CXCL1, CCL2, and CCL5 modulation by microbial and biomechanical signals in periodontal cells and tissues—in vitro and in vivo studies

Rath-Deschner, Birgit; Memmert, Svenja; Damanaki, Anna; Nokhbehsaim, Marjan; Eick, Sigrun; Cirelli, Joni Augusto; Götz, Werner; Deschner, James; Jäger, Andreas; Nogueira, Andressa Vilas Boas

doi:10.1007/s00784-020-03244-1

Cited by 24 publications

(27 citation statements)

References 41 publications

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“…Fibroblasts were treated with F. nucleatum ATCC 25586 (OD 660 : 0.05) for 1 d. The microorganisms had been suspended in phosphate-buffered saline (OD 660 = 1.0, equivalent to 1.2 × 10 9 bacterial cells/mL) and subjected twice to ultra-sonication (160 W for 15 min) before the experiments. Fibroblasts were also subjected to constant tensile strain (CTS) with a cell strain device for 1 d, as in our previous studies ( Figure 7 a,b) [ 60 , 61 , 62 ]. In addition, fibroblasts were exposed simultaneously to F. nucleatum and CTS.…”

Section: Methodsmentioning

confidence: 99%

“…Approval of the Ethics Committee of the University of Bonn and written informed consent from the patients or their parents were obtained (#043/11). Gingival tissues were either stored immediately in RNA stabilization reagent (RNAlater) (Qiagen, Hilden, Germany) and kept in the −80 °C freezer until use or fixed in formaldehyde for histological examination [ 60 , 61 , 63 ].…”

Section: Methodsmentioning

confidence: 99%

“…In order to study the regulation of microbial actions by orthodontic forces in vivo, an animal model was applied [ 60 , 63 ]. The in-vivo experiments were carried out according to the ARRIVE (Animal Research: Reporting of In-Vivo Experiments) guidelines.…”

Section: Methodsmentioning

confidence: 99%

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Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues

Rath-Deschner

Nogueira

Memmert

et al. 2021

IJMS

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The aim of the study was to clarify whether orthodontic forces and periodontitis interact with respect to the anti-apoptotic molecules superoxide dismutase 2 (SOD2) and baculoviral IAP repeat-containing protein 3 (BIRC3). SOD2, BIRC3, and the apoptotic markers caspases 3 (CASP3) and 9 (CASP9) were analyzed in gingiva from periodontally healthy and periodontitis subjects by real-time PCR and immunohistochemistry. SOD2 and BIRC3 were also studied in gingiva from rats with experimental periodontitis and/or orthodontic tooth movement. Additionally, SOD2 and BIRC3 levels were examined in human periodontal fibroblasts incubated with Fusobacterium nucleatum and/or subjected to mechanical forces. Gingiva from periodontitis patients showed significantly higher SOD2, BIRC3, CASP3, and CASP9 levels than periodontally healthy gingiva. SOD2 and BIRC3 expressions were also significantly increased in the gingiva from rats with experimental periodontitis, but the upregulation of both molecules was significantly diminished in the concomitant presence of orthodontic tooth movement. In vitro, SOD2 and BIRC3 levels were significantly increased by F. nucleatum, but this stimulatory effect was also significantly inhibited by mechanical forces. Our study suggests that SOD2 and BIRC3 are produced in periodontal infection as a protective mechanism against exaggerated apoptosis. In the concomitant presence of orthodontic forces, this protective anti-apoptotic mechanism may get lost.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues

