Journals / Selcuk Dental Journal / 2021 / Cilt: 8 - Sayı: 1

Periodontal Disease and Cardiovascular Diseases

Periodontal Hastalık ve Kardiyovasküler Hastalıklar

Pages
229–237
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

These review focuses on the possible mechanisms between periodontal disease and cardiovascular disease.

📌 3 Key Takeaways

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Objective & Hypothesis:Inflammation plays a role in the pathogenesis of periodontal and cardiovascular diseases.
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Key Findings & Data:Systemic circulatory infiltration of periodontal pathogens through inflamed and ulcerated gingival epithelium is considered to be a possible mechanism.
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Conclusion & Impact:These review focuses on the possible mechanisms between periodontal disease and cardiovascular disease.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Inflammation plays a role in the pathogenesis of periodontal and cardiovascular diseases. Recent studies have indicated that periodontal disease may have an impact on the development and progression of cardiovascular disease. Oral pathogens detected in atheromatous lesions strengthen the possible link between the two diseases. Systemic circulatory infiltration of periodontal pathogens through inflamed and ulcerated gingival epithelium is considered to be a possible mechanism. Oral pathogens affecting vascular tissues as a result of bacterial infiltration are thought to progress in the systemic circulation and initiate destructive reactions to the cardiovascular structures. Additionally, ulcerated gingival epithelium is a source of proinflammatory cytokines/chemokines that may cause the synthesis of acute phase proteins. Chronic bacteriemia is able to stimulate the acquired immune response. Antibodies produced in response to periodontal pathogens can stimulate cross-reaction between endothelial cells and modified lipids. These reactions are believed to increase the lipid concentration within the vessel wall. Moreover, it is discussed that some antibodies and inflammatory cytokines increase the activation of macrophages in the atheroma by stimulating T helper-1 response. It is believed that all these mechanisms contribute to the initiation and progression of atherogenesis. These review focuses on the possible mechanisms between periodontal disease and cardiovascular disease.

Özet

Periodontal ve kardiyovasküler hastalıklar, patogenezinde enflamasyonun rol oynadığı durumlardır. Yakın dönemde yapılan çalışmalar, periodontal hastalığın kardiyovasküler hastalık oluşumu ve ilerlemesi üzerine etkili olabileceğini ortaya koymuştur. Aterom lezyonlarında tespit edilen oral patojenler iki hastalık arasındaki olası ilişkiyi kuvvetlendirmektedir. İltihaplı ve ülsere dişeti epiteli yolu ile periodontal patojenlerin sistemik dolaşıma infiltrasyonu olası mekanizma olarak kabul edilmektedir. Bakteriyel infiltrasyon sonucunda vasküler dokuları etkileyen oral patojenlerin, sistemik dolaşımda ilerleyerek kardiyovasküler sistem için zararlı reaksiyonları başlattıkları düşünülmektedir. Ayrıca, ülsere dişetinden proenflamatuvar sitokin/kemokin sızıntısı akut faz proteinlerinin sentezine neden olabilir. Kronik bakteriyemi kazanılmış bağışıklık cevabını etkileyebilir. Periodontal patojenlere cevap olarak üretilen antikorlar, endotel hücreleri ve modifiye lipidler arasındaki çapraz reaksiyonları uyarabilmektedir. Bu reaksiyonların damar duvarında lipid yoğunluğunu arttırabileceği düşünülmektedir. Bunlara ek olarak, bazı antikorların ve enflamatuvar sitokinlerin T yardımcı hücre-1 cevabını uyararak aterom lezyonlarındaki makrofajların aktivasyonunu arttırdıkları savunulmaktadır. Tüm bu mekanizmaların aterogenezin başlamasına ve ilerlemesine katkıda bulunduğu düşünülmektedir. Bu derleme, periodontal hastalık ve kardiyovasküler hastalık arasındaki ilişkide olası mekanizmalara değinmektedir.

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Cite This Article

KEŞİR, S. S. S., HENDEK, M. K., OLGUN, E. (2021). Periodontal Disease and Cardiovascular Diseases. Selcuk Dental Journal, Cilt: 8 - Sayı: 1, 229–237. https://ajindex.com/articles/319763

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