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Figure 2. Chemokines and bone tissue. A schematic representation of chemokine networks in bone tissue, in which both osteoclasts and osteoblasts can be targets of chemokines. Chemokines such as MCP-1/CCL2, SDF-1
/CXCL12, MIP-1/CCL3, and MIP-1
/CCL9 can induce the chemotaxis and differentiation of osteoclast precursors into osteoclasts. Other chemokines, such as IL-8/CXCL1, MCP-3/CCL7, CKß8/CCL23, and IP-10/CXCL10, also act in osteoclasts. However, the activation of osteoclasts is achieved only with RANKL, which also induces chemokine production, generating an amplification loop to potentiate bone resorption. Chemokines such as SDF-1/CXCL12, BCA-1/CXCL13, and RANTES/CCL5 act on osteoblast precursors, driving their proliferation and cell survival, chemotaxis, and the production of type-I collagen, which can result in increased bone formation. The osteoblasts are also an important source of chemokines, produced in response to a wide range of stimuli, such as microbial products, inflammatory mediators, or dentin proteins. While osteoblast-derived MCP-1/CCL2 and SDF-1/CXCL12 participate in an interesting chemokine cross-talk between osteoblasts and osteoclasts, chemokines such as LIX/CXCL5 and BCA-1/CXCL13 can also attract different leukocyte subsets, suggesting an important role for osteoblasts in the inflammatory-immune reaction.