Rath-Deschner

Nogueira

Memmert

et al. 2021

IJMS

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“…F. nucleatum plays a significant etiopathogenetic role in gingivitis and periodontitis [12][13][14][15][16]. Previous studies by our research group have shown that mechanical/orthodontic forces can regulate the bacteria-induced levels of some proinflammatory and anti-apoptotic molecules [17][18][19]. The synthesis of some of these molecules during periodontal inflammation is further enhanced by mechanical/orthodontic forces, whereas other molecules tend to be downregulated [17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Interaction of periodontitis and orthodontic tooth movement—an in vitro and in vivo study

et al. 2021

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Objectives The aim of this in vitro and in vivo study was to investigate the interaction of periodontitis and orthodontic tooth movement on interleukin (IL)-6 and C-X-C motif chemokine 2 (CXCL2). Materials and methods The effect of periodontitis and/or orthodontic tooth movement (OTM) on alveolar bone and gingival IL-6 and CXCL2 expressions was studied in rats by histology and RT-PCR, respectively. The animals were assigned to four groups (control, periodontitis, OTM, and combination of periodontitis and OTM). The IL-6 and CXCL2 levels were also studied in human gingival biopsies from periodontally healthy and periodontitis subjects by RT-PCR and immunohistochemistry. Additionally, the synthesis of IL-6 and CXCL2 in response to the periodontopathogen Fusobacterium nucleatum and/or mechanical strain was studied in periodontal fibroblasts by RT-PCR and ELISA. Results Periodontitis caused an increase in gingival levels of IL-6 and CXCL2 in the animal model. Moreover, orthodontic tooth movement further enhanced the bacteria-induced periodontal destruction and gingival IL-6 gene expression. Elevated IL-6 and CXCL2 gingival levels were also found in human periodontitis. Furthermore, mechanical strain increased the stimulatory effect of F. nucleatum on IL-6 protein in vitro. Conclusions Our study suggests that orthodontic tooth movement can enhance bacteria-induced periodontal inflammation and thus destruction and that IL-6 may play a pivotal role in this process. Clinical relevance Orthodontic tooth movement should only be performed after periodontal therapy. In case of periodontitis relapse, orthodontic therapy should be suspended until the periodontal inflammation has been successfully treated and thus the periodontal disease is controlled again.

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“…In conclusion, using cytokine antagonists to treat PD in this scope needs to be further examined properly to obtain conclusive and effective treatment modalities. Recently, Rath-Deschner et al reported higher levels of CXCL 1 (motif chemokine ligand 1), CCL 2 (motif chemokine ligand 2), and CCL 5 (motif chemokine ligand 5) chemokines in vitro and in vivo in human and rat gingiva in sites with periodontitis [38]. CXCL 1 , also known as GRO-alpha, is a potent chemoattractant for neutrophils [39], whereas CCL 2 and CCL 5, also known as MCP-1 and RANTES, are primarily responsible for the recruitment of monocytes, macrophages and T-lymphocytes [38].…”

Section: Cytokines Proteases and Prostaglandinsmentioning

confidence: 99%

An Evidence-Based Update on the Molecular Mechanisms Underlying Periodontal Diseases

Qasim

Alotaibi

Jasser

et al. 2020

IJMS

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Several investigators have reported about the intricate molecular mechanism underlying periodontal diseases (PD). Nevertheless, the role of specific genes, cells, or cellular mechanisms involved in the pathogenesis of periodontitis are still unclear. Although periodontitis is one of the most prevalent oral diseases globally, there are no pre-diagnostic markers or therapeutic targets available for such inflammatory lesions. A pivotal role is played by pro- and anti-inflammatory markers in modulating pathophysiological and physiological processes in repairing damaged tissues. In addition, effects on osteoimmunology is ever evolving due to the ongoing research in understanding the molecular mechanism lying beneath periodontal diseases. The aim of the current review is to deliver an evidence-based update on the molecular mechanism of periodontitis with a particular focus on recent developments. Reports regarding the molecular mechanism of these diseases have revealed unforeseen results indicative of the fact that significant advances have been made to the periodontal medicine over the past decade. There is integrated hypothesis-driven research going on. Although a wide picture of association of periodontal diseases with immune response has been further clarified with present ongoing research, small parts of the puzzle remain a mystery and require further investigations.

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CXCL1, CCL2, and CCL5 modulation by microbial and biomechanical signals in periodontal cells and tissues—in vitro and in vivo studies

Cited by 24 publications

References 41 publications

Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues

Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues

Interaction of periodontitis and orthodontic tooth movement—an in vitro and in vivo study

An Evidence-Based Update on the Molecular Mechanisms Underlying Periodontal Diseases

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