Elevated expression of genes assigned to NF-κB and apoptotic pathways in human periodontal ligament fibroblasts following mechanical stretch

2007 ◽  
Vol 328 (3) ◽  
pp. 537-548 ◽  
Author(s):  
Nina Ritter ◽  
Eva Mussig ◽  
Thorsten Steinberg ◽  
Annette Kohl ◽  
Gerda Komposch ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Mechanical Stretch ◽  
Periodontal Ligament Fibroblasts ◽  
Expression Of Genes ◽  
Elevated Expression ◽  
Human Periodontal Ligament Fibroblasts ◽  
Apoptotic Pathways

scholarly journals In Vitro Compression Model for Orthodontic Tooth Movement Modulates Human Periodontal Ligament Fibroblast Proliferation, Apoptosis and Cell Cycle

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 932
Author(s):  
Julia Brockhaus ◽  
Rogerio B. Craveiro ◽  
Irma Azraq ◽  
Christian Niederau ◽  
Sarah K. Schröder ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Periodontal Ligament ◽  
Environmental Changes ◽  
Tooth Movement ◽  
Orthodontic Tooth Movement ◽  
Compressive Force ◽  
Periodontal Ligament Fibroblasts ◽  
Human Periodontal Ligament Fibroblasts

Human Periodontal Ligament Fibroblasts (hPDLF), as part of the periodontal apparatus, modulate inflammation, regeneration and bone remodeling. Interferences are clinically manifested as attachment loss, tooth loosening and root resorption. During orthodontic tooth movement (OTM), remodeling and adaptation of the periodontium is required in order to enable tooth movement. hPDLF involvement in the early phase-OTM compression side was investigated for a 72-h period through a well-studied in vitro model. Changes in the morphology, cell proliferation and cell death were analyzed. Specific markers of the cell cycle were investigated by RT-qPCR and Western blot. The study showed that the morphology of hPDLF changes towards more unstructured, unsorted filaments under mechanical compression. The total cell numbers were significantly reduced with a higher cell death rate over the whole observation period. hPDLF started to recover to pretreatment conditions after 48 h. Furthermore, key molecules involved in the cell cycle were significantly reduced under compressive force at the gene expression and protein levels. These findings revealed important information for a better understanding of the preservation and remodeling processes within the periodontium through Periodontal Ligament Fibroblasts during orthodontic tooth movement. OTM initially decelerates the hPDLF cell cycle and proliferation. After adapting to environmental changes, human Periodontal Ligament Fibroblasts can regain homeostasis of the periodontium, affecting its reorganization.

scholarly journals Myeloid HIF1α Is Involved in the Extent of Orthodontically Induced Tooth Movement

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 796
Author(s):  
Christian Kirschneck ◽  
Nadine Straßmair ◽  
Fabian Cieplik ◽  
Eva Paddenberg ◽  
Jonathan Jantsch ◽  
...  
Keyword(s):  
Bone Density ◽  
Periodontal Ligament ◽  
Tooth Movement ◽  
Hypoxia Inducible Factor ◽  
Myeloid Cells ◽  
Orthodontic Tooth Movement ◽  
Periodontal Ligament Fibroblasts ◽  
Expression Of Genes ◽  
Periodontal Bone Loss

During orthodontic tooth movement, transcription factor hypoxia-inducible factor 1α (HIF1α) is stabilised in the periodontal ligament. While HIF1α in periodontal ligament fibroblasts can be stabilised by mechanical compression, in macrophages pressure application alone is not sufficient to stabilise HIF1α. The present study was conducted to investigate the role of myeloid HIF1α during orthodontic tooth movement. Orthodontic tooth movement was performed in wildtype and Hif1αΔmyel mice lacking HIF1α expression in myeloid cells. Subsequently, µCT images were obtained to determine periodontal bone loss, extent of orthodontic tooth movement and bone density. RNA was isolated from the periodontal ligament of the control side and the orthodontically treated side, and the expression of genes involved in bone remodelling was investigated. The extent of tooth movement was increased in Hif1αΔmyel mice. This may be due to the lower bone density of the Hif1αΔmyel mice. Deletion of myeloid Hif1α was associated with increased expression of Ctsk and Acp5, while both Rankl and its decoy receptor Opg were increased. HIF1α from myeloid cells thus appears to play a regulatory role in orthodontic tooth movement.

scholarly journals Elevated Expression of Cathepsin K in Periodontal Ligament Fibroblast by Inflammatory Cytokines Accelerates Osteoclastogenesis via Paracrine Mechanism in Periodontal Disease

2021 ◽  
Vol 22 (2) ◽  
pp. 695
Author(s):  
Soon Chul Heo ◽  
Yu Na Kim ◽  
YunJeong Choi ◽  
Ji-Young Joo ◽  
Jae Joon Hwang ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Inflammatory Cytokines ◽  
Periodontal Ligament ◽  
Cathepsin K ◽  
Periodontal Ligament Fibroblasts ◽  
Supporting Cells ◽  
Inflammatory Conditions ◽  
Elevated Expression ◽  
Macrophage Colony

Cathepsin K (CTSK) is a cysteine protease that is mainly produced from mature osteoclasts and contributes to the destruction of connective tissues and mineralized matrix as a consequence of periodontal disease (PD). However, few studies have reported its regulatory role in osteoclastogenesis-supporting cells in inflammatory conditions. Here, we investigated the role of CTSK in osteoclastogenesis-supporting cells, focusing on the modulation of paracrine function. Microarray data showed that CTSK was upregulated in PD patients compared with healthy individuals, which was further supported by immunohistochemistry and qPCR analyses performed with human gingival tissues. The expression of CTSK in the osteoclastogenesis-supporting cells, including dental pulp stem cells, gingival fibroblasts, and periodontal ligament fibroblasts (PDLFs) was significantly elevated by treatment with inflammatory cytokines such as TNFα and IL-1β. Moreover, TNFα stimulation potentiated the PDLF-mediated osteoclastogenesis of bone marrow-derived macrophages. Interestingly, small interfering RNA-mediated silencing of CTSK in PDLF noticeably attenuated the TNFα-triggered upregulation of receptor activator of nuclear factor kappa-B ligand (RANKL), macrophage colony-stimulating factor, and RANKL/osteoprotegerin ratio, thereby abrogating the enhanced osteoclastogenesis-supporting activity of PDLF. Collectively, these results suggest a novel role of CTSK in the paracrine function of osteoclastogenesis-supporting cells in periodontal disease.

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