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Review
. 2022 Sep 19;17(1):1240-1248.
doi: 10.1515/biol-2022-0474. eCollection 2022.

Osteogenic differentiation of periodontal membrane stem cells in inflammatory environments

Shenghao Jin  1 , Haitao Jiang  1 , Yue Sun  1 , Fang Li  1 , Jianglan Xia  1 , Yaxin Li  1 , Jiwei Zheng  1   2 , Ying Qin  1   2
Affiliations
Review

Osteogenic differentiation of periodontal membrane stem cells in inflammatory environments

Shenghao Jin et al. Open Life Sci. .

Abstract

Periodontitis is a common disease that is difficult to treat, and if not controlled in time, it causes severe conditions, such as alveolar bone resorption and tooth loosening and loss. Periodontal ligament stem cells constitute a promising cell source for regenerative treatment of periodontitis due to their high osteogenic differentiation capacity. PDLSC osteogenesis plays a central role in periodontal regeneration through successive cytokine-mediated signaling pathways and various biochemical and physicochemical factors. However, this process is inhibited in the inflammatory periodontitis environment due to high concentrations of lipopolysaccharide. Here, we review the mechanisms that influence the osteogenic differentiation of periodontal stem cells in this inflammatory microenvironment.

Keywords: inflammatory environment; lipopolysaccharide; osteogenic differentiation; periodontal membrane stem cells.

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Conflict of interest statement

Conflict of interest: Authors state no conflict of interest.

Figures

Figure 1
Figure 1
Multi-directional differentiation potential of periodontal stem cells. (Description: This figure describes the multidirectional differentiation potential of PDLSCs. According to the sources of endoderm, mesoderm, and ectoderm, PDLSCs can differentiate into a variety of cells in the figure. We can use this feature to study its role in repairing bone and other tissue defects in the treatment of periodontitis.).
Figure 2
Figure 2
Mechanism of Wnt/β-catenin signaling pathway (Description: Wnt/β-catenin pathway is important for osteogenic differentiation of PDLSCs. In the presence of LPS, histone acetyltransferase GCN5 can inhibit this pathway through the acetylation regulation of DDK1. TAZ, which is necessary for LPS-induced osteogenesis, is a downstream component of this signal pathway. Interference with it by ShRNA or under the influence of phospholipase notum can inhibit Wnt/β-catenin pathway-mediated osteogenic differentiation of PDLSCs, and LiCl could reverse the effect of Notum).
Figure 3
Figure 3
Mechanism of Toll-like receptor TLR 4/nuclear factor NF-κB signaling pathway (Description: transmembrane receptor TLR4 can participate in the activation of signal pathways under inflammatory conditions. In LPS-mediated environment, TLR4 receptor activation decreased the expression of osteogenic markers, such as ALP, Runx, and OCN, activated NF-kB pathway, and downregulated the mRNA expression of osteogenic marker EphrinB2. All these make the osteogenic differentiation of PDLSCs inhibited. The activation of TLR1,4,6 can inhibit the activation of Akt and osteogenic differentiation of PDLSCs through Myd88- or TRIF-dependent signaling pathways. In addition, some studies have found that the inhibition of NF-kb pathway can be reversed by rutin, extracellular vesicles or astaxanthin).
See this image and copyright information in PMC

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