Abstract
The hypoxic microenvironment caused by oral pathogens is the most important cause of the disruption of dynamic hemostasis between the oral microbiome and the immune system. Periodontal infection exacerbates the inflammatory response with increased hypoxia and causes vascular changes. The chronicity of inflammation becomes systemic as a link between oral and systemic diseases. The vascular network plays a central role in controlling infection and regulating the immune response. In this review, we focus on the local and systemic vascular network change mechanisms of periodontal inflammation and the pathological processes of inflammatory diseases. Understanding how the vascular network influences the pathology of periodontal diseases and the systemic complication associated with this pathology is essential for the discovery of both local and systemic proactive control mechanisms.
Highlights
Overview of the Vascular Impact of Periodontal andOral InflammationPhysical barriers are the first lines of defense against pathogenic microorganisms.The skin covering the outer surface of the body and the mucosal surfaces covering the internal spaces prevent external agents, including the microorganisms, from penetrating deeper tissue compartments and causing disease in the host
This review focuses on local and systemic vascular network change mechanisms of periodontal inflammation and pathological processes of inflammatory diseases
The homeostatic dynamics of the oral cavity are constantly changing with microenvironmental conditions, histological differentiation, and contact of host and oral microorganisms
Summary
Physical barriers are the first lines of defense against pathogenic microorganisms. The skin covering the outer surface of the body and the mucosal surfaces covering the internal spaces prevent external agents, including the microorganisms, from penetrating deeper tissue compartments and causing disease in the host. Inflammation appears to be tissue-specific; it can lead to pathologies in distant tissues or organs when the process becomes chronic It is, plausible that there is a link between inflammatory diseases, considering that mediators, cells, and mechanisms play a similar role in local and systemic processes. Studies have shown that patients with atherosclerosis and periodontitis have similar cytokine profiles [1,15,16,17] with high pro-inflammatory cytokines such as IL-6 [18], TNF-α [19], and acute-phase proteins (e.g., CRP) [18,20] in serum These inflammatory mediators can trigger endothelial cell activation, leading to vascular inflammation, mononuclear cell inflammation, adhesion molecule expression, platelet aggregation, foam cell formation, and atherosclerotic plaque formation. This review focuses on local and systemic vascular network change mechanisms of periodontal inflammation and pathological processes of inflammatory diseases
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