Current models of mucosal surfaces of oral, gut, lung, and skin tissue postulate that local bacterial antigens, derived from biofilms on surfaces, regulate local tolerance, local immune response, and systemic response by way of an "information relay system" through a series of nuclear factor-kappa beta pathways to synthesize and secrete cytokines and chemokines to regulate the inflammatory process at local as well as distant sites. Evidence is also accumulating that the predominant cells of the periodontium, gingival fibroblasts, are capable of producing prostaglandins, interleukins (IL-1beta [β], IL-6, IL-8), tumor necrosis factor-alpha (TNF-α), and interferon- gamma (IFN-γ). It is hypothesized that these mediators modulate inflammation locally as well as at a distant site of infection.
One presupposes the direct role of oral bacteria or their products in the pathogenesis of atherosclerotic plaque in myocardial infarctions. An alternative explanation is the possible role of mediators in inflammation initiated by periodontal pathogens in the development of chronic complications. There is general agreement that chronic diseases, such as atherosclerosis, stroke, and diabetes, are multifactorial in origin. But there is growing evidence that these diseases are influenced by gingival inflammation and chronic periodontal infections. In a series of cross-sectional studies, a strong relationship has been found between acutephase C-reactive protein (CRP) in serum and the severity of periodontal diseases. CRP is triggered by infections, trauma, necrosis, and malignancy, and is also linked to heart disease and diabetes. CRP is synthesized in the liver in response to proinflammatory cytokines such as IL-1α, IL-1β, and IL-6. TNF-α, IFN-γ, and transforming growth factor also participate in the production.
The current therapeutic strategy to control periodontal infections involves mechanical removal of deposits, both supra- and subgingival.