have been recently reported as the only non-immune cell capable of synthesising all complement proteins [34]. After complement activation, biologically active fragments are released. Recent investigation of these fragments revealed their involvement in the pulp anti-inflammatory and regeneration processes. Indeed, pulp complement can be activated by lipoteichoic acids of Gram-positive bacteria, such as S. mutans and S. sanguinis. Upon activation, several biologically active molecules are released. Among these, C5a has been shown to be involved in the recruitment of pulp stem cells [35] and in the guidance of nerve growth to the stimulation site [36]. Another fragment, C3a, is involved in the proliferation of both pulp fibroblasts and stem cells and in guiding fibroblast migration to the stimulation site [37]. This clearly illustrates the involvement of complement in the pulp regeneration process facing bacterial infiltration during carious disease. Indeed, reparative dentine is efficient in arresting the carious injury progression (Fig. 3). This may be partially explained by the fact that pulp complement activation also leads to the synthesis of a complex molecular structure called membrane attack complex. This complex structure can be produced by the fibroblasts and has been shown not only to be fixed on S. mutans and S. sanguinis, but also to kill these cariogenic bacteria [33]. When this complex polymerises on bacteria walls, it creates numerous holes leading to the entry of electrolytes and water, which results in bacteria destruction. Thus, the fibroblasts dampen down, and may even arrest the bacterial invasion to the pulp and provide the adequate signals not only to kill cariogenic bacteria, but also to initiate the regeneration process by recruiting the stem cells and nerve regeneration.
Overall, a carious lesion should be regarded as a dynamic process. Its progression does not only depend on the bacterial infiltration and the local environment, but also on the host pulp response.
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