Efficacy of combined orthodontic-periodontic treatment for patients with periodontitis and its effect on inflammatory cytokines: A comparative study

Zhang, Jin; Zhang, Aimin; Zhang, Zong-Mei; Jia, Jinlin; Sui, Xinxin; Yu, Lu-Rui; Liu, Haitao

doi:10.1016/j.ajodo.2017.01.028

Cited by 33 publications

(25 citation statements)

References 18 publications

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“…Concentration of GCF IL-1β and TNF-α were extensively studied in local inflammatory conditions as periodontitis 35,36,37,38 and perimplantitis 39,40,41,42,43,44 or even as a systemic inflammatory condition like diabetes 45,46 or connective tissue disease 47,48,49,50 . Comparing to these inflammatory conditions, cytokines were infrequently investigated in dental caries, especially in GCF of caries teeth 51,52,53 .…”

Section: Discussionmentioning

confidence: 99%

The effect of dental caries and restorative biomaterials on IL-1 β and TNF-α levels in the gingival crevicular fluid

et al. 2021

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Background/Aim.To estimate the concentrations of the proinflammatory cytokines (IL-1β TNF-in the gingival crevicular fluid (GCF) samples from caries affected teeth and intact teeth, and to correlate them with caries extension, tooth position, and different restorative biomaterials. Methods.GCF samples were collected from the 90 periodontally healthy patients demonstrating at least one tooth with proximal caries and one intact tooth, at the baseline, 7 and 30 days post-treatment. The biomarkers profile was investigated in relation to the different level of caries extension (superficial, pulpitis, gangrenous, root affection), defect size and restorative biomaterial. Results. Before therapy, caries level was significantly associated with GCF IL-1β concentration, demonstrating lowest level in gangrenous (C4) and superficial caries (C2). 30d after therapy, root affection (C5) was characterized by the highest IL-1β concentration. Different dental fillings showed various GCF cytokine change. CPC induced a significant IL-1β increase in more than 70% of treated patients. Caries lesion size was insignificantly associated with GCF levels of these proinflammatory cytokines, where larger defects were followed with average cytokine increase. Considering tooth position, before therapy, IL-1β had the highest level in GCF samples from caries affected canines and second molars while TNF-α showed highest levels from canines GCF. Dental restoration induced cytokine increase in canines (IL-1β and TNF-α), 1st and 2nd molars GCF (IL-1β). Conclusion. Before inflammation intensity of tooth structures was directly reflected with IL-1β and TNF-α concentration. Dental restoration significantly affects IL-1β and TNF-α depending on the used dental filling-type material. Profile of these cytokines varied in GCF samples of the tooth with different anatomical position, where canines and molars demonstrated the highest level. An increase of these proinflammatory cytokines in the absence of any symptomatic manifestation of inflammatory response has to be reconsidered as a possible tooth reparation parametar. Clinical relevance. The concentration of GCF cytokines is illustrative in depicting processes in tooth structures. Their relevance must be inspected with aspects of tooth position and caries lesion level. Different impact of dental restoration materials on GCF IL-1β and TNF-αcould be used as parameter for estimating local inflammation.

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Section: Discussionmentioning

confidence: 99%

The effect of dental caries and restorative biomaterials on IL-1 β and TNF-α levels in the gingival crevicular fluid

et al. 2021

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“…Gingivitis is thought to be an early periodontal disease that may or may not develop into periodontitis (Van Dyke et al, 1986). Periodontitis is a chronic inflammatory disease of dental support tissue with high incidence and alternating relief and acute exacerbation (Zhang et al, 2017). Periodontitis is described as persistent leukocyte infiltration, possibly regulated by the production of topical chemokine, but its pathogenesis has not been fully elucidated (Bostrom et al, 2015).…”

