Abstract
Parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP) are two peptides that regulate mineral ion homeostasis, skeletal development, and bone turnover by activating parathyroid hormone 1 receptor (PTH1R). PTH1R signaling is of profound clinical interest for its potential to stimulate bone formation and regeneration. Recent pre-clinical animal studies and clinical trials have investigated the effects of PTH and PTHrP analogs in the orofacial region. Dental mesenchymal stem cells (MSCs) are targets of PTH1R signaling and have long been known as major factors in tissue repair and regeneration. Previous studies have begun to reveal important roles for PTH1R signaling in modulating the proliferation and differentiation of MSCs in the orofacial region. A better understanding of the molecular networks and underlying mechanisms for modulating MSCs in dental diseases will pave the way for the therapeutic applications of PTH and PTHrP in the future. Here we review recent studies involving dental MSCs, focusing on relationships with PTH1R. We also summarize recent basic and clinical observations of PTH and PTHrP treatment to help understand their use in MSCs-based dental and bone regeneration.
Highlights
Parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP) are two peptides that regulate mineral ion homeostasis, skeletal development, and bone turnover by activating parathyroid hormone 1 receptor (PTH1R)
There are a variety of stem cell populations that can be identified in teeth and their supporting structures, including dental pulp stem cells (DPSCs), stem cells from human exfoliated deciduous teeth (SHEDs), periodontal ligament stem cells (PDLSCs), dental follicle progenitor cells (DFPCs), stem cells from apical papilla (SCAPs), orofacial bone/bone-marrow-derived mesenchymal stem cells (MSCs) (OMSCs), tooth germ progenitor cells (TGPCs), and gingival MSCs (GMSCs) (Zheng et al, 2019)
It is important to note that p-extracellular signal-regulated kinase (ERK) was increased in PTH-treated DPSCs in conjunction with osteo-differentiation enhancement, suggesting that the nature of the crosstalk between PTH1R signaling and Jun N-terminal kinase (JNK), P38 mitogen-activated protein kinase (MAPK) pathways could be different in specific stem cell lineages (Ge et al, 2020)
Summary
PTH is an 84 amino-acid (AA) endocrine hormone secreted by the parathyroid glands and serves as the mediator of extracellular calcium and phosphate levels and skeletal homeostasis (Wein and Kronenberg, 2018). IPTH treatment shifted the differentiation of LepR-positive progenitor cells from an adipo-lineage toward an osteo-lineage, accompanied by higher expression of osteogenic markers and reduced adipocyte markers (Yang M. et al, 2019) These data emphasize the central role of PTH1R signaling in guiding BMMSCs toward an osteoblast lineage and away from adipogenesis. There are a variety of stem cell populations that can be identified in teeth and their supporting structures, including dental pulp stem cells (DPSCs), stem cells from human exfoliated deciduous teeth (SHEDs), periodontal ligament stem cells (PDLSCs), dental follicle progenitor cells (DFPCs), stem cells from apical papilla (SCAPs), orofacial bone/bone-marrow-derived MSCs (OMSCs), tooth germ progenitor cells (TGPCs), and gingival MSCs (GMSCs) (Zheng et al, 2019) These stem cells express distinct surface markers and have multi-lineage differentiation capacities with region-specific characteristics.
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