Damage-regulated autophagy modulator 1 in oral inflammation and infection

Memmert, Svenja; Nogueira, Andressa Vilas Boas; Damanaki, Anna; Nokhbehsaim, Marjan; Eick, Sigrun; Divnic‐Resnik, Tihana; Spahr, Axel; Rath-Deschner, Birgit; Till, Andreas; Götz, Werner; Cirelli, Joni Augusto; Jäger, Andreas; Deschner, James

doi:10.1007/s00784-018-2381-6

Cited by 20 publications

(20 citation statements)

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“…And in vivo, DRAM1 expression was also significantly enhanced in rat and human gingival tissues with periodontitis, compared to that in healthy gingiva (Memmert et al, 2018).…”

Section: Autophagy and Periodontal Infl Ammationmentioning

confidence: 91%

“…DRAM1 is a lysosomal membrane protein regulated as part of the p53 signal transduction pathway and promotes the induction of autophagy in a p53‐dependent manner (Crighton et al, ; Crighton, Wilkinson, & Ryan, ). The expression of DRAM1 was up‐regulated under inflammatory conditions in human periodontal ligament fibroblasts stimulated by IL‐1β in vitro (Memmert et al, ). And in vivo, DRAM1 expression was also significantly enhanced in rat and human gingival tissues with periodontitis, compared to that in healthy gingiva (Memmert et al, ).…”

Section: Autophagy and Periodontal Inflammationmentioning

confidence: 99%

“…The expression of DRAM1 was up‐regulated under inflammatory conditions in human periodontal ligament fibroblasts stimulated by IL‐1β in vitro (Memmert et al, ). And in vivo, DRAM1 expression was also significantly enhanced in rat and human gingival tissues with periodontitis, compared to that in healthy gingiva (Memmert et al, ).…”

Section: Autophagy and Periodontal Inflammationmentioning

confidence: 99%

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The role of autophagy in the pathogenesis of periodontal disease

Jiang

Zhu

2019

Oral Diseases

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Periodontal disease is a chronic inflammatory disease leading to destruction of periodontal tissues. As a local inflammation, periodontopathic bacterium, pro‐inflammatory mediators, and local immune response play pivotal role in the progress of periodontal disease. Besides, cigarette smoke has long been associated with periodontal disease and tooth loss. Autophagy is an intracellular degradation process highly conserved from yeast to humans. As a lysosomal degradation pathway of self‐digestion, it is critical for maintaining cells homeostasis and development. The role of autophagy has been investigated in oral diseases, such as oral cancer, periapical lesions, and oral candidiasis. Recently, increasing studies investigated the role of autophagy in periodontal disease. In this review, we try to illustrate the effect of autophagy on periodontal disease pathogenesis from 5 aspects: autophagy affects the intracellular infection and survival of bacteria; autophagy has an interaction with periodontal inflammation; autophagy is pivotal in periodontal cells biology and periodontal tissues destruction and reconstruction; autophagy can be induced by cigarette smoke; last but not least, autophagy may affect periodontal disease via endoplasmic reticulum stress.

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“…And in vivo, DRAM1 expression was also significantly enhanced in rat and human gingival tissues with periodontitis, compared to that in healthy gingiva (Memmert et al, 2018).…”

Section: Autophagy and Periodontal Infl Ammationmentioning

confidence: 91%

Section: Autophagy and Periodontal Inflammationmentioning

confidence: 99%

Section: Autophagy and Periodontal Inflammationmentioning

confidence: 99%

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The role of autophagy in the pathogenesis of periodontal disease

Jiang

Zhu

2019

Oral Diseases

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“…Gingival biopsies of 7 periodontally healthy donors (mean age: 22.1 years, min–max: 18–26 years; gender: 2 male/5 female) and 7 periodontally-diseased patients (mean age: 58.4 years, min–max: 29–81 years; gender: 5 male/2 female) were used for our experiments. These biopsies were obtained during wisdom tooth extraction and extractions for orthodontic or periodontal reasons in the Department of Oral Surgery of the University of Bonn [44]. Written and informed consent by the subjects and approval by the Ethics Committee of the University of Bonn (#043/11) were provided.…”

Section: Materials Und Methodsmentioning

confidence: 99%

“…No clinical inflammation (GI = 0), a PD below 3 mm and neither clinical nor radiographic bone loss were categorized as periodontally healthy. Periodontitis patients were identified by sites with a GI > 1 and PD ≥ 5 mm and clinical as well as radiographic bone loss ≥3 mm, as previously described [21, 44, 45]. Smokers as well as patients taking any medication were excluded from the study.…”

Section: Materials Und Methodsmentioning

confidence: 99%

Regulation of somatostatin receptor 2 by proinflammatory, microbial and obesity-related signals in periodontal cells and tissues

et al. 2019

Self Cite

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BackgroundPeriodontitis is a chronic disease characterized by a progressive and irreversible destruction of the tooth-supporting tissues, including gingiva and periodontal ligament (PDL). Microorganisms, such as Fusobacterium nucleatum, evoke an inflammatory host response, which leads to increased levels of inflammatory mediators, such as interleukin (IL)-1β. Periodontitis has been linked to obesity, and adipokines have been suggested to represent a pathomechanistic link. The hormone somatostatin (SST) exerts antiproliferative, antiangiogenetic, proapoptotic, anti-nociceptive and other effects through binding to its receptors, such as SSTR2. Therefore, the objective of the present study was to examine the regulation of SSTR2 in periodontal cells and tissues under inflammatory, microbial and obesity-related conditions.MethodsIn-vitro, human PDL fibroblasts were exposed to IL-1β, F. nucleatum, leptin or visfatin. The SSTR2 regulation was assessed by real-time PCR and immunocytochemistry. In-vivo, the SSTR2 expression was analyzed in gingival biopsies of periodontally diseased and healthy subjects by real-time PCR and immunohistochemistry. Additionally, the SSTR2 expression was determined in gingival biopsies of rats with ligature-induced periodontitis, rats with diet-induced obesity, and periodontally and systemically healthy control animals. For statistical analyses, the Mann-Whitney-U test and ANOVA with post-hoc tests were applied (p < 0.05).ResultsExposure of PDL cells to IL-1β and F. nucleatum caused a significant SSTR2 upregulation by 2.6-fold and 6.4-fold, respectively. Additionally, leptin and visfatin increased significantly the SSTR2 gene expression by 3.0-fold and 2.8-fold, respectively. These stimulatory effects were also observed at protein level. SSTR2 expressions in human gingival biopsies from sites of periodontitis were significantly higher than those in healthy biopsies. Similarly, SSTR2 expression levels were significantly enhanced at periodontally-diseased sites in rat experimental periodontitis. Finally, the SSTR2 expression was significantly upregulated in gingival biopsies of obese rats as compared to normal weight control animals.ConclusionsOur study provides original insights into the SSTR2 regulation in cells and tissues of the periodontium. We demonstrate for the first time that proinflammatory, microbial and obesity-associated molecules result in an SSTR2 upregulation. Since SST has been shown to be antiproliferative, antiangiogenetic, and proapoptotic, our study suggests that SSTR2 might play a critical role in the aetiopathogenesis of periodontitis.

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Current Trends in In Vitro Modeling to Mimic Cellular Crosstalk in Periodontal Tissue

Aveic

Craveiro

Wolf

et al. 2020

Adv Healthcare Materials

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Clinical evidence indicates that in physiological and therapeutic conditions a continuous remodeling of the tooth root cementum and the periodontal apparatus is required to maintain tissue strength, to prevent damage, and to secure teeth anchorage. Within the tooth's surrounding tissues, tooth root cementum and the periodontal ligament are the key regulators of a functional tissue homeostasis. While the root cementum anchors the periodontal fibers to the tooth root, the periodontal ligament itself is the key regulator of tissue resorption, the remodeling process, and mechanical signal transduction. Thus, a balanced crosstalk of both tissues is mandatory for maintaining the homeostasis of this complex system. However, the mechanobiological mechanisms that shape the remodeling process and the interaction between the tissues are largely unknown. In recent years, numerous 2D and 3D in vitro models have sought to mimic the physiological and pathophysiological conditions of periodontal tissue. They have been proposed to unravel the underlying nature of the cell–cell and the cell–extracellular matrix interactions. The present review provides an overview of recent in vitro models and relevant biomaterials used to enhance the understanding of periodontal crosstalk and aims to provide a scientific basis for advanced regenerative strategies.

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Damage-regulated autophagy modulator 1 in oral inflammation and infection

Abstract: DRAM1 might be a promising target in future diagnostic and treatment strategies for periodontitis.

Cited by 20 publications

References 49 publications

The role of autophagy in the pathogenesis of periodontal disease

The role of autophagy in the pathogenesis of periodontal disease

Regulation of somatostatin receptor 2 by proinflammatory, microbial and obesity-related signals in periodontal cells and tissues

Current Trends in In Vitro Modeling to Mimic Cellular Crosstalk in Periodontal Tissue

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