Periapical bone resorption is the hallmark of periradicular disease initiated by the invasion of bacteria and their byproduct from the infected root canal system1). Many recent studies have demonstrated that interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) are potent inflammatory cytokines having bone-resorbing activity2-4). Since these cytokines are produced by monocytes/macrophages, the recruitment of inflammatory cells is of particular importance in the root canal system and periapical tissue because it is likely that cells will be challenged with bacteria during acute infection and once localized, these cells in periapical tissue may play a functional role in the pathogenic mechanism(s) of periapical disease through production of these cytokines5). Periapical infections may result in the exposure of periodontal ligament (PDL) cells to microbial products as well as to proinflammatory cytokines liberated from neighboring tissue. These cytokines affect the functions of PDL cells.
Periodontal ligament resides between the cementum of the roots of teeth and the alveolar bone. In this location, PDL cells are uniquely situated to maintain the overall integrity of the periodontal ligament. Among the PDL cells, fibroblasts are the predominant cell type and play a central role in the maintenance of the periodontium since they are responsible for the synthesis and degradation of collagen and are involved in the regulation of alveolar bone remodeling. It is now clear that the fibroblasts are a key sentinel cells that have important functions in fibrosis, wound healing, maintenance of tissue integrity, as well as the regulation of immune responses in various tissues. In order to execute these functions, fibroblasts should synthesize and release a wide array of cytokines including chemokines6).
Chemokines are chemotactic cytokines that stimulate recruitment of leukocytes to the site of inflammatory reactions7-8). Monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α) and RANTES(regulated on activation, normal T cell expressed and secreted) are 3 well-characterized CC-chemokines that regulate mononuclear cell recruitment.
MCP-1 is expressed by mononuclear phagocytes and endothelial cells, MIP-1α is produced by activated inflammatory cells, such as macrophages and eosinophils, and noninflammatory cells including fibroblasts, myofibroblasts, endothelial cells and epithelial cells. The role of RANTES in allergic inflammation has been well defined and one of the major eosinophil chemoattractants in allergic inflammatory diseases8). Despite of the fact that some of these chemokines are secreted by various normal cell types, including fibroblasts, epithelial cells, and leukocytes9), there are few studies on the expression of chemokines from the PDL fibroblasts.
In this regard, Safronova et al.10) have demonstrated that MCP-1 was expressed in human synovial fibroblasts and Hanazawa et al.11) showed that gingival fibroblasts also produced MCP-1.
Bacterial lipopolysaccharide (LPS) is a major component of the outer membranes of Gram-negative bacteria. It functions as a virulence factor and has the ability to induce a number of inflammatory and immunopathological reactions by stimulating inflammatory cells to release a variety of cytokines, which in turn leads to the destruction of host tissue. In last few years, although many studies have investigated the role of anaerobic bacterial LPS, the role of endodontopathic bacterial LPS and the interaction between these bacterial LPS and inflammatory cells have received less attention12-14).
P. endodontalis, an asaccharolytic, black-pigmented bacteria, is found in approximately 50% of chronic endodontic lesions and exclusively found in infections of endodontic origin, suggesting that there is a specific association between P. endodontalis and pulpal and periapical diseases15-16). Recently, Ko et al.17) demonstrated that human peripheral polymor-phonuclear neutrophils (PMNs) have the ability to release MIP-1α and MIP-1β after stimulation of P.endodontalis LPS.
It is postulated as a possibility that chemokines, MCP-1, MIP-1α and RANTES expressions in the PDL fibroblasts may be induced by the action of cell components of P. endodontalis. Therefore, the purpose of present study was to evaluate the protein level of these chemokines expression in PDL fibroblasts stimulated with P. endodontalis LPS
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