Periodontal tissue stem cells and mesenchymal stem cells in the periodontal ligament

Iwayama, Tomoaki; Sakashita, Hiromi; Takedachi, Masahide; Murakami, Shinya

doi:10.1016/j.jdsr.2022.04.001

Cited by 19 publications

(16 citation statements)

References 88 publications

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“…PDL fibroblasts are mesenchymal cells with multifunctional properties that participate in various cellular activities and respond to inflammatory stimuli ( 16 , 17 ). PDL cells exhibit similarities to tendon cells and immature mesenchymal cells with some osteoblastic characteristics as demonstrated by 2.5kb collagen-1α1 promoter reporter activity in vivo .…”

Section: Osteoblasts Osteocytes Periodontal Ligament and Osteoclast C...mentioning

confidence: 99%

Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

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Periodontitis involves the loss of connective tissue attachment and alveolar bone. Single cell RNA-seq experiments have provided new insight into how resident cells and infiltrating immune cells function in response to bacterial challenge in periodontal tissues. Periodontal disease is induced by a combined innate and adaptive immune response to bacterial dysbiosis that is initiated by resident cells including epithelial cells and fibroblasts, which recruit immune cells. Chemokines and cytokines stimulate recruitment of osteoclast precursors and osteoclastogenesis in response to TNF, IL-1β, IL-6, IL-17, RANKL and other factors. Inflammation also suppresses coupled bone formation to limit repair of osteolytic lesions. Bone lining cells, osteocytes and periodontal ligament cells play a key role in both processes. The periodontal ligament contains cells that exhibit similarities to tendon cells, osteoblast-lineage cells and mesenchymal stem cells. Bone lining cells consisting of mesenchymal stem cells, osteoprogenitors and osteoblasts are influenced by osteocytes and stimulate formation of osteoclast precursors through MCSF and RANKL, which directly induce osteoclastogenesis. Following bone resorption, factors are released from resorbed bone matrix and by osteoclasts and osteal macrophages that recruit osteoblast precursors to the resorbed bone surface. Osteoblast differentiation and coupled bone formation are regulated by multiple signaling pathways including Wnt, Notch, FGF, IGF-1, BMP, and Hedgehog pathways. Diabetes, cigarette smoking and aging enhance the pathologic processes to increase bone resorption and inhibit coupled bone formation to accelerate bone loss. Other bone pathologies such as rheumatoid arthritis, post-menopausal osteoporosis and bone unloading/disuse also affect osteoblast lineage cells and participate in formation of osteolytic lesions by promoting bone resorption and inhibiting coupled bone formation. Thus, periodontitis involves the activation of an inflammatory response that involves a large number of cells to stimulate bone resorption and limit osseous repair processes.

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Section: Osteoblasts Osteocytes Periodontal Ligament and Osteoclast C...mentioning

confidence: 99%

Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

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“…Recent studies indicate that PDLSCs play a crucial role in the maintenance of periodontal homeostasis. 31 The normal periodontal milieu is in a dynamic equilibrium of cell proliferation and apoptosis, 32 and the invasion of periodontal pathogens could impair the self-renewal function of PDLSCs. 33 In our study, we demonstrated that F. nucleatum inhibited cell proliferation and promoted apoptosis in PDLSCs and first showed that F. nucleatum could induce ferroptosis by intervening in iron metabolism in PDLSCs.…”

Section: Discussionmentioning

confidence: 99%

Study of the inflammatory activating process in the early stage of Fusobacterium nucleatum infected PDLSCs

Wang

Sun

et al. 2023

Int J Oral Sci

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Fusobacterium nucleatum (F. nucleatum) is an early pathogenic colonizer in periodontitis, but the host response to infection with this pathogen remains unclear. In this study, we built an F. nucleatum infectious model with human periodontal ligament stem cells (PDLSCs) and showed that F. nucleatum could inhibit proliferation, and facilitate apoptosis, ferroptosis, and inflammatory cytokine production in a dose-dependent manner. The F. nucleatum adhesin FadA acted as a proinflammatory virulence factor and increased the expression of interleukin(IL)-1β, IL-6 and IL-8. Further study showed that FadA could bind with PEBP1 to activate the Raf1-MAPK and IKK-NF-κB signaling pathways. Time-course RNA-sequencing analyses showed the cascade of gene activation process in PDLSCs with increasing durations of F. nucleatum infection. NFκB1 and NFκB2 upregulated after 3 h of F. nucleatum-infection, and the inflammatory-related genes in the NF-κB signaling pathway were serially elevated with time. Using computational drug repositioning analysis, we predicted and validated that two potential drugs (piperlongumine and fisetin) could attenuate the negative effects of F. nucleatum-infection. Collectively, this study unveils the potential pathogenic mechanisms of F. nucleatum and the host inflammatory response at the early stage of F. nucleatum infection.

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“…Recent studies indicate that PDLSCs play a crucial role in the maintenance of periodontal homeostasis 31 .Normal periodontal milieu is in dynamic equilibrium of cell proliferation and apoptosis 32 , and the invasion of periodontal pathogens could impair the self-renewal function of PDLSCs 33 . In our study, we demonstrated that F. nucleatum inhibited the cell proliferation and promoted the apoptosis of PDLSCs, and rstly found that F. nucleatum could induce ferroptosis through intervening iron metabolism in PDLSCs.…”

Section: Discussionmentioning

confidence: 99%

Study of the inflammatory activating process in the early stage of Fusobacterium nucleatum infected PDLSCs

Feng

Wang

et al. 2022

Preprint

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Fusobacterium nucleatum (F. nucleatum) is the early pathogenic colonizer of periodontitis, while the host response to this pathogen infection remains unclear yet. In this study, we built the F. nucleatum infectious model with human periodontal ligament stem cells (PDLSCs) and showed that F. nucleatum could inhibit proliferation, facilitates apoptosis, ferroptosis, and inflammatory cytokines production in a dose-dependent manner. F. nucleatum adhesin FadA acted as a proinflammatory virulence factor and increased the expression of IL-1β, IL-6 and IL-8. Further study showed FadA could bind with PEBP1 to active Raf1-MAPK and IKK-NF-κB signaling pathways. Time-course RNA-sequencing analyses showed the cascade of gene activation process of PDLSCs with the increasing duration of F. nucleatum infection. NFκB1 and NFκB2 were up-regulated since 3 h of F. nucleatum-infection and time serially elevated the inflammatory related genes on the NF-κB signaling pathway. Using computational drug repositioning analysis, we predicted and validated that two potential drugs (piperlongumine and fisetin) could attenuate the negative effects of F. nucleatum-infection. Collectively, this study unveils the potential pathogenic mechanisms of F. nucleatum and the host inflammatory response at the early stage of F. nucleatum-infection.

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Periodontal tissue stem cells and mesenchymal stem cells in the periodontal ligament

Cited by 19 publications

References 88 publications

Impact of the host response and osteoblast lineage cells on periodontal disease

Impact of the host response and osteoblast lineage cells on periodontal disease

Study of the inflammatory activating process in the early stage of Fusobacterium nucleatum infected PDLSCs

Study of the inflammatory activating process in the early stage of Fusobacterium nucleatum infected PDLSCs

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