Inflammation: The Relationship Between Oral Health And Systemic Disease
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Author: JoAnn R. Gurenlian, RDH, PhD
Since the mid 1990s, both the scientific community and the public have been inundated with articles addressing the association between systemic diseases and oral health. It seems that almost monthly there is an article in a fashion magazine reminding the public that tooth brushing and flossing can save their life. Some articles point to the notion that oral infection and bacteria may be linked to heart attack and stroke. Others dispel the association, indicating that there is not enough research to determine any relationship between the two. The questions that have been raised focusing on the relationship between periodontal diseases and systemic conditions now extend beyond cardiovascular disease and include diabetes, respiratory disease and adverse pregnancy outcomes. Research has demonstrated that the association between oral inflammation and systemic inflammation may be the key to understanding the deleterious effects on multiple organ systems. However, is the relationship so complex that it is like trying to crack the DaVinci Code, or can health care professionals and the public understand the role of inflammation in oral and systemic health?
The purpose of this article is to review how the inflammatory process functions in the human body. The role of inflammation in oral and systemic health will be discussed. Translating this information into practical application for dental hygiene professionals will be addressed so that both inquiring patients and astute clinicians will capitalize on the opportunities for improving total health.
What is inflammation? Isn't this the process that is supposed to be good for our bodies? How can it now be something that causes harm to so many different aspects of the body? As we learn more about the biological mechanisms of inflammation, it becomes clear that this process is more complicated than was once thought.
Inflammation is the body's response to cellular injury. Despite the fact that the press has emphasized the harmful effects of inflammation, the fact remains that without this process, our bodies could not survive. Inflammation represents a protective response designed to rid the body of the initial cause of cell injury and the consequences of that injury. Cell injury may occur due to trauma, genetic defects, physical and chemical agents, tissue necrosis, foreign bodies, immune reactions and infections.
Inflammation is a local reactive change that involves the release of antibacterial agents from nearby cells that defend the host against infection. It also facilitates early tissue healing and repair. It contains—or "walls off "—the infectious or injurious agent and serves as a defense mechanism that the body can use to restore itself to a normal morphological form and function.
The inflammatory response consists of a vascular and a cellular reaction. These reactions are mediated by chemical factors derived from plasma proteins or cells. The classic signs of inflammation are redness, swelling, heat, pain and loss of function. The physiologic explanations for these signs appear in Table I. Other signs of inflammation include fever, leukocytosis or an increase in the number of circulating white blood cells, the presence of acute-phase proteins including C-reactive proteins (CRP), fibrinogen and serum amyloid A protein (SAA), and sepsis.
There are two types of inflammation: acute and chronic. Acute inflammation is characterized by a rapid onset and short duration. It manifests with exudation of fluid and plasma proteins, and emigration of leukocytes, most notably neutrophils. Chronic inflammation is of prolonged duration and manifests histologically by the presence of lymphocytes and macrophages and results in fibrosis and tissue necrosis. When inflammation continues for prolonged periods of time, it can be thought of as the healing process in overdrive, and deleterious changes can occur to localized tissues as well as the entire body.
In appreciating the inflammatory process, it is important to understand the role of chemical mediators. These are the substances that tend to direct the inflammatory response. These inflammatory mediators come from plasma proteins or cells including mast cells, platelets, neutrophils and monocytes/macrophages. They are triggered by bacterial products or host proteins. Chemical mediators bind to specific receptors on target cells and can increase vascular permeability and neutrophil chemotaxis, stimulate smooth muscle contraction, have direct enzymatic activity, induce pain or mediate oxidative damage. Most mediators are short-lived but cause harmful effects.1 Examples of chemical mediators include vasoactive amines (histamine, serotonin), arachadonic acids (prostaglandins, leukotrienes) and cytokines (tumor necrosis factor and interleukin–1).
The inflammatory process significantly affects the periodontium. Plaque biofilm releases a variety of biologically active products as gram-positive and gram-negative bacteria colonize the tooth surface around the gingival margin and interproximal areas. These products include endotoxins, cytokines and protein toxins.2 These molecules penetrate the gingival epithelium and initiate a host response that eventually results in gingivitis. Evidence of this can be seen clinically with changes in tissue color from pink to red, swelling, and bleeding upon probing.3 Because gingivitis is typically not painful, it may remain untreated for years. Worse, it may be viewed by practitioners as something that requires less concern than periodontitis. Nevertheless, chronic gingivitis that persists for years may provide the basis for greater concern for systemic health than a periodontitis condition that is more readily treated.
As the biofilm continues to proliferate, soluble compounds penetrate the sulcular epithelium. This, in turn, signals the gingival epithelium to produce chemical mediators including interleukin–1 beta (IL-1‚), prostaglandins, tumor necrosis factor alpha (TNF-α), and matrix metalloproteinases.4 These products recruit neutrophils to the area and influence chemotaxis, and can cause increased permeability of gingival vessels that permits plasma proteins to emigrate from the blood vessels into the tissue. As the inflammatory process progresses, additional mediators are produced, and more cell types are recruited to the area including neutrophils, T-cells, and monocytes. Continued inflammation results in signaling of fibroblasts and production of proinflammatory cytokines in the tissues. Antibodies specific to oral bacteria circulate in the peripheral blood. The acute-phase response becomes activated and CRP, fibrinogen and complement are produced both by local cells and within the liver.5,6 These proteins may further exacerbate and adverse pregnancy outcomes has been closely investigated. The basis for the biological mechanism of this relationship is beginning to emerge and further study may lead to an understanding of whether or not a true causal relationship exists.
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