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Background: Phthalates are widely used plasticizers, which were identified as risk factors in the development of many human diseases. However, the effects of phthalates in the periodontitis are unknown. We aimed to investigated the relationship of periodontitis and phthalate exposure as well as the underlying mechanisms., Materials and Methods: Univariate and multivariate logistic regressions were employed to evaluate the association between phthalate metabolites and periodontitis. The generalized additive model and piecewise logistic regression were conducted to investigate the dose-response relationship. Cell and animal models were used to explore the role and mechanism of DEHP in the development of periodontitis. Transcriptome sequencing, bioinformatics analysis, western blot, immunofluorescence and mice model of periodontitis were also employed., Results: MEHP (OR 1.14, 95% CI 1.05-1.24), MCPP (OR 1.08, 95% CI 1.00-1.17), MEHHP (OR 1.18, 95% CI 1.08-1.29), MEOHP (OR 1.18, 95% CI 1.07-1.29), MiBP (OR 1.15, 95% CI 1.04-1.28), and MECPP (OR 1.20, 95% CI 1.09-1.32) were independent risk factors. And MEHHP, the metabolite of DEHP, showed the relative most important effects on periodontitis with the highest weight (0.34) among all risk factors assessed. And the increase of inflammation and the activation of NFκB pathway in the periodontitis model mice and cells were observed., Conclusion: Exposure to multiple phthalates was positively associated with periodontitis in US adults between 30 and 80 years old. And DEHP aggravated inflammation in periodontitis by activating NFκB pathway., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Periodontal disease is the most common cause of tooth loss in humans, is an inflammatory disease initiated by oral microbial biofilm. Given the involvement of the inflammatory pathway in this type of pathology, the main pharmacological strategy for the treatment of periodontitis, is the inhibition of the inflammatory process in order to prevent tissue destruction and bone resorption, a condition associated with a painful state. To do this, the best class of drugs are Non-steroidal anti-inflammatory drugs (NSAIDs), however, the presence of side effects, especially at the gastrointestinal tract, limits their use for long-term therapy. Recently, some evidence shows that derivatives of NSAIDs capable of releasing hydrogen sulphide exhibit lower collateral effects, particularly at the gastric level. In fact, H2S is an endogenous gaseous mediator with a cytoprotective role at the gastric level. In this study, we have compared the protective effects of ketoprofen with ATB-352, a hydrogen sulfide-releasing derivative of ketoprofen, in an experimental model of periodontitis in rat. Periodontitis was induced by a single intragingival injection of 1 μl LPS (10 μg/μl), Our results show that 14 h after intragingival injection of LPS, there was a high tissue damage associated with bone resorption, and in gingivomucosal tissues there was a significant expression of NF-kb p65 and pro-inflammatory cytokine as well as a higher expression of COX-2 and iNOS, activation of the apoptotic process, and also increased levels of NGF expression, often associated with a higher nociceptive perception. Treatment with ATB-352 at the dose of 20mg\kg, was able to reduce the inflammatory process associated with intragingival LPS injection and also had a positive effect on bone resorption and tissue damage., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background and Overview: There is a lack of clinical research on the potential effect of cannabis use on the periodontium as well as its effect on treatment outcomes. The aim of this case report is to illustrate the clinical presentation of periodontal disease in a young woman who was a chronic cannabis user, as well as successful treatment involving motivating the patient to quit cannabis use and undergo nonsurgical and surgical therapy., Case Description: A 23-year-old woman sought care at the dental clinic for periodontal treatment. During a review of her medical history, the patient reported using cannabis frequently during a 3-year period, which coincided with the occurrence of gingival inflammation. She used cannabis in the form of cigarettes that were placed at the mandibular anterior region of her mouth for prolonged periods. Localized prominent papillary and marginal gingival enlargement of the anterior mandible were present. The mandibular anterior teeth showed localized severe chronic periodontitis. The clinicians informed the patient about the potentially detrimental consequences of continued cannabis use; she was encouraged to quit, which she did. The clinicians performed nonsurgical therapy (scaling and root planing) and osseous surgery. The treatment outcome was evaluated over 6 months; improved radiographic and clinical results were observed throughout the follow-up period., Conclusions and Practical Implications: Substantial availability and usage of cannabis, specifically among young adults, requires dentists to be vigilant about clinical indications of cannabis use and to provide appropriate treatments. Behavioral modification, nonsurgical therapy, and surgical therapy offer the potential for successful management of cannabis-related periodontitis., (Copyright © 2017 American Dental Association. Published by Elsevier Inc. All rights reserved.)

