Periodontium regeneration and repair is a controversial and difficult point in the treatment of periodontosis. The proliferation, differentiation, migration and adhesion of periodontal ligament cells and the dynamic relationship between periodontal ligament cells and their extracellular matrix proteins are the basis of periodontium morphological reconstruction, functional maintenance and tissue repair. This article reviews the mechanism of estrogen-regulated periodontal membrane fine repair and periodontal tissue reconstruction to provide the basis for follow-up research on the treatment of periodontitis and the promotion of periodontal tissue repair and reconstruction by exogenous estrogen-mediated periodontal membranes. Under the regulation of certain concentrations of estrogen, the proliferation and differentiation ability of periodontal ligament stem cells (PDLSCs) and bone mesenchymal stem cells (BMSCs) to other periodontal ligament cells were enhanced. At the same time, PDLSCs, BMSCs, human periodontal ligament fibroblasts (HPLFSs), osteoblasts and cementoblasts synthesized and secreted collagen I (COLI), osteopontin (OPN), bone sialoprotein (BSP) and osteocalcin (OCN) into the extracellular matrix. They interact with fibronectin (FN) and cementum attachment protein (CAP) in the extracellular matrix to form a variety of chain complexes and regulate each other, thus promoting the growth, migration, adhesion and fibrosis of periodontal ligament cells, repairing the collagen fiber skeleton of the periodontal ligament and adhering the two ends to the new cementum and the inherent alveolar bone.
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Open Access
Review Article
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Open Access
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To investigate the effects of type Ⅱ a histone deacetylase inhibitor LMK-235 during early osteoblast/odontoblast differentiation in hPDLCs.
hPDLCs were obtained by the collagenase digestion method. hPDLCs at the 3rd passage were treated with medium containing 10% fetal bovine serum mixed with different concentrations of LMK-235 (0, 50, 100, 250, 500 nmol/L), respectively. Proliferative capability of hPDLCs was tested by MTT and qRT-PCR was used to detect mRNA expression levels of Runx2, ALP and DMP-1 3 d later.
MTT assay showed that cell proliferation in hPDLCs treated with 100 nmol/L LMK-235 was increased significantly compared with the control group (P<0.05). The expression of Runx2 mRNA in the 100 nmol/L group was 1.77 times of the control groups (P<0.05). The expressions of ALP mRNA in all the experimental groups were significantly higher than that in control groups (P<0.05), and the expression in the 100 nmol/L groups was the highest. The expressions of DMP-1 mRNA in the 50 and 100 nmol/L groups were higher than the control groups (P<0.05).
Type Ⅱ a histone deacetylase inhibitor LMK-235 could accelerate cell proliferation in hPDLCs at the concentration of 100 nmol/L, and regulate early osteoblast/odontoblast differentiation by upregulating the mRNA expressions of Runx2, ALP and DMP-1.
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