Analysis of HIF-1α, MDA, and GPX4 in Peri-Implant Crevicular Fluid
NCT ID: NCT06863116
Last Updated: 2025-03-07
Study Results
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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COMPLETED
45 participants
OBSERVATIONAL
2023-05-15
2024-07-16
Brief Summary
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A total of 45 participants with 62 dental implants were included in the study. They were divided into three groups: peri-implant health, peri-implant mucositis, and peri-implantitis. Peri-implant crevicular fluid (PICF) samples were collected, and the levels of HIF-1α, GPX-4, and MDA were measured using laboratory tests.
The study aims to determine whether hypoxia affects ferroptosis-related pathways by altering GPX-4 and MDA levels. Understanding these mechanisms could provide new insights into peri-implant disease progression and help develop improved treatment strategies.
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Detailed Description
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This cross-sectional study aims to evaluate the relationship between hypoxia and ferroptosis in peri-implant diseases by measuring the levels of HIF-1α, GPX-4, and MDA in peri-implant crevicular fluid (PICF). A total of 45 participants with 62 dental implants were included in the study, categorized into peri-implant health (PH), peri-implant mucositis (PM), and peri-implantitis (PP) groups. PICF samples were collected using standardized paper strips, and biomarker levels were quantified via enzyme-linked immunosorbent assay (ELISA). Statistical analyses, including Kruskal-Wallis and Spearman correlation tests, were performed to assess differences among groups and potential associations between biomarkers.
The findings demonstrated that MDA levels were significantly lower in the peri-implantitis and peri-implant mucositis groups compared to peri-implant health, while GPX-4 levels were elevated in peri-implant mucositis and decreased in peri-implantitis. HIF-1α levels showed no significant differences among groups, but a positive correlation was observed between HIF-1α and GPX-4, suggesting a potential interaction between hypoxia and ferroptotic regulation in peri-implant tissues. These results imply that hypoxic conditions in peri-implant diseases may inhibit ferroptosis by modulating GPX-4 activity and reducing lipid peroxidation.
The study provides novel insights into the pathophysiology of peri-implant diseases, suggesting that the peri-implant microenvironment may exhibit unique regulatory mechanisms affecting ferroptotic pathways. While these findings contribute to our understanding of peri-implant disease pathogenesis, further longitudinal studies are needed to establish causal relationships and explore potential therapeutic strategies targeting hypoxia-ferroptosis interactions.
Conditions
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Study Design
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CASE_CONTROL
CROSS_SECTIONAL
Study Groups
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Peri-Implant Health
Participants with no clinical signs of peri-implant disease. These individuals exhibit healthy peri-implant soft tissues with no bleeding on probing (BOP), probing depth (PD) ≤ 4 mm, and no radiographic bone loss.
No interventions assigned to this group
Peri-Implant Mucositis
Participants diagnosed with peri-implant mucositis, characterized by bleeding on probing (BOP) and/or signs of inflammation (redness, swelling), but without radiographic bone loss beyond early remodeling.
No interventions assigned to this group
Peri-Implantitis
Participants diagnosed with peri-implantitis, defined by increased probing depth (PD \> 5 mm), bleeding on probing (BOP) or suppuration, and radiographic evidence of bone loss beyond initial remodeling.
No interventions assigned to this group
Eligibility Criteria
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Inclusion Criteria
* No history of systemic diseases.
* No periodontal treatments (surgical or non-surgical) in the past six months.
* No use of antibiotics or other medications within the past six months.
Exclusion Criteria
Diabetes mellitus Rheumatoid arthritis Cardiovascular disorders Immunological disorders Mucocutaneous diseases Contagious or communicable diseases
* Medication use, including:
Immunosuppressants Steroids Non-steroidal anti-inflammatory drugs (NSAIDs) Antiepileptics Calcium channel blockers Beta-blockers Anticoagulants Hormonal contraceptives Nutritional supplements
* Pregnant or lactating women.
* Use of orthodontic appliances or removable partial dentures.
* Poorly maintained implant-supported prostheses that may interfere with peri-implant crevicular fluid collection.
18 Years
ALL
Yes
Sponsors
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Ege University
OTHER
Responsible Party
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Büşra Yılmaz
Professor
Locations
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Ege University, Faculty of Dentistry, Department of Periodontology
Izmir, , Turkey (Türkiye)
Countries
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References
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Gao X, Hu W, Qian D, Bai X, He H, Li L, Sun S. The Mechanisms of Ferroptosis Under Hypoxia. Cell Mol Neurobiol. 2023 Oct;43(7):3329-3341. doi: 10.1007/s10571-023-01388-8. Epub 2023 Jul 17.
Hsieh CH, Lin YJ, Chen WL, Huang YC, Chang CW, Cheng FC, Liu RS, Shyu WC. HIF-1alpha triggers long-lasting glutamate excitotoxicity via system xc- in cerebral ischaemia-reperfusion. J Pathol. 2017 Feb;241(3):337-349. doi: 10.1002/path.4838. Epub 2016 Dec 29.
Fan Y, Ma L, Fang X, Du S, Mauck J, Loor JJ, Sun X, Jia H, Xu C, Xu Q. Role of hypoxia-inducible-factor-1alpha (HIF-1alpha) in ferroptosis of adipose tissue during ketosis. J Dairy Sci. 2024 Dec;107(12):10611-10627. doi: 10.3168/jds.2024-24822. Epub 2024 Jul 26.
Afacan B, Ozturk VO, Pasali C, Bozkurt E, Kose T, Emingil G. Gingival crevicular fluid and salivary HIF-1alpha, VEGF, and TNF-alpha levels in periodontal health and disease. J Periodontol. 2019 Jul;90(7):788-797. doi: 10.1002/JPER.18-0412. Epub 2018 Dec 11.
Xing L, Dong W, Chen Y, Dai W, Xiao X, Liu Z, Zhang X, Bai D, Xu H. Fibroblast ferroptosis is involved in periodontitis-induced tissue damage and bone loss. Int Immunopharmacol. 2023 Jan;114:109607. doi: 10.1016/j.intimp.2022.109607. Epub 2022 Dec 22.
Qiao S, Li B, Cai Q, Li Z, Yin Z, He J, Li Y, Meng W. Involvement of ferroptosis in Porphyromonas gingivalis lipopolysaccharide-stimulated periodontitis in vitro and in vivo. Oral Dis. 2023 Nov;29(8):3571-3582. doi: 10.1111/odi.14292. Epub 2022 Jul 12.
Other Identifiers
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23-4.1T/14
Identifier Type: -
Identifier Source: org_study_id
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