Experimental gingivitis induces systemic inflammatory markers in young healthy individuals: a single-subject interventional study
Open accessAbstract
OBJECTIVES: We here investigated whether experimental gingivitis enhances systemic markers of inflammation which are also known as surrogate markers of atherosclerotic plaque development. BACKGROUND: Gingivitis is a low-level oral infection induced by bacterial deposits with a high prevalence within Western populations. A potential link between the more severe oral disease periodontitis and cardiovascular disease has already been shown. METHODS: 37 non-smoking young volunteers with no inflammatory disease or any cardiovascular risk factors participated in this single-subject interventional study with an intra-individual control. Intentionally experimental oral inflammation was induced by the interruption of oral hygiene for 21 days, followed by a 21-days resolving phase after reinitiation of oral hygiene. Primary outcome measures at baseline, day 21 and 42 were concentrations of hsCRP, IL-6, and MCP-1, as well as adhesion capacity and oxLDL uptake of isolated blood monocytes. RESULTS: The partial cessation of oral hygiene procedures was followed by the significant increase of gingival bleeding (34.0%, P<0.0001). This local inflammation was associated with a systemic increase in hsCRP (0.24 mg/L, P = 0.038), IL-6 (12.52 ng/L, P = 0.0002) and MCP-1 (9.10 ng/l, P = 0.124) in peripheral blood samples between baseline and day 21, which decreased at day 42. Monocytes showed an enhanced adherence to endothelial cells and increased foam cell formation after oxLDL uptake (P<0.050) at day 21 of gingivitis. CONCLUSIONS: Bacterial-induced gingival low-level inflammation induced a systemic increase in inflammatory markers. Dental hygiene almost completely reversed this experimental inflammatory process, suggesting that appropriate dental prophylaxis may also limit systemic markers of inflammation in subjects with natural gingivitis. International Clinical Trials Register Platform of the World Health Organization, registry number: DRKS00003366, URL: http://apps.who.int/trialsearch/Default.aspx.
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Although mechanisms were not directly tested, the attenuated vasodilation may be caused by elevated systemic inflammation due to increased diffusion of extravascular metabolic products from oral plaque.
“Although we did not directly test mechanisms, the attenuated vasodilation may be caused by the elevated level of systemic inflammation because of the increased diffusion of extravascular metabolic products from the oral plaque (6, 8, 15, 32, 34).”
From Oral inflammatory load predicts vascular function in a young adult population: a pilot study (2023) · cites this paper as [34]
The Results and Discussion report elevated systemic inflammatory markers during experimental gingivitis. The Discussion also proposes that oral biofilm organisms or their products can enter the circulation, while saying the mechanisms remain largely unknown. The paper does not link this process to attenuated vasodilation or specifically describe diffusion of extravascular metabolic products from oral plaque. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMetabolic products in plaque bacteria can move via diffusion into the blood stream, thereby enhancing systemic inflammation.
“The metabolic products in the plaque bacteria can move via diffusion into the blood stream thereby enhancing systemic inflammation (34).”
From Oral inflammatory load predicts vascular function in a young adult population: a pilot study (2023) · cites this paper as [34]
The Discussion says that gingival ulceration can facilitate the entry of biofilm organisms or their products into the circulation, and that circulating infection products can increase inflammatory markers. It does not identify those products as metabolic products or describe diffusion as their route into the bloodstream. (LLM, conf=0.86)
Experimental — accuracy not yet measuredExtravascular metabolic products can enhance systemic inflammatory cytokines and may lead to disruptive effects on the endothelium, including reduced ability to produce nitric oxide.
“These extravascular metabolic products can enhance systemic inflammatory cytokines (34) and may lead to disruptive effects on the blood vessel's endothelium, including the reduced ability for the endothelium to produce nitric oxide (6, 7, 30, 31).”
From Oral inflammatory load predicts vascular function in a young adult population: a pilot study (2023) · cites this paper as [34]
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- Authors
- Eberhard, J., Grote, K., Luchtefeld, M., Heuer, W., Schuett, H., Divchev, D., Scherer, R., Schmitz-Streit, R., Langfeldt, D., Stumpp, N., Staufenbiel, I., Schieffer, B., & Stiesch, M.
- Affiliations
- Medizinische Hochschule Hannover (DE)
- Christian-Albrechts-Universität zu Kiel (DE)
- Corresponding author
- Eberhard, Jörg
- ORCID
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-02-07
- Volume
- 8
- Issue
- 2
- Pages
- e55265
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3567060
- OpenAlex
- W2071694400
- Cited by
- 75
- References
- 46
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 5 · 2023: 6 · 2022: 6 · 2021: 8 · 2020: 7 · 2019: 7 · 2018: 5 · 2017: 5 · 2016: 10 · 2015: 2 · 2014: 2 · 2013: 1
- FWCI
- 6.08
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- Deutsche Forschungsgemeinschaft (EB 223/5-1)
- Topics
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Health Sciences › Health Professions › Pharmacy › Oral and gingival health research
- Health Sciences › Dentistry › General Dentistry › Dental Research and COVID-19
- Keywords
- experimental gingivitis, systemic inflammation, atherosclerosis, high-sensitivity C-reactive protein, interleukin-6, MCP-1, monocyte adhesion, oxidized LDL uptake, foam cell formation, oral hygiene, dental prophylaxis, gingival bleeding, cardiovascular risk, periodontitis
- MeSH terms
- Adult, Base Sequence, Cells, Cultured, Dental Plaque, Female, Gingivitis, Humans, Inflammation, Male, Reference Values, Biomarkers, Polymerase Chain Reaction, DNA Primers, Young Adult
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