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Figure 4. Pulpal and periapical scenarios orchestrated by chemokines. A schematic representation of periapical lesion formation, supported by an inflammatory and immune response against micro-organisms that invade and destroy the dental pulp. In inflamed pulp, the chemokines MIP-3
/CCL20 (a CCR6 ligand), IL-8/CXCL-8, and MCP-1/CCL-2 expression contribute to inflammatory cell infiltration. The progression of pulpal inflammation to the periapex and colonization of the root canal system by micro-organisms leads to soft- and hard-tissue destruction. In the periapex, chemokine production, which can be invoked by micro-organisms, dentin proteins, and dental materials, supports migration of leukocyte subsets, lymphocytes, and bone cells. Gram-negative flora is able to induce the production of IL-8/CXCL8 by pulp fibroblasts, osteoblasts, and the production of MIP-1/CCL3 and MIP-1ß/CCL4 by neutrophils. CXCR1 expression was detected in neutrophils, which are attracted by IL-8/CXCL8. Chemokines and receptors expressed in cysts and granulomas comprise, CCR1—expressed in monocytes/macrophages, lymphocytes and osteoclasts—and its ligands MIP-1/CCL3 and RANTES/CCL5. CCR2 and CCR5 are found in monocytes/macrophages and lymphocytes, and their ligands are MCP-1/CCL2 (CCR2), MIP-1/CCL3, MIP-1ß/CCL4, and RANTES/CCL5 (CCR5 ligands). CXCR3 and CCR3 are expressed in lymphocytes, and their ligands are MCP-2/CCL8 (CCR3) and IP-10/CXCL10 (CXCR3). Chemokine expression in apical periodontitis contributes to persistent inflammatory cell infiltration and the chronicity of apical lesions.
