Abstract
Chronic Periodontitis is an inflammatory disease initiated and maintained by bacterial plaque and its metabolic products that trigger the local infiltration of inflammatory cells associated with the breakdown of collagenous extracellular matrices(ECMs). The degradation of gingival connective tissue during periodontitis could be a disturbance of cell-cell and cell-matrix interactions involving the production of enzymes, activators, inhibitors, and regulatory molecules such as cytokines and growth factors. In periodontitis, although some tissuedestructive enzyme activities may derive from specific bacteria, it is more likely that plaque bacteria inaddition to their other pro-inflammatory effects, generate proteinases that activate latent forms of mammalian collagenase, or even stimulate the release of collagenase and other matrix metalloproteinases(MMPs) from host cells 4) . MMPs are a family of zinc-dependent endopeptidases that collectively degrade all extracellular matrix proteins and basement membrane at neutral pH and are essential for cellular migration and tissue remodeling under physiological and pathological conditions. Most of them are secreted as inactive form(proenzyme) and are activated in the extracellular compartment or in the vicinity of the cell membranes by other MMPs or serine proteinases 7) . Interstitial collagenase, including matrix metalloproteinase-1(MMP-1) and MMP-8, serve as ini-
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