Background: The present study was designed to examine whether the intermittent local periodontal inflammation induces endothelial dysfunction of the systemic artery caused by oxidative stress and if increased levels of hydrogen peroxide coexisted with overexpression of superoxide dismutase (SOD) as well as NADPH oxidase contribute to the oxidative stress., Methods: The rats in lipopolysaccharides (LPS) group received 1500μg LPS injection to bilateral gingiva of the lower jaw a week interval from eight- to eleven-week-old. Isolated mandibles or aortas were subjected to the evaluation of histopathological changes, isometric force recordings, reactive oxygen species using 2',7'-dichlorofluorescin diacetate (10(-5)mol/L) and protein expression of NADPH oxidase subunits and SOD, respectively., Results: Mandible sections demonstrated the periodontal inflammation only in the LPS group at three days, but not seven days, after the LSP injection. Acetylcholine (10(-9) to 10(-5)mol/L)-induced relaxation was reduced only in aortas from the LPS group. Gp91ds-tat and PEG-catalase restored the impaired dilation in arteries from the LPS group. Levels of reactive oxygen species were enhanced in aortas from the LPS group, whereas the increment was abolished by the treatment with gp91-ds-tat or PEG-catalase. Expression of a NADPH oxidase subunit p47phox and CuZn-SOD increased in the LPS group., Conclusions: The intermittent local periodontal inflammation induces systemic endothelial dysfunction caused by overproduction of reactive oxygen species in the systemic artery of rats and that overexpression of CuZn-SOD as well as a NADPH oxidase cytosolic subunit contributes to increased levels of hydrogen peroxide in blood vessels of this animal model., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Resveratrol is an antioxidant and anti-inflammatory polyphenol. Periodontitis is induced by oral pathogens, where a systemic inflammatory response accompanied by oxidative stress is the major event initiating disease. We investigated how resveratrol modulates cellular responses and the mechanisms related to this modulation in lipopolysaccharide (LPS)-stimulated human gingival fibroblasts (hGFs). We also explored whether resveratrol protects rats against alveolar bone loss in an experimental periodontitis model. Periodontitis was induced around the first upper molar of the rats by applying ligature infused with LPS. Stimulating hGFs with 5μg/ml LPS augmented the expression of cyclooxygenase-2, matrix metalloproteinase (MMP)-2, MMP-9, and Toll-like receptor-4. LPS treatment also stimulated the production of reactive oxygen species (ROS) and the phosphorylation of several protein kinases in the cells. However, the expression of heme oxygenase-1 (HO-1) and nuclear factor-E2 related factor 2 (Nrf2) was inhibited by the addition of LPS. Resveratrol treatment almost completely inhibited all of these changes in LPS-stimulated cells. Specifically, resveratrol alone augmented HO-1 induction via Nrf2-mediated signaling. Histological and micro-CT analyses revealed that administration of resveratrol (5mg/kg body weight) improved ligature/LPS-mediated alveolar bone loss in rats. Resveratrol also attenuated the production of inflammation-related proteins, the formation of osteoclasts, and the production of circulating ROS in periodontitis rats. Furthermore, resveratrol suppressed LPS-mediated decreases in HO-1 and Nrf2 levels in the inflamed periodontal tissues. Collectively, our findings suggest that resveratrol protects rats from periodontitic tissue damage by inhibiting inflammatory responses and by stimulating antioxidant defense systems., Statement of Significance: The aims of this study were to investigate how resveratrol modulates cellular responses and the mechanisms related to this modulation in lipopolysaccharide (LPS)-stimulated human gingival fibroblasts (hGFs) and protects rats against alveolar bone disruption in an experimental periodontitis model. Our findings suggest that resveratrol protects rats from periodontitic tissue damage by inhibiting inflammatory responses and by stimulating antioxidant defense systems. On the basis of our experiment studies, we proposed that resveratrol could be used as novel bioactive materials or therapeutic drug for the treatment of periodontitis or other inflammatory bone diseases like osteoporosis, arthritis etc. Furthermore, it could be also used for the modification or coating of implant materials as an antiinflammatory molecules which will help to accelerate bone formation. There are a few of reports suggesting antioxidant and anti-inflammatory potentials of resveratrol. However, our results highlight the cellular mechanisms by which resveratrol inhibits LPS-mediated cellular damages using human-originated gingival fibroblasts and also support the potential of resveratrol to suppress periodontitis-mediated tissue damages. We believe that the present findings might improve a clinical approach of using of resveratrol on human, although further detailed experiments will be needed., (Copyright © 2015 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.)

Objective: The aim of this study was to investigate the oral mucosal disorders associated with habitual gutka consumption., Methods: Databases were searched from 1956 to June 2009 using the following terms: "gutka," "gutkha," "ghutka," "guttkha," "smokeless tobacco," "areca nut," "betel nut," "slaked lime," "dental," "oral," "periodontal," "inflammation," "submucous fibrosis," "carcinoma," and "cancer." The eligibility criteria included: human and experimental studies, use of control subjects, and articles published in English. Unpublished data were not sought. Odds ratios (ORs) and 95% confidence intervals (CIs) were computed., Results: Twelve studies were included. Three studies associated gutka consumption with periodontal inflammation (ORs 1.64 [CI 1.2-2.1], 2.20 [CI 1.1-4.9], and 3.56 [CI 1.9-5.5]). Five studies showed a direct relationship between gutka usage and oral submucous fibrosis (ORs 1.65 [CI 1.2-2.3], 2.33 [CI 1.9-4.5], 2.98 [CI 1.5-3.9], 3.56 [CI 1.3-4.7], and 5.08 [CI 3.7-6.4]). An increased frequency of gutka usage was associated with malignant transformations in oral submucous fibrosis by 2 studies (ORs 4.59 [CI 2-5.6] and 18 [CI 5.8-61.6]). Two studies showed an extension of oral submucous fibrosis into the hypopharynx and esophagus in gutka users (ORs 4.59 [CI 2-5.6] and 33 [CI 2.2-46.6])., Conclusions: Habitual gutka usage is associated with severe oral mucosal disorders, and the consequences may extend beyond the oral cavity., (Copyright 2010 Mosby, Inc. All rights reserved.)