Abstract
IntroductionPeriodontitis is initiated and sustained by bacteria. However, the mechanism of bacteria induced periodontitis is still unknown. We hypothesized that bacterial components can affect the functions of stem cells in the periodontium. In this study, we comparatively investigated the influence of Lipopolysaccharide (LPS) on the osteogenesis potential of human periodontal ligament stem cells (PDLSCs) and bone marrow mesenchymal stem cells (BMMSCs).MethodsHuman PDLSCs and BMMSCs were harvested and mineralized nodule formation was assessed by alizarin red S staining. Expression level of osteogenic related gene was detected by quantitative RT-PCR (qRT-PCR). The expression of Toll-like receptor 4 (TLR4) and its downstream signaling pathway were examined by western blot. The role of TLR4 and related signaling pathway in LPS impairing the osteogenic potential of human PDLSCs and BMMSCs were also studied by alizarin red S staining and qRT-PCR. Experimental periodontitis was induced in adult Sprague–Dawley rats and the alveolar bone loss was measured by micro computed tomography analysis. The expression of alkaline phosphatase (ALP) was assessed by immunohistochemistry and the number of osteoclasts was shown by Tartrate-resistant acid phosphatase (TRAP) staining.ResultsLPS decreased the osteogenic differentiation of human PDLSCs through TLR4 regulated nuclear factor (NF)-κB pathway, but not for BMMSCs. Blocking TLR4 or NF-κB signaling partially reversed the decreased osteogenic potential of PDLSCs and prevented the alveolar bone loss caused by LPS experimental periodontitis in rats. The ALP expression in the periodontal ligament was elevated after treatment with anti-TLR4 antibody or pyrrolidinedithiocarbamate, whereas there was no statistical significance among groups for the number of osteoclasts.ConclusionsThese data suggest that LPS can activate TLR4 regulated NF-κB pathway of human PDLSCs, thus decreasing their osteogenic potential. Blockage of TLR4 or NF-κB pathway might provide a new approach for periodontitis treatment.
Highlights
Periodontitis is initiated and sustained by bacteria
LPS decreased the osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) through toll-like receptor 4 (TLR4) regulated nuclear factor (NF)-κB pathway, but not for bone marrow mesenchymal stem cells (BMMSCs)
Blocking TLR4 or nuclear factor-κB (NF-κB) signaling partially reversed the decreased osteogenic potential of PDLSCs and prevented the alveolar bone loss caused by LPS experimental periodontitis in rats
Summary
Periodontitis is initiated and sustained by bacteria. the mechanism of bacteria induced periodontitis is still unknown. Periodontitis is characterized by the inflammatory reaction of the surroundings of the teeth, mostly caused by an oral microbial biofilm and perpetuated by an uncoordinated immune-inflammatory response, which leads to progressive destruction of the tissues supporting the teeth [1] It is until now the major cause of tooth loss and is associated with a number of systemic diseases, such as diabetes and cardiovascular diseases [2], while no appropriate method has been developed to provide a functional and predictable method for periodontal regeneration. Lipopolysaccharide (LPS), a cell wall component of gramnegative bacteria, is mainly recognized by toll-like receptor 4 (TLR4) of the host. This bimolecular compound penetrates periodontal tissue [3,4] and is considered to be a major nexus for virulence in periodontitis [5,6]. The underlying molecular mechanism of LPS-host interaction is still unclear
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