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Bacteria in Dental Plaque and Atheroma Plaque

Bacteria in Dental Plaque and Atheroma Plaque

Status
Recruiting
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT07100574
Enrollment
60
Registered
2025-08-03
Start date
2024-12-10
Completion date
2026-03-30
Last updated
2025-08-03

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Atheroma Plaque, Dental Plaque, Gingival Inflammation, Oral Bacteria

Brief summary

Periodontitis is considered a focus of infection where oral bacteria, bacterial by-products or inflammatory mediators can interact with other parts of the organism via the blood. Periodontal pathogen components such as DNA, RNA or specific antigens of P. gingivalis, Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Treponema denticola (T. denticola), Fusobacterium nucleatum (F. nucleatum) or Campylobacter rectus have been isolated from different tissues such as atheroma plaques, placenta, amniotic sac and respiratory tract. It has been reported that periodontitis may contribute to endothelial dysfunction leading to the formation of atherosclerosis.

Detailed description

Periodontitis is considered a focus of infection where oral bacteria, bacterial by-products or inflammatory mediators can interact with other parts of the organism via the blood. Periodontal pathogen components such as DNA, RNA or specific antigens of P. gingivalis, Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Treponema denticola (T. denticola), Fusobacterium nucleatum (F. nucleatum) or Campylobacter rectus have been isolated from different tissues such as atheroma plaques, placenta, amniotic sac and respiratory tract. It has been reported that periodontitis may contribute to endothelial dysfunction leading to the formation of atherosclerosis. Severe chronic generalized periodontitis may result in systemic inflammation and endothelial dysfunction. Periodontal bacteria produce endotoxins in the form of lipopolysaccharide (LPS). Circulating LPS causes an early systemic inflammatory response in the intima. The aim of this study is to assess the relationship between bacteria in atheroma plaque, and dental plaque in patients grouped using the new periodontal classification. In addition, the relationship between demographic findings and bacterial count and frequency will be evaluated.

Interventions

During the endarterectomy procedure, samples will be collected for study from some of the atheroma plaques routinely taken for pathology from patients.

OTHERdental plaque

Subgingival plaque samples will be collected from patients before the endarterectomy procedure.

Sponsors

Istanbul Saglik Bilimleri University
Lead SponsorOTHER

Study design

Observational model
OTHER
Time perspective
CROSS_SECTIONAL

Eligibility

Sex/Gender
ALL
Age
18 Years to 85 Years

Inclusion criteria

* Diagnosed with endarterectomy * Not receiving chemotherapy * Not having received this treatment before

Exclusion criteria

* Having systemic infection * Patients with severe heart disease

Design outcomes

Primary

MeasureTime frameDescription
Number of bacteriathrough study completion, an average of 2 monthsSubgingival plaque

Countries

Turkey (Türkiye)

Contacts

Primary ContactAyşe Toraman
draysetoraman@gmail.com05385025422

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026