Inflammation and Oral Health

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 the local inflammatory response and may affect the initiation or progression of systemic disease (i.e., atherosclerosis).7,8 This process of chronic gingivitis is represented in Figure 1.

It is important to note that even though an individual may have established or chronic gingivitis, the condition is still reversible. Thorough dental hygiene debridement and regular home oral hygiene care could return the gingival tissues to a state of health. In some individuals when the inflammatory process continues and expands, the collagen of the periodontal ligament breaks down and bone resorption occurs, thus resulting in periodontitis. Individuals with periodontitis have the same increased levels of proinflammatory mediators as those with chronic gingivitis, including CRP, fibrinogen, and IL-1 and 6. Fortunately, when periodontal treatment is performed and clinical inflammation decreases, the serum levels of these inflammatory mediators also decrease.9