The role of CD14 and Toll-like receptors on the release of MMP-8 in the LPS recognition pathway

Periodontal diseases are infections that are caused by microorganisms which are colonized on the tooth surface at or below the gingival margin, and these initiate the breakdown of connective tissue attachment to the tooth and alveolar bone loss. For a periodontal pathogenesis, it is essential that the pathogen should be able to colonize the subgingival area and produce factors that either directly damage the host tissue or lead to the host tissue damaging itself. It has been designated that A. actinomycetemcomitans, P. gingivalis and B. forsythus were major periodontal pathogens among oral microflora 1) . Among them, P. gingivalis species produce collagenase, an array of proteases, hemolysins, endotoxin etc. and can inhibit migration of polymorphonuclear leukocytes (PMNs) across an epithelial barrier 2) .1) The pathogenicity of microorganisms relates as much to the particular host s innate and/or inflammatory and/or immune capabilities, as to the virulence of the bacteria themselves. Some of substances produced by the biofilm can be directly injure host cells and tissues. Other microbial constituents may activate inflammatory or cellular and humoral immune systems which secondarily damage the periodontium. Among the enzymes released by bacteria, lipopolysaccharides (LPS) of Gram-negative microorganisms are capable of invoking both the inflammatory and immune responses as they interact with host cells. LPS binding protein(LBP), CD14, and Toll-like receptors(TLRs) are parts of major innate host defense inflammatory activation pathway that recognize and facilitate the host inflammatory response to LPS 3-5) . One role of