Section: Periodontal Diseasesmentioning

confidence: 99%

A Review of the Anti-Inflammatory Effects of Rosmarinic Acid on Inflammatory Diseases

et al. 2020

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Inflammatory diseases are caused by abnormal immune responses and are characterized by an imbalance of inflammatory mediators and cells. In recent years, the antiinflammatory activity of natural products has attracted wide attention. Rosmarinic acid (RosA) is a water-soluble phenolic compound that is an ester of caffeic acid and 3, 4dihydroxyphenyl lactic acid. It is discovered in many plants, like those of the Boraginaceae and Lamiaceae families. RosA has a wide range of pharmacological effects, including antioxidative, anti-apoptotic, anti-tumorigenic, and anti-inflammatory effects. The antiinflammatory effects of RosA have been revealed through in vitro and in vivo studies of various inflammatory diseases like arthritis, colitis, and atopic dermatitis. This article mainly describes the preclinical research of RosA on inflammatory diseases and depicts a small amount of clinical research data. The purpose of this review is to discuss the antiinflammatory effects of RosA in inflammatory diseases and its underlying mechanism.

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“…Periodontitis is one of the most common infectious diseases and the main reason for tooth loss worldwide (Frencken et al., 2017). Periodontitis is characterized by the loss of alveolar bone periodontal ligament and gingival tissue, and is resulted from various factors, including traumatic misalignment of the teeth, the deposition of bacterial plaque on the teeth, and imbalance of the inflammatory and immune response (Ahmad et al., 2019; Zhang et al., 2017). Additionally, periodontitis is closely associated with systemic disease, including cancer, hypertension, cardiovascular disease, and dementia (Barton, 2017; Harding, Robinson, Crean, & Singhrao, 2017; Merchant & Virani, 2017).…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA TUG1 participates in LPS‐induced periodontitis by regulating miR‐498/RORA pathway

Huang

Sun

et al. 2020

Oral Diseases

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Aim This study was aimed to investigate the role of TUG1 in LPS‐stimulated hPDLCs and to evaluate the potential functions of TUG1 in the pathogenesis of periodontitis. Methods LPS‐stimulated hPDLCs were established as the cell model. CCK‐8 assay was performed to assess cell proliferation ability. Flow cytometry was performed to detect cell cycle distribution, and quantitative RT‐PCR and Western blotting were conducted to measure gene expressions. ELISA kits were used to evaluate the production of inflammatory cytokines. The putative binding site between TUG1 and miR‐498 was verified using luciferase reporter and RNA immunoprecipitation assays. Results TUG1 was downregulated upon LPS stimulation in hPDLCs. TUG1 overexpression promoted cell proliferation through regulating the cell cycle distribution, along with the decreased expression of p21 and increased expression of CDK2 and cyclin D1. Besides, TUG1 overexpression decreased the production of inflammatory cytokines. The effects were opposite upon TUG1 knockdown. TUG1 negatively regulated its target miR‐498, and influenced the expression of RORA, the direct target of miR‐498. Simultaneous TUG1 overexpression and miR‐498 reversed the effect of TUG1 overexpression alone on alleviating LPS‐induced cell injury and inhibition of Wnt/β‐catenin signaling, which was further changeover after co‐overexpression with RORA. Conclusion Therefore, TUG1 could protect against periodontitis via regulating miR‐498/RORA mediated Wnt/β‐catenin signaling.

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Efficacy of combined orthodontic-periodontic treatment for patients with periodontitis and its effect on inflammatory cytokines: A comparative study

Cited by 33 publications

References 18 publications

The effect of dental caries and restorative biomaterials on IL-1 β and TNF-α levels in the gingival crevicular fluid

The effect of dental caries and restorative biomaterials on IL-1 β and TNF-α levels in the gingival crevicular fluid

A Review of the Anti-Inflammatory Effects of Rosmarinic Acid on Inflammatory Diseases

Long non‐coding RNA TUG1 participates in LPS‐induced periodontitis by regulating miR‐498/RORA pathway

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