancy to try to prevent periodontal disease from developing with frequent preventative appointments with their family dentist.


Periodontal status has been shown to have a large impact on glycemic control in patients with diabetes. It is estimated that 12 to 14 million individuals in the United States have diabetes, with only half of the affected individuals diagnosed (Harris et al. 1987). Type 2 DM accounts for 85 to 90% of the cases and Type 1 only 5 to 10 %. The remaining diabetes cases are associated with pregnancy and are called gestational diabetes.

In initial studies to investigate a relationship between periodontal disease and Type 1 DM, it was shown that patients with Type 1 DM have an increased risk of developing periodontal disease with age and that the severity increases with the increased duration of diabetes (Cianciola et al. 1982). Furthermore, it has been shown that poorly controlled diabetics have more attachment and bone loss than well-controlled patients (Safkan-Seppala and Ainamo, 1992). In Type II DM patients, studies have demonstrated increased attachment loss and bone loss irrespective of age (Shlossman et al. 1990). The study reported that attachment loss occurs more frequently and to a greater extent in moderate and poorly controlled diabetic patients.

The mechanisms for the association of periodontal disease and diabetes are reduced polymorphonuclear leukocyte (PMN) function and production of advanced glycosylation end-products as well as decreased collagen production. First, the severity of periodontitis has been correlated with defective chemotaxis (Manoucherhr-Pour et al. 1981 and Manoucherhr-Pour et al. 1981). It was reported that diabetic patients with severe periodontitis had depressed PMN chemotaxis compared to those with mild periodontitis or non-diabetic subjects with severe or mild periodontitis. It has been suggested that a local effect may be responsible since the PMN phagocytic activity of gingival sulcular PMNs was less than that of peripheral blood PMNs. Also, the functional activity of PMNs collected from diseased sites was less than that at healthy sites.

In the hyperglycemic environment, numerous proteins including collagen undergo a non-enzymatic glycosylation process to form advanced glycosylation end products (AGE). AGE play a central role in diabetic complications because they accumulate in the tissues with chronic hyperglycemia (Brownlee, 1994). AGE formation alters the extracellular matrix components and alters tissue structure. This affects collagen stability and vascular integrity. AGE accumulation in collagen results in increased cross-linking between collagen molecules which results in decreased turnover rates (Vlassara, 1991). This may render the poorly controlled diabetic patient with periodontal disease more susceptible to significant tissue damage (Schmidt et al. 1996).


A final aspect of periodontal disease addressed by periodontal medicine is the genetic predisposition of some individuals to advanced tissue destruction. Some evidence has arisen from epidemiological, familial, and twin aggregation studies that periodontal disease, especially aggressive forms, may have a genetic basis (Hart, 1994 and Hart, 1996). The main focus of current studies is the interleukin-1 genotype (Kornman et al. 1997). It is thought that certain people may be more susceptible to the effects of interleukin1 which is known to be associated with bone loss in chronic adult periodontitis. When subjected to the right conditions for periodontal disease, these patients will exhibit more severe bone loss and attachment loss than patients without this genotype. It may be determined from further studies that patients positive for the interleukin-1 genotype may need more aggressive treatment early on in the disease process as well as more rigorous maintenance after treatment is completed.

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