Pathology

Is a significant improvement in oral health closely correlated with analogous changes in coronary heart disease?
Nobody wants a heart attack. Individual who suffers from chronic coronary heart disease has an urge to seek measures to preventing its recurrence or even to curing the disease. Researchers are establishing a link of oral health to coronary heart disease (CHD) based on findings from recent researches; however, there are also studies reporting no significant association between these two diseases other than a socioeconomic one. Though opinions split the issue, but we certainly see the benefits of investigating into both sides of the controversy, so that we may logically arrive a reasonable recommendation for you and your colleagues. Firstly, we shall discuss the analogous risk/contributing factors for these two diseases, with reference to the medical, dental and social histories of our patient of interest in the following tables (Tables 1 and 2). CHD is multifactorial, and often the risk/contributing factors will occur in a cluster; moreover, different individuals may have different combination of the factors leading to CHD. (Little et al, 1993 & Frohlich et al, 1998). While the true risk factor identified for PD is smoking, there are also other factors contributing to the incidence of this disease. To start with, we draw analogous risk/contributing factors of these two diseases side by side, and attempt to reveal the possible linkage between them. Secondly, we shall attempt to draw an analogy between the two diseases by comparing the pathogenesis of CHD with the pathogenesis of PD.

What is coronary heart disease?

Coronary heart disease (CHD) is the a myocardial disorder in most cases caused by coronary atherosclerosis. Most often it is due to inadequate blood supply, which not only

causes myocardial hypoxia or anoxia, but also reduces the availability of nutrients and impedes the removal of metabolic degradation products (Frohlich et al, 1998). The main underlying pathological process of CHD is the atherosclerosis of one or more of the four coronary arteries. In humans, no single factor can account for all the causes of CHD. Our patient has a cluster of the risk factors for his chronic heart disease condition. These include his male gender, over 40 years of age, smoking 2 cigarettes per day, high blood pressure of 148/110 mmHg. His scotch-like halitosis may be a sign of his advanced and active periodontitis, or an evidence of his drinking too much alcohol. In addition to his adenocarcinoma history and the follow-up chemotherapy, his health and life style have brought him a lot of stress too! Inevitably, he is chosen as a candidate for CHD. However, a substantial proportion of CHD patients do not have these traditional risk factors. Recent data suggest that chronic infectious diseases may play an important role in the development of atherosclerosis, or they may intensify the effect of other risk factors. The association of CHD and Clamydia pnemoniae infection is firmly established, but causality is yet to be proven. The link with other infectious agents or conditions, such as cytomegalovirus, herpes simplex virus, Helicobactor pyloris and periodontitis, is more controversial (Fong, 2000). In fact, some researchers suggest that traditional risk factors are not significant predictors of coronary event, when included in a model that contained oral health variables such as periodontal condition of the patient. Furthermore, the inflammatory markers in the blood that have been associated or correlated with risk of CHD include highly sensitive C-reactive protein, fibrinogen, serum amyloid and interleukins, tumour necrosis factor- (TNF- ), interleukin-6, and vascular and cellular fibrinogen adhesion molecules (Ridker, 1999). To appreciate the correlation of this possible role of periodontal disease as one of these infectious diseases, it is necessary to understand the pathogenesis of coronary atherosclerosis.

What is the pathogenesis of coronary atherosclerosis?

The initiating event is an irreversible injury to the endothelial cells of the coronary artery, which elicit a series of on site host inflammatory response. The injured endothethial cells lose their barrier capacity, allowing the influx of various substances from the plasma into the vessel wall. Loss of anti-thrombogenic functions of endothelial cells is accompanied by attachment of platelets to the luminal surface. Growth factors such as platelet-derived growth factor or fibroblast growth factor released

from the platelets stimulate the proliferation of smooth muscle cells, which grow into the intima of the artery and become lipid-laden. At the same time, macrophages enter the vessel wall and take up the lipid, transforming it into a foam cells. The lipid released from dead and dying smooth muscle cells and macrophages become oxidized and broken down. Cholesterol crystals and a mixture of cell debris, altered collagen, and other intercellular matrix molecules formed a softened area in the vessel wall, known as atheroma. Tissue damage heals by scarring, but it also elicits a lymphocytic response. Lymphocytes are a major source of growth factors and mediators that act on macrophages, smooth muscle cells, and fibroblasts, perpetuating the pathologic process that ultimately destroy all layers of the blood vessel. The fibrotic scar tissue and lipid-rich atheroma attract calcium salt and, accordingly, most advanced atheromatous lesions are heavily calcified (fig.1). Coronary atherosclerosis is localized at the heart vessels. The clinical symptoms developed due to ischemia caused by the progressive narrowing or the complete occlusion of the arterial lumen by the atherosclerotic plaques. Rupture of coronary atherosclerotic plaques is often accompanied by the formation of thrombi, which develop suddenly and typically cause acute infarction in the area supplied by the affected coronary artery or arteries. Coronary atherosclerosis results in coronary heart disease. Moreover, one form of clinical syndromes of severe CHD is chronic heart disease. Apart form the existing severe coronary atherosclerosis, our patients condition may present as a gradually progressive myocardial ischemia, or as a series of repeated infarct, resulting in myocardial fibrosis, and in most cases he should have a history of angina or previous myocardial infarction (Frohlich et al, 1998).