الفهرس 
Review of LiterautreOnly 14 pages are availabe for public view
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Abstract
Periodontitis is a chronic infection that results from the interaction of periodontopathogenic bacteria and host inflammatory and immune responses and is the most common bacterial infection worldwide. Estimates reveal that 10 - 15 % of adults have advanced periodontitis, and periodontal disease can contribute to widespread oral health dysfunction and enhanced susceptibility to other systemic diseases (Pussinen et al., 2007).
Bacterial biofilms are considered to be the primary etiological factor in the initiation ofgingival inflammation and the following destruction of periodontal tissues (Offenbacher, 1996). Three primary specific pathogens have been repeatedly identified as etiologic agents namely Aggregatibacter (Actinobacillus) actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg) and Tannerella forsythia (Tf) (Socransky et al., 1998).
Although chronic exposure to bacteria and their products is a main reason for gingival inflammation and periodontal tissue destruction to occur, the major causative factor of soft- and hard- tissue breakdown associated with periodontitis is currently contributed to the host’s immune-inflammatory response to bacterial challenge. Also the nature of the inflammatory response might determine the destructive character of the disease (Gemmell et al., 2002).
The biologic phenotype underlying chronic periodontitis, including the biofilm and the host response, tend to vary among individuals despite a similar clinical diagnostic category (Offenbacher et al., 2007). Consequently, disease screening should ideally be based on clinical determinations and the biologic phenotype (Page and Kornman, 1997).
Other involved factors include environmental exposures, differences in genetic and also epigenetic composition (Page and Kornman, 1997).
The biological changes underlying the transition process from gingival health to early inflammatory changes include local increase in vascular permeability, edema and the recruitment and activation of polymorphonuclear neutrophils (PMN) (Delima and Van Dyke, 2003). Acquired immune response becomes involved when antigen-presenting cells interact with immunocompetent cells, such as T and B lymphocytes, leading to the expansion of antibody-secreting plasma cells and the development of the chronic lesion (Gemmell and Seymour, 2004).
Bacterial–host interactions at the biofilm–periodontium interface induce the synthesis of cytokines and other inflammatory mediators that induce the release of enzymes and bone-associated molecules that finally induce the alterations of the connective tissue metabolism and the destruction of the tooth supporting alveolar bone (Shapira et al., 2007).
In addition to local periodontal tissue involvement, chronic infection of the periodontium together with continuous up-regulation of pro-inflammatory responses and immune mediators may assist in systemic sequel including diabetes, preterm delivery of low weight birth babies, lung inflammation, arthritis and cardiovascular diseases (CVD). In fact, numerous case-control and cohort studies have explained that periodontitis patients have increased risk for CVD, acute myocardial infarction (AMI), peripheral arterial disease and CVD, relative to patients with healthy periodontium (Mattila et al., 2005).
Although the associations of periodontal diseases with CVD have been investigated in several clinical studies the pathogenic mechanisms and links between both diseases are not completely clarified (Buduneli et al., 2011).