IADR Abstract Archives
Immunoregulatory Function of Stem Cells of the Apical Papilla
Objectives: Clinicians are often faced with the challenge of treating immature teeth with pulpal necrosis. Regenerative endodontics procedures have emerged as a viable stem-cell based treatment alternative for these cases. The apical papilla is likely a main source of stem cells in these procedures. These cells are exposed to a myriad of microbial antigens during the progressive process of pulpal necrosis. Although there is growing recognition that mesenchymal stem cells are participants in immune reactions, the immune-competency of stem cells of the apical papilla (SCAP) remains largely unknown. We hypothesized that SCAP are able to recognize pathogen patterns (antigens), and release key inflammatory mediators in response to a microbial challenge thereby mediating the initial immune response.
Methods: To test this hypothesis, SCAP were exposed to heat-killed E. coli and gene and protein expression were evaluated by PCR and protein arrays. In addition, SCAP-mediated chemotaxis of macrophages and leukocytes was evaluated using a real-time dual chamber model in presence of bacterial challenge. Data were analyzed with one way-ANOVA with Bonferroni’s post hoc test (p<0.05).
Results: SCAP express all major toll-like receptors including TLR2, TLR3, TLR4, TLR5 and TLR9. Exposure of SCAP to bacterial antigens results in the selective upregulation of several genes encoding chemotactic factors. The protein expression and the release of these chemokines were significantly upregulated in bacterially challenged SCAP. Subsequently, this resulted in robust migration of macrophages and lymphocytes towards the SCAP exposed to bacteria.
Conclusions: Collectively, these results demonstrate that SCAP play an active role in microbial recognition and immune cell recruitment to the inflammatory site. Thus, SCAP are likely to be involved in the apical recruitment of immune cells during the process of pulp necrosis, and in the development and maintenance of apical periodontitis in immature teeth with pulpal necrosis.
Methods: To test this hypothesis, SCAP were exposed to heat-killed E. coli and gene and protein expression were evaluated by PCR and protein arrays. In addition, SCAP-mediated chemotaxis of macrophages and leukocytes was evaluated using a real-time dual chamber model in presence of bacterial challenge. Data were analyzed with one way-ANOVA with Bonferroni’s post hoc test (p<0.05).
Results: SCAP express all major toll-like receptors including TLR2, TLR3, TLR4, TLR5 and TLR9. Exposure of SCAP to bacterial antigens results in the selective upregulation of several genes encoding chemotactic factors. The protein expression and the release of these chemokines were significantly upregulated in bacterially challenged SCAP. Subsequently, this resulted in robust migration of macrophages and lymphocytes towards the SCAP exposed to bacteria.
Conclusions: Collectively, these results demonstrate that SCAP play an active role in microbial recognition and immune cell recruitment to the inflammatory site. Thus, SCAP are likely to be involved in the apical recruitment of immune cells during the process of pulp necrosis, and in the development and maintenance of apical periodontitis in immature teeth with pulpal necrosis.