Lipopolysaccharide from Escherichia coli but not from Porphyromonas gingivalis induce pro-inflammatory cytokines and alkaline phosphatase in dental follicle cells.

OBJECTIVES: Dental follicle cells (DFCs) as periodontal precursor cells are the natural source for cellular therapies of periodontitis. Periodontitis is initiated after the infection of the periodontium with oral pathogens such as the Gram-negative bacteria Porphyromonas gingivalis. Lipopolysaccharide (LPS) is the major component of the outer membrane of gram-negative bacteria. Previous studies have shown that especially P. gingivalis LPS induces the expression of pro-inflammatory cytokines in PDL cells and disturbs the differentiation of dental stem cells. Our study investigated the administration of LPS to DFCs for the first time.
MATERIALS AND METHODS: We evaluated cell proliferation (WST1 assay), expression of cytokines IL1β, IL8 and IL6 (real-time RT-PCR) and the osteogenic differentiation of DFCs (ALP-activity and Alizarin red staining) in the presence of P. gingivalis LPS and Escherichia coli LPS.
RESULTS: All tested pro-inflammatory cytokines were highly increased after E. coli LPS treatment. P. gingivalis LPS induces only the expression of IL8, but this expression was significantly lower than that after E. coli LPS administration. The ALP activity was significantly higher in DFCs after the administration of E. coli LPS than after administration of P. gingivalis LPS or under normal cell differentiation conditions. However, the mineralization was inhibited with LPS from both bacterial species.
CONCLUSION: LPS disturbs osteogenic differentiation in DFCs. Moreover, the failure of pro-inflammatory cytokines induction in DFCs after the administration of P. gingivalis LPS differs greatly from that of PDL fibroblasts. These immunological properties of DFCs have to be considered for cellular therapies of periodontitis with DFCs.