Resveratrol prevents alveolar bone loss in an experimental rat model of periodontitis

Bhattarai, Govinda; Poudel, Sher Bahadur; Kook, Sung‐Ho; Lee, Jeong-Chae

doi:10.1016/j.actbio.2015.10.031

Cited by 187 publications

(183 citation statements)

References 46 publications

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“…Resveratrol mediated inhibition of CSI‐induced increases in bone loss seen in EP agree with previous studies done by our research group and others . Reduced periodontal damage related to use of resveratrol is high if not solely related to its effects on levels of IL‐17, IFN‐γ, IL‐4, and TH17/TH2 response .…”

Section: Discussionsupporting

confidence: 91%

Resveratrol attenuates oxidative stress during experimental periodontitis in rats exposed to cigarette smoke inhalation

Corrêa¹,

Absy²,

Tenenbaum

et al. 2018

J of Periodontal Research

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Objectives This study aimed at investigating the effect of the systemic administration of resveratrol (RESV) on oxidative stress during experimental periodontitis in rats subjected to cigarette smoke inhalation. Material and Methods Experimental periodontitis (EP) was induced in 26 male Wistar rats by the insertion of a ligature around one of the first mandibular and maxillary molars. The animals were assigned randomly to the following groups: cigarette smoke inhalation (CSI; 3 times/d, 8 minutes/d) + resveratrol (10 mg/Kg), that is, SMK + RESV (n = 13) and cigarette smoke inhalation + placebo, that is, SMK + PLAC (n = 13). The substances were administered daily for 30 days (19 days prior and 11 days following EP induction), and then, the animals were euthanized. The maxillary specimens were processed for morphometric analysis of bone loss, and the tissue surrounding the first maxillary molars was collected for mRNA quantification of Sirtuin 1 (SIRT1) by real‐time PCR. The gingival tissues surrounding the mandibular first molars were collected for quantification of superoxide dismutase 1 (SOD1) and nicotinamide adenine dinucleotide phosphatase oxidase (NADPH) using an ELISA assay. Results Reduced bone loss was demonstrated in animals in the SMK + RESV group as compared to those in the SMK + PLAC (P < 0.05) group on the basis of morphometric analysis. Resveratrol promoted higher levels of SIRT and SOD (P < 0.05) as well as reduced levels of NADPH oxidase (P < 0.05) were found in tissues derived from animals in the SMK + RESV group when compared to those in the SMK + PLAC group. Conclusion Resveratrol is an efficient therapeutic agent that reduces exacerbation of bone loss found in animals with EP that were also exposed to smoke. The results suggest that its effects could be mediated, at least in part, by its antioxidant and anti‐inflammatory properties which attenuate the effects of oxidative stress on EP in the presence of cigarette smoke.

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Section: Discussionsupporting

confidence: 91%

Resveratrol attenuates oxidative stress during experimental periodontitis in rats exposed to cigarette smoke inhalation

Corrêa¹,

Absy²,

Tenenbaum

et al. 2018

J of Periodontal Research

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“…Western blotting for the determination of protein level of Nrf2 and HO‐1 was carried out according to the methods described previously . Briefly, whole protein lysates were obtained from hPLFs and then separated by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis (SDS‐PAGE) on 10% gels followed by electroblotting onto polyvinylidene difluoride membrane.…”

Section: Methodsmentioning

confidence: 99%

Oral supplementation with p‐coumaric acid protects mice against diabetes‐associated spontaneous destruction of periodontal tissue

Bhattarai

Min

Jeon

et al. 2019

J of Periodontal Research

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Objective Dietary bioactive materials having anti‐inflammatory and antioxidant potentials are able to inhibit diabetes‐associated periodontal complications. Although numerous studies indicate that administration of p‐coumaric acid (p‐CA) ameliorates diabetes and diabetes‐related complications, the roles of p‐CA on periodontal tissue destruction in diabetic mice and the possible mechanisms therein are not completely understood. In this study, we evaluated whether supplementation with p‐CA protects mice against diabetes‐associated spontaneous periodontal destruction and also explored the associated mechanism therein using in vivo and in vitro experimental systems. Materials and Methods C57BL/6 male mice were divided into sham, streptozotocin (STZ), and STZ+CA groups (n = 5/group). Sham group was intraperitoneally injected with sodium buffer, whereas other two groups were injected with the buffer containing 160 mg/kg of STZ. STZ‐induced diabetic mice received oral gavage with p‐CA (50 mg/kg) (STZ+CA group) or with buffer only (STZ group) daily for 6 weeks. The effect of p‐CA on diabetes‐associated spontaneous periodontal destruction was evaluated using μCT analysis, hematoxylin and eosin staining, tartrate‐resistant acid phosphatase staining, and immunohistochemical staining methods. The efficacies of p‐CA on cell proliferation, osteoblast differentiation, reactive oxygen species (ROS) accumulation, and antioxidant‐related marker expression were examined using human periodontal ligament fibroblasts (hPLFs) cultured under high glucose condition. Results Streptozotocin group exhibited periodontal tissue destruction along with increased inflammation, oxidative stress, and osteoclast formation, as well as with decreased osteogenesis. However, oral administration with p‐CA protected mice against STZ‐induced periodontal destruction by inhibiting inflammation and osteoclastic activation. STZ+CA group also showed higher expression of antioxidant and osteogenic markers in periodontal tissue than did STZ group. Treatment with high glucose concentration (30 mmol/L) impaired proliferation and osteoblast differentiation of hPLFs along with cellular ROS accumulation, whereas these impairments were almost completely disappeared by supplementation with p‐CA. Conclusion These findings demonstrate that supplementation with p‐CA inhibits diabetes‐associated spontaneous destruction of periodontal tissue by enhancing anti‐inflammatory, anti‐osteoclastogenic, and antioxidant defense systems in STZ‐treated mice.

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“…In addition, neutrophils from patients with severe chronic periodontitis exhibited hyper-reactivity to bacterial stimuli (Dias et al, 2013). Conversely, activation of NRF2 prevented alveolar bone loss in an experimental animal study (Bhattarai et al, 2016). In this context, downregulation of NRF2 pathway might lead to the increase in ROS, which causes tissue destruction.…”

Section: Mechanisms That Protect Against Oxidative Stressmentioning

confidence: 99%

“…Indeed, RANKL stimulation decreases expression of NRF2-dependent cytoprotective enzymes, thereby facilitating intracellular ROS signaling (Kanzaki et al, 2013, 2016b). Induction of cytoprotective enzymes by NRF2 activation subsequently inhibits osteoclastogenesis (Kanzaki et al, 2013, 2014, 2015; Sakai et al, 2013; Gambari et al, 2014; Lee et al, 2014; Lu et al, 2015; Bhattarai et al, 2016). Inversely, augmented osteoclastogenesis and bone destruction was observed with NRF2 deficiency (Rana et al, 2012; Hyeon et al, 2013; Ibanez et al, 2014; Lippross et al, 2014; Sun et al, 2015).…”

Section: Mechanisms That Protect Against Oxidative Stressmentioning

confidence: 99%

Pathways that Regulate ROS Scavenging Enzymes, and Their Role in Defense Against Tissue Destruction in Periodontitis

et al. 2017

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Periodontitis, an inflammatory disease that affects the tissues surrounding the teeth, is a common disease worldwide. It is caused by a dysregulation of the host inflammatory response to bacterial infection, which leads to soft and hard tissue destruction. In particular, it is the excessive inflammation in response to bacterial plaque that leads to the release of reactive oxygen species (ROS) from neutrophils, which, then play a critical role in the destruction of periodontal tissue. Generally, ROS produced from immune cells exhibit an anti-bacterial effect and play a role in host defense and immune regulation. Excessive ROS, however, can exert cytotoxic effects, cause oxidative damage to proteins, and DNA, can interfere with cell growth and cell cycle progression, and induce apoptosis of gingival fibroblasts. Collectively, these effects enable ROS to directly induce periodontal tissue damage. Some ROS also act as intracellular signaling molecules during osteoclastogenesis, and can thus also play an indirect role in bone destruction. Cells have several protective mechanisms to manage such oxidative stress, most of which involve production of cytoprotective enzymes that scavenge ROS. These enzymes are transcriptionally regulated via NRF2, Sirtuin, and FOXO. Some reports indicate an association between periodontitis and these cytoprotective enzymes' regulatory axes, with superoxide dismutase (SOD) the most extensively investigated. In this review article, we discuss the role of oxidative stress in the tissue destruction manifest in periodontitis, and the mechanisms that protect against this oxidative stress.

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Resveratrol prevents alveolar bone loss in an experimental rat model of periodontitis

Cited by 187 publications

References 46 publications

Resveratrol attenuates oxidative stress during experimental periodontitis in rats exposed to cigarette smoke inhalation

Resveratrol attenuates oxidative stress during experimental periodontitis in rats exposed to cigarette smoke inhalation

Oral supplementation with p‐coumaric acid protects mice against diabetes‐associated spontaneous destruction of periodontal tissue

Pathways that Regulate ROS Scavenging Enzymes, and Their Role in Defense Against Tissue Destruction in Periodontitis

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