The key etiological bacteria of enamel caries are Streptococcus mutans in association with secondary colonisators like Lactobacilli and Actinomyces. One of the main virulence factors of S. mutans is its ability to adhere to the dental surface by adhesins like antigen I/II, a family of cell-surface-anchored proteins. Progressive caries is defined by the diffusion of bacterial substances into the pulp by dentinal tubules. In response to this carious bacterial infection, the dental pulp initiates inflammatory and immune reactions by two types of cells, odontoblasts and pulpal fibroblasts. Previously to the pulpal immune response, pathogenesis of caries leads to the stimulation of the innate immunity in the pulp by the induction of antimicrobial peptides.
The present study focuses on the ability of human pulpal fibroblasts and human odontoblasts to produce the antimicrobial protein S100A7 after stimulation with antigen I/II from S.mutans. Antimicrobial activity of S100A7 against caries-causing bacteria including S. mutans, L. acidophilus and A. naeslundii was tested as well.
Method:
Cloning of S100A7, immunoblot analysis, enzyme linked immunosorbant assay (ELISA), bacterial culture
Result:
S100A7 protein is expressed in a concentration and time dependent manner by pulpal fibroblasts and odontoblasts after stimulation with antigen I/II. Simultaneously, S100A7 was secreted into the cell culture supernatant both by human pulpal fibroblasts and odontoblasts. S100A7 showed antimicrobial activity against Streptococcus mutans, Lactobacilli and Actinomyces.
Conclusion:
Our results suggest an important role of pulpal fibroblasts and odontoblasts in the activation and modulation of innate immune responses during specific caries-causing bacterial infection in the pulp. The antibacterial potential of S100A7 produced by pulpal fibroblasts and odontoblasts reveals the key role in innate immunity of the pulp-dentine formation and the possibility to be used as an specific adjunct natural regimen for elimininating specifically caries-causing bacteria without disturbing the natural balance of the microbial flora in the oral cavity.