In the emerging field of osteoimmunology, the role of complement in bone biology in general and fracture healing in particular has started to raise interest. Although some direct interactions between the immune system and bone cells have been found (65, 66) , few studies demonstrated the presence of complement components in bone cells. In particular, the expression of various complement factors might depend on the cell differentiation state. Murine osteoblastic cells were shown to produce C3 in response to vitamin D3 (67, 68) . During osteoblastic differentiation in murine osteoblasts and in human cell lines, the complement components C1q, C4, C1 inhibitor, C3a receptor (C3aR), properdin and the complement factor H were upregulated (69), whereas the expression of the subcomponents C1r and C1s together with factor H was decreased (70) . The expression of functionally active C5a receptor (C5aR; CD88) that modulated IL-6 production was described in a human osteoblastic cell line (71, 72) . Recently, mRNA and protein expression of C3aR and C5aR in human MSC were reported (73) .