Benzo[a]pyrene/aryl hydrocarbon receptor signaling inhibits osteoblastic differentiation and collagen synthesis of human periodontal ligament cells

Monnouchi, Satoshi; Maeda, Hidefumi; Yuda, Atsushi; Serita, S.; Wada, Naohisa; Tomokiyo, Atsushi; Akamine, Akifumi

doi:10.1111/jre.12355

Cited by 24 publications

(10 citation statements)

References 51 publications

(62 reference statements)

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“…Similar results were found in human periodontal ligament cells. In this recent study, the addition of benzo[a]pyrene decreased the levels of mRNA expressed by osteogenic genes and also reduced alkaline phosphatase activity 99 . In the current literature, there is evidence demonstrating the inhibitory effects of aryl hydrocarbon receptor and RANKL signaling pathways on bone metabolism, more specifically, osteoclastogenesis 100,101 .…”

Section: Conditions and Behaviors That Stimulate Oxidative Stressmentioning

confidence: 79%

“…99 In the current literature, there is evidence demonstrating the inhibitory effects of aryl hydrocarbon receptor and RANKL signaling pathways on bone metabolism, more specifically, osteoclastogenesis. 100,101 It can be postulated that the destructive effects on the structure of tooth-supporting tissues are enhanced by long-term exposure to aryl hydrocarbons in a dose-dependent manner, and a representative group of experimental in vitro and in vivo studies have tested the ability of different aryl hydrocarbon receptor antagonists to counteract these deleterious effects, 93,[98][99][100][101] which will be discussed in more detail below. The data also suggest, quite strongly, that the deleterious effects of smoking on inflammatory disease, and in this case, periodontitis, are probably mediated, at least in part, by activation of the aryl hydrocarbon receptor, as will also be discussed below.…”

Section: Diabetesmentioning

confidence: 99%

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Periodontitis is an inflammatory disease of oxidative stress: We should treat it that way

Sczepanik

Grossi

Casati

et al. 2020

Periodontology 2000

341

244

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Periodontitis is a highly prevalent disease. As it progresses, it causes serious morbidity in the form of periodontal abscesses and tooth loss and, in the latter stages, pain. It is also now known that periodontitis is strongly associated with several nonoral diseases. Thus, patients with periodontitis are at greater risk for the development and/or exacerbation of diabetes, chronic obstructive pulmonary disease, and cardiovascular diseases, among other conditions. Although it is without question that specific groups of oral bacteria which populate dental plaque play a causative role in the development of periodontitis, it is now thought that once this disease has been triggered, other factors play an equal, and possibly more important, role in its progression, particularly in severe cases or in cases that prove difficult to treat. In this regard, we allude to the host response, specifically the notion that the host, once infected with oral periodontal pathogenic bacteria, will mount a defense response mediated largely through the innate immune system. The most abundant cell type of the innate immune system – polymorphonuclear neutrophils – can, when protecting the host from microbial invasion, mount a response that includes upregulation of proinflammatory cytokines, matrix metalloproteinases, and reactive oxygen species, all of which then contribute to the tissue damage and loss of teeth commonly associated with periodontitis. Of the mechanisms referred to here, we suggest that upregulation of reactive oxygen species might play one of the most important roles in the establishment and progression of periodontitis (as well as in other diseases of inflammation) through the development of oxidative stress. In this overview, we discuss both innate and epigenetic factors (eg, diabetes, smoking) that lead to the development of oxidative stress. This oxidative stress then provides an environment conducive to the destructive processes observed in periodontitis. Therefore, we shall describe some of the fundamental characteristics of oxidative stress and its effects on the periodontium, discuss the diseases and other factors that cause oxidative stress, and, finally, review potentially novel therapeutic approaches for the management (and possibly even the reversal) of periodontitis, which rely on the use of therapies, such as resveratrol and other antioxidants, that provide increased antioxidant activity in the host.

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Section: Conditions and Behaviors That Stimulate Oxidative Stressmentioning

confidence: 79%

Section: Diabetesmentioning

confidence: 99%

Periodontitis is an inflammatory disease of oxidative stress: We should treat it that way

Sczepanik

Grossi

Casati

et al. 2020

Periodontology 2000

341

244

View full text Add to dashboard Cite

show abstract

“…Correspondingly, the ALP staining was also suppressed by 0.1, 1 or 100 nM TCDD (Tong et al, ). In human PDLCs, another AhR ligand benzo[α]pyrene (BaP), a content of cigarettes, was studied (Monnouchi et al, ). In normal cell culture medium or osteogenic differentiation medium, PDLCs treated with 1 μM BaP for 7 days showed a significant reduced mRNA expression of ALP, BSP and ALP activity.…”

Section: Discussionmentioning

confidence: 99%

Protective roles of FICZ and aryl hydrocarbon receptor axis on alveolar bone loss and inflammation in experimental periodontitis

Huang

Cai

et al. 2019

J Clinic Periodontology

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Aim: The aryl hydrocarbon receptor (AhR)-ligand axis has been shown to be involved in inflammatory diseases and bone homeostasis. However, the activation of AhR signalling pathway and the possible functions of AhR ligands in periodontitis are underexplored. This study investigated the expression of the AhR target gene cytochrome P450 subfamily B member 1 (CYP1B1) and the functions and mechanisms of the AhR ligand 6 formylindolo[3,2-b]carbazole (FICZ) in periodontitis. Materials and Methods: CYP1B1 expression was detected in human periodontitis samples, mice with ligature-induced periodontitis and lipopolysaccharide (LPS)-induced inflammation in periodontal ligament cells (PDLCs) in vitro. FICZ was administered topically or systemically. The therapeutic functions of FICZ were detected via qPCR, micro-computed tomography and immunohistochemistry. Finally, the mechanisms of AhR signalling in periodontitis were investigated by cell assays. Results: CYP1B1 expression was downregulated in periodontitis. FICZ rescued the alveolar bone loss and mitigated the inflammatory cytokines in periodontitis mice. In vitro, FICZ pre-treatment reduced the LPS-induced inflammation in PDLCs via the increased phosphorylation of STAT3. Additionally, FICZ prompted the mineralization of PDLCs via activation of the Wnt/β-catenin signalling pathway. Conclusion: AhR signalling pathway is suppressed in periodontitis and the AhR ligand FICZ can prevent periodontitis. K E Y W O R D S AhR signalling, CYP1B1, FICZ, inflammation, periodontitis | 883 HUANG et Al.

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“…CSI not only increases risk for development of periodontitis but also enhances its severity and predisposes patients to respond poorly to treatment 2 , 6 . Pathways that link tobacco use and in particular various components of smoke, ranging from nicotine to products of combustion such as aryl hydrocarbons, and their potential effects on the periodontium have been investigated 7 . Overall, effects of smoking on periodontal breakdown could be attributed to different molecular mechanisms, including oxidative stress (production of reactive oxygen species [ROS]), dysfunction in microcirculation, and alterations in osteo‐immunoinflammatory systems 8 , 9 …”

mentioning

confidence: 99%

Resveratrol Inhibits Periodontitis‐Related Bone Loss in Rats Subjected to Cigarette Smoke Inhalation

Ribeiro

Pino

Franck

et al. 2017

Journal of Periodontology

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Benzo[a]pyrene/aryl hydrocarbon receptor signaling inhibits osteoblastic differentiation and collagen synthesis of human periodontal ligament cells

Cited by 24 publications

References 51 publications

Periodontitis is an inflammatory disease of oxidative stress: We should treat it that way

Periodontitis is an inflammatory disease of oxidative stress: We should treat it that way

Protective roles of FICZ and aryl hydrocarbon receptor axis on alveolar bone loss and inflammation in experimental periodontitis

Resveratrol Inhibits Periodontitis‐Related Bone Loss in Rats Subjected to Cigarette Smoke Inhalation

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