Copyright © 2014, Zahedan University of Medical Sciences. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Chronic periodontitis (CP) is a common complex infectious disease resulting in inflammation within tissues supporting teeth, which leads to progressive attachment loss, bone loss and eventually tooth loss (1). It is characterized by degradation of extracellular matrix (ECM) components associated with an infiltration of several inflammatory cell populations into the gingival epithelium and connective tissue (2, 3). The first etiologic factor of CP is the accumulation of bacteria in gingival groove. Dental plaque bacteria and calculus have direct and indirect roles in destruction of periodontal tissues. The direct impact is due totoxins, enzymes, and metabolites of bacteria present in dental plaque, which play a key role in the initiation of immune response and induces tissue destruction indirectly by activating host defense cells, which in turns produce and release inflammatory mediators. It stimulates effectors of connective tissue breakdown. Bacteria-derived pathogenic factors such as lipopolysaccharides can activate junctional epithelial cells to release potent cytokines and proteases, leading to inflammation and connective tissue breakdown and bone resorption (4, 5). Fibroblasts, macrophages, osteoblasts, keratinocytes, and endothelial cells are activated in response to stimulus, contributing with the synthesis of cytokines and MMPs (6). Epidemiological studies revealed that differences in periodontitis among individuals could not be explained by differences in oral hygiene alone and that not everybody is equally susceptible (7). The pathogenesis of periodontitis depends on the interactions between host and microorganism and may be complicated by genetic and environmental risk factors (8). There is local infiltration of inflammatory cells and degradation of ECM macromolecules in gingival connective tissue of patients with CP. Among matrix macromolecules, collagen fibers constitute the major compartment of the gingival lamina propria and have an important role in its normal histological architecture. Loss of Collagenous compartment may reflect the severity of periodontitis (8). During the progression of periodontal inflammation, periodontal ligament and gingival fibroblasts secrete high levels of cytokines and chemokines (9). Proinflammatory cytokines play crucial roles in microbe-induced destructive inflammation (8). These molecules contribute to the breakdown of type I collagen and also promote bone resorption by stimulating proliferation, differentiation, and activation of osteoclasts (10, 11). Tissue destruction seems to be regulated by four major pathways of plasminogen-dependent, phagocytic, osteoclastic and matrix metalloproteinase (MMP) ones. It seems that the MMPs pathway is the most relevant in periodontitis. MMPs are a family of metal ions-dependent endopeptidases capable of degrading all matrix macromolecules, including collagen fibers and basement membrane constituents (12). Four major subgroups of MMPs directly related to degradation of periodontal tissues include: collagenases, gelatinases, stromelysins and membrane-type MMPs (MT-MMP). Collagenases due to their helicase activity are capable of degradation of type I collagen. Then degradation of the collagen fibrils is done by gelatinases, or lysosomal proteinases (phagocytic pathway). MMP-2 degrades fibrillar type I collagen (10, 11). Stromelysins (MMP-3) and MT-MMPs play a pivotal role during activation of other MMPs (13). Studies have reported that some cytokines are encoded by polymorphic genes, showing genotypes associated with inflammatory diseases that may confer susceptibility to periodontal disease (9). Therefore, most genetic researches in periodontitis have focused on gene polymorphisms playing role in immune system, tissue destructive processes, or metabolic mechanisms (7, 14). Gene polymorphisms are mechanisms through which individuals may exhibit variations within the range of what is considered biologically normal (7). Polymorphisms represent natural sequence variants (alleles), which may occur with more Ar h ve of S ID
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