Periodontal cell mechanotransduction

Chukkapalli, Sasanka S.; Lele, Tanmay P.

doi:10.1098/rsob.180053

Cited by 38 publications

(37 citation statements)

References 133 publications

(174 reference statements)

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“…Our data suggest that palmitate treatment rather induce cellular senescence and cell death as cause for the diminished secretion of osteoclastogenesis-modulating factors. In particular, cells that are compromised in their survival due to external cues may not be able to properly perform their regulatory functions due to changes in their metabolism as well as their morphology and cellular contacts [70][71][72] . However, these results seems to be in contradiction with studies showing that palmitic acid enhances osteoclastic differentiation and activity 30 .…”

Section: Discussionmentioning

confidence: 99%

Distinguish fatty acids impact survival, differentiation and cellular function of periodontal ligament fibroblasts

Symmank

Chorus

Appel

et al. 2020

Sci Rep

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Alveolar bone (AB) remodeling is necessary for the adaption to mechanical stimuli occurring during mastication and orthodontic tooth movement (OTM). Thereby, bone degradation and assembly are strongly regulated processes that can be altered in obese patients. Further, increased fatty acids (FA) serum levels affect bone remodeling cells and we, therefore, investigated whether they also influence the function of periodontal ligament fibroblast (PdLF). PdLF are a major cell type regulating the differentiation and function of osteoblasts and osteoclasts localized in the AB. We stimulated human PdLF (HPdLF) in vitro with palmitic (PA) or oleic acid (OA) and analyzed their metabolic activity, growth, survival and expression of osteogenic markers and calcium deposits. Our results emphasize that PA increased cell death of HPdLF, whereas OA induced their osteoblastic differentiation. Moreover, quantitative expression analysis of OPG and RANKL revealed altered levels in mechanically stimulated PA-treated HPdLF. Furthermore, osteoclasts stimulated with culture medium of mechanical stressed FA-treated HPdLF revealed significant changes in cell differentiation upon FA-treatment. For the first time, our results highlight a potential role of specific FA in the function of HPdLF-modulated AB remodeling and help to elucidate the complex interplay of bone metabolism, mechanical stimulation and obesity-induced alterations.

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Section: Discussionmentioning

confidence: 99%

Distinguish fatty acids impact survival, differentiation and cellular function of periodontal ligament fibroblasts

Symmank

Chorus

Appel

et al. 2020

Sci Rep

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“…Rapid alveolar bone loss is generally associated with cases of combined inflammation and occlusal trauma. While the effects of mechanical forces against fibroblasts such as periodontal ligament cells 46 have been reported, there still remain unknown details about the relationships between DAMPs and occlusal forces against periodontal tissue.…”

Section: Discussionmentioning

confidence: 99%

RNA sequencing for ligature induced periodontitis in mice revealed important role of S100A8 and S100A9 for periodontal destruction

Maekawa

Onizuka

Katagiri

et al. 2019

Sci Rep

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Periodontitis is an inflammatory disease caused by pathogenic oral microorganisms that induce the destruction of periodontal tissue. We sought to identify the relevant differentially expressed genes (DEGs) and clarify the mechanism underlying the rapid alveolar bone loss by using ligature-induced periodontitis in mice. A silk ligature was tied around the maxillary left second molar in 9-week-old C57BL/6 J male mice. In-vivo micro-CT analysis revealed that ligation induced severe bone loss. RNA-sequencing analysis, to examine host responses at 3 days post-ligation, detected 12,853 genes with fragments per kilobase of exon per million mapped reads ≥ 1, and 78 DEGs. Gene ontology term enrichment analysis revealed the expression profiles related to neutrophil chemotaxis and inflammatory responses were significantly enriched in the ligated gingiva. The expression levels of innate immune response-related genes, including S100a8 and S100a9, were significantly higher in the ligated side. S100A8 was strongly detected by immunohistochemistry at the attached epithelium in ligated sites. Inhibition of S100A8 and S100A9 expression revealed that they regulated IL1B and CTSK expression in Ca9-22 cells. Thus, innate immune response-related molecules might be associated with the burst-destruction of periodontal tissue in ligature-induced periodontitis. Especially, S100A8 and S100A9 may play an important role in alveolar bone resorption.

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“…Cytopathic mechanisms in mechanotransduction are facilitated by cytoskeletal interaction with the ECM ( Humphrey et al., 2014 ) and include ECM degradation and remodeling ( Tsuji et al., 2004 ; Manokawinchoke et al., 2015 ), altered cellular differentiation ( Kanzaki et al., 2002 ), altered cellular migration, and altered cellular adhesion or de-adhesion processes ( Kang et al., 2010 ; Wang et al., 2019 ). A failure of mechanotransduction and actin organization within the periodontium results in loss of regeneration of periodontal tissues, remodeling of the ECM, and progression of disease; processes highly regulated within the PDL ( Chukkapalli and Lele, 2018 ). The disease process is initiated by pathogenic microbes under conditions of microbial dysbiosis.…”

Section: Introductionmentioning

confidence: 99%

Treponema denticola-Induced RASA4 Upregulation Mediates Cytoskeletal Dysfunction and MMP-2 Activity in Periodontal Fibroblasts

Malone

Ganther

Mena

et al. 2021

Front. Cell. Infect. Microbiol.

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The periodontal complex consists of the periodontal ligament (PDL), alveolar bone, and cementum, which work together to turn mechanical load into biological responses that are responsible for maintaining a homeostatic environment. However oral microbes, under conditions of dysbiosis, may challenge the actin dynamic properties of the PDL in the context of periodontal disease. To study this process, we examined host-microbial interactions in the context of the periodontium via molecular and functional cell assays and showed that human PDL cell interactions with Treponema denticola induce actin depolymerization through a novel actin reorganization signaling mechanism. This actin reorganization mechanism and loss of cell adhesion is a pathological response characterized by an initial upregulation of RASA4 mRNA expression resulting in an increase in matrix metalloproteinase-2 activity. This mechanism is specific to the T. denticola effector protein, dentilisin, thereby uncovering a novel effect for Treponema denticola-mediated RASA4 transcriptional activation and actin depolymerization in primary human PDL cells.

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Periodontal cell mechanotransduction

Cited by 38 publications

References 133 publications

Distinguish fatty acids impact survival, differentiation and cellular function of periodontal ligament fibroblasts

Distinguish fatty acids impact survival, differentiation and cellular function of periodontal ligament fibroblasts

RNA sequencing for ligature induced periodontitis in mice revealed important role of S100A8 and S100A9 for periodontal destruction

Treponema denticola-Induced RASA4 Upregulation Mediates Cytoskeletal Dysfunction and MMP-2 Activity in Periodontal Fibroblasts